Psilocybin analogs, salts, compositions, and methods of use

Abstract

The present disclosure relates to psilocin compounds and pharmaceutically acceptable salts, polymorphs, stereoisomers, or solvates thereof, to pharmaceutical compositions, and in some embodiments, to serotonin 5-HT2 receptor agonists and uses in the treatment of diseases associated with a 5-HT2 receptor.

Description

CROSS REFERENCE TO RELATED APPLICATIONS This application claims the benefit of U.S. Provisional Application No. 63 / 162,749 filed March 18, 2021, and U.S. Provisional Application No. 63 / 276,117 filed November 5, 2021, each incorporated herein by reference in its entirety. FIELD The present disclosure relates generally to psilocin compounds and pharmaceutically acceptable salts, polymorphs, stereoisomers, or solvates thereof, compositions, and, in some embodiments, to serotonin 5-HT2 receptor agonists and uses in the treatment of diseases associated with a 5-HT2 receptor. BACKGROUND Psilocybin (PY) and psilocin (PI) are tryptamine alkaloids and structural analogs of the neurotransmitter serotonin. Psilocybin is a prodrug of psilocin. That is, when consumed, psilocybin is rapidly metabolized into the active form, psilocin (4-hydroxy-N,N-dimethyltryptamine). Specifically, a chemical process called dephosphorylation removes the phosphate group on psilocybin, creating psilocin. Psaocytm ■              Psilocin.-                   Serotorw Outside the body, psilocin is reported to be a short-lived and unstable molecule. Therefore, therapeutic applications involving the use of psilocin are generally accomplished by administration of the precursor, psilocybin, or other prodrug approaches. However, psilocybin has slow onset and a long duration of drug action, often requiring 7-8 hours of supervised clinical observation of a patient before discharge. Therefore, there is a need for a stabilized psilocin, that does not rely on breakdown of a prodrug to provide pharmacologically active drug, and that has a faster / quicker therapeutic onset and a shorter duration of drug action (i.e., shorter duration of therapeutic effect) than psilocybin. SUMMARY The present disclosure is based at least in part on the identification of novel stabilized forms of psilocin and deuterated psilocin, including novel polymorphs of psilocin / deuterated psilocin, novel salt forms of psilocin / deuterated psilocin and their polymorphs, as well as compositions thereof, which provide a fast therapeutic onset, a shortened duration of drug action, and less variability in drug exposure (e g., compared to psilocybin or other prodrug approaches), and methods of using the same to treat diseases associated with a serotonin 5-HT2 receptor. More specifically, the present disclosure provides stabilized forms of psilocin and deuterated psilocin and compositions thereof, that can be used to treat neuropsychiatric disorders, central nervous system (CNS) disorders, and other disorders, such as those associated with inflammation, for example, through various dosing regimens (e.g., once-daily, once-weekly, sub-psychedelic dosing, etc.) to selectively engage 5-HT2aRs without producing psychedelic side effects. The disclosed stabilized forms of psilocin and deuterated psilocin do not rely on prodrug metabolism for release of active agent, as is the case with psilocybin administration or related prodrug approaches, and thus have a faster / quicker therapeutic onset, a shorter duration of drug action (i.e., short duration of therapeutic effect), and less inter-subject variability. Further, certain dosage forms of these stabilized forms of psilocin and deuterated psilocin, such as oral disintegrating tablets (ODT) and immediate release (IR) tablets, have also been found to enhance these stability and / or fast onset characteristics, as they provide for immediate disintegration and rapid release of the compounds / salts herein—particularly ODT and related dosage forms which allow for pre-gastric absorption of the compounds / salts herein, e.g., when administered through the mucosal linings of the oral cavity. Thus, the present disclosure provides: (1) A pharmaceutically acceptable salt of a compound of Formula (I), or a polymorph, stereoisomer, or solvate thereof, r8 ----- r7 wherein: R2, Rs, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium, Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, and Xi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium. (2) The pharmaceutically acceptable salt of (1), wherein R2, Rs, Re, and R7 are hydrogen. (3) The pharmaceutically acceptable salt of (1), wherein at least one of R2, Rs, Re, and R7 is deuterium. (4) The pharmaceutically acceptable salt of any one of (1) to (3), wherein Rs and Rgare -CH3. (5) The pharmaceutically acceptable salt of any one of (1) to (3), wherein Rs and Rgare -CD3. (6) The pharmaceutically acceptable salt of any one of (1) to (5), wherein Xi, X2, Yi, and Y2 are deuterium. (7) The pharmaceutically acceptable salt of any one of (1) to (6), wherein Xi and X2 are 3 deuterium. (8) The pharmaceutically acceptable salt of any one of (1) to (7), wherein Yi and Y2 are deuterium. (9) The pharmaceutically acceptable salt of any one of (1) to (5) or (7), wherein Yi and Y2 are hydrogen. (10) The pharmaceutically acceptable salt of any one of (1) to (9), wherein the compound of Formula (I) is selected from the group consisting of: D                                   (1-1), D                                   (1-2), (1-4), (1-6), (1-8), (11) The pharmaceutically acceptable salt of any one of (1) to (10), wherein the compound of Formula (I) is (12) The pharmaceutically acceptable salt of any one of (1) to (10), wherein the compound of Formula (I) is (13) The pharmaceutically acceptable salt of any one of (1) to (12), wherein the compound of Formula (I) is an agonist of a serotonin 5-HT2 receptor. (14) The pharmaceutically acceptable salt of any one of (1) to (13), wherein the compound of Formula (I) is an agonist of a serotonin 5-HT2A receptor. (15) The pharmaceutically acceptable salt of any one of (1) to (14), which is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, a salicylate salt, an ascorbate salt, a hydrochloride salt, a maleate salt, a malate salt, a methanesulfonate salt, a toluenesulfonate salt, a glucuronate salt, or a glutarate salt of the compound of Formula (I). (16) The pharmaceutically acceptable salt of any one of (1) to (15), which is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, or a salicylate salt of the compound of Formula (I). (17) The pharmaceutically acceptable salt of any one of (1) to (16), which is a benzenesulfonate salt or a benzoate salt of the compound of Formula (I). (18) The pharmaceutically acceptable salt of any one of (1) to (17), which is a benzenesulfonate salt of the compound of Formula (I). (19) The pharmaceutically acceptable salt of any one of (1) to (17), which is a benzoate salt of the compound of Formula (I). (20) The pharmaceutically acceptable salt of any one of (1) to (16), which is a citrate salt of the compound of Formula (I). (21) The pharmaceutically acceptable salt of any one of (1) to (16), which is a tartrate salt of the compound of Formula (I). (22) The pharmaceutically acceptable salt of any one of (1) to (18), which is a benzenesulfonate salt of 3-(2-(bis(methyl-4 / 3)amino)ethyl-l,l,2,2-4 / 4)-lH-indol-4-ol (I-3a). (23) The pharmaceutically acceptable salt of (22), wherein the benzenesulfonate salt of 3-(2-(bis(methyl-d3)amino)ethyl-1,1,2,2-4 / 4)-17 / -indol-4-ol (1-3a) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ±0.2°) selected from the group consisting of7.023°, 7.767°, 11.822°, 12.550°, 12.860°, 13.994°, 15.521°, 18.436°, 19.503°, 20.760°, 21.070°, 22.007°, 22.745°, 23.340°, 24.187°, 25.532°, 26.880°, 27.856°, 28.163°, 31.267°, 33.024°, 35.030°, 36.835°, 39.312°, 40.545°, and 40.988°. (24) The pharmaceutically acceptable salt of any one of (1) to (18), which is a benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-12 / -indol-4-ol (I-7a). (25) The pharmaceutically acceptable salt of (24), wherein the benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-l / / -indol-4-ol (I-7a) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.002°, 7.733°, 11.768°, 12.516°, 12.882°, 13.546°, 13.968°, 14.788°, 15.225°, 15.474°, 18.370°, 19.737°, 20.703°, 21.050°, 21.873°, 21.982°, 22.315°, 22.639°, 23.282°, 23.775°, 24.125°, 25.193°, 25.475°, 25.931°, 26.813°, 27.778°, 28.127°, 30.866°, 31.207°, 32.941°, 33.222°, 33.698°, 36.803°, 38.668°, and 39.289°. (26) The pharmaceutically acceptable salt of any one of (1) to (17) or (19), which is a benzoate salt of 3-(2-(bis(methyl-<73)amino)ethyl-l, 1,2,2-di)- 127-indol-4-ol (I-3j). (27) The pharmaceutically acceptable salt of (26), wherein the benzoate salt of 3-(2-(bis(methyl-d3)amino)ethyl-l, 1,2,2-^)-l / Z-indol-4-ol (I-3j) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 9.486°, 11.006°, 12.379°, 13.428°, 14.608°, 15.446°, 16.389°, 18.247°, 18.977°, 19.346°, 19.831°, 20.868°, 21.447°, 22.860°, 23.878°, 24.944°, 25.737°, 26.144°, 26.341°, 26.990°, 27.708°, 28.595°, 30.048°, 30.763°, 31.127°, 31.839°, 32.800°, 34.460°, 35.444°, 37.725°, and 38.597°. (28) The pharmaceutically acceptable salt of any one of (1) to (17) or (19), which is a benzoate salt of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (I-7j). (29) The pharmaceutically acceptable salt of (28), wherein benzoate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7j) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 9.492°, 11.011°, 12.391°, 13.440°, 14.609°, 15.432°, 16.394°, 18.259°, 18.967°, 19.356°, 19.827°, 20.843°, 21.476°, 22.062°, 22.805°, 23.862°, 24.963°, 25.734°, 26.170°, 26.992°, 27.738°, 28.593°, 30.073°, 30.746°, 31.041°, 31.799°, 32.794°, 33.551°, 34.480°, 35.430°, 37.685°, and 38.643°. (30) The pharmaceutically acceptable salt of any one of (1) to (16) or (20), which is a citrate salt of 3-(2-(bis(methyl-t / 3)ammo)ethyl-l,l,2,2-J4)-lH-indol-4-ol (I-3e). (31) The pharmaceutically acceptable salt of (30), wherein the citrate salt of 3-(2-(bis(methyl-J3)amino)ethyl-1,1,2,2-^)-l / f-indol-4-ol (I-3e) is amorphous by X-ray powder diffraction. (32) The pharmaceutically acceptable salt of any one of (1) to (16) or (20), which is a citrate salt of 3-(2-(dimethylamino)ethyl)-l / f-indol-4-ol (I-7e). (33) The pharmaceutically acceptable salt of (32), wherein citrate salt of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (I-7e) is amorphous by X-ray powder diffraction. (34) The pharmaceutically acceptable salt of any one of (1) to (16) or (21), which is a tartrate salt of 3-(2-(bis(methyl-<73)amino)ethyl-1,1,2,2-^)-l.H-indol-4-ol (I-3b). (35) The pharmaceutically acceptable salt of (34), wherein the tartrate salt of 3-(2-(bis(methyl-J3)amino)ethyl-1,1,2,2-^)- 177-indol-4-ol (I-3b) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0.2°) selected from the group consisting of 6.732°, 12.708°, 13.470°, 14.774°, 15.921°, 16.268°, 17.295°, 18.869°, 20.079°, 20.208°, 20.877°, 21.894°, 22.657°, 23.491°, 23.702°, 24.636°, 24.882°, 25.569°, 26.685°, 27.060°, 27.502°, 28.179°, 28.597°, 29.035°, 29.257°, 29.527°, 31.017°, 31.527°, 32.059°, 32.307°, 33.012°, 34.024°, 34.388°, 34.905°, 35.361°, 36.183°, 37.372°, 37.764°, 38.657°, 41.049°. (36) The pharmaceutically acceptable salt of any one of (1) to (16) or (21), which is a tartrate salt of 3-(2-(dimethylamino)ethyl)-l / f-indol-4-ol (I-7b). (37) The pharmaceutically acceptable salt of (36), wherein the tartrate salt of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (I-7b) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 6.798°, 11.360°, 12.764°, 13.535°, 14.837°, 15.973°, 16.351°, 17.367°, 18.937°, 20.168°, 20.929°, 21.946°, 22.719°, 23.604°, 23.814°, 24.874°, 25.609°, 26.745°, 27.111°, 27.558°, 28.653°, 29.630°, 31.129°, 31.567°, 32.180°, 33.073°, 34.096°, 34.460°, 36.226°, 37.497°, 38.727°. (38) The pharmaceutically acceptable salt of any one of (1) to (37), wherein the pharmaceutically acceptable salt of the compound of Formula (I) has a water solubility from about 1 mg / mL to about 400 mg / mL. (39) The pharmaceutically acceptable salt of any one of (1) to (14), which is a fatty acid salt of the compound of Formula (I). (40) The pharmaceutically acceptable salt of (39), which is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, a caprylate salt, a palmitate salt, a sebacate salt, an undecylenate salt, or a caproate salt of the compound of Formula (I). (41) The pharmaceutically acceptable salt of (39) or (40), which is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, or a caprylate salt of the compound of Formula (I). (42) The pharmaceutically acceptable salt of any one of (39) to (41), which is a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, or a caprylate salt of the compound of Formula (I). (43) The pharmaceutically acceptable salt of any one of (39) to (42), which is a laurate salt, a linoleate salt, a caprate salt, or a caprylate salt of the compound of Formula (I). (44) A pharmaceutical composition comprising the pharmaceutically acceptable salt of any one of (1) to (43), and a pharmaceutically acceptable vehicle. (45) The pharmaceutical composition of (44), which is adapted for intraoral administration. (46) The pharmaceutical composition of (44) or (45), wherein the pharmaceutical composition is in an orodispersible dosage form. (47) The pharmaceutical composition of any one of (44) to (46), wherein the pharmaceutical composition is in a form of an orally disintegrating tablet (ODT). (48) The pharmaceutical composition of any one of (44) to (47), wherein the pharmaceutically acceptable vehicle comprises a water-soluble polymer and a matrix material, filler, or diluent. (49) The pharmaceutical composition of (48), wherein the water-soluble polymer is gelatin, and the matrix material, filler, or diluent is mannitol. (50) The pharmaceutical composition of (48) or (49), wherein the pharmaceutically acceptable vehicle further comprises an acid. (51) The pharmaceutical composition of (50), wherein the acid is citric acid and / or tartaric acid. (52) The pharmaceutical composition of any one of (44) to (46), wherein the pharmaceutical composition is in a form of an orodispersible film (ODF). (53) The pharmaceutical composition of (44), wherein the pharmaceutical composition is in an immediate release (IR) dosage form. (54) The pharmaceutical composition of (53), wherein the immediate release (IR) dosage form is an immediate release (IR) tablet. (55) The pharmaceutical composition of (54), wherein the immediate release (IR) tablet comprises microcrystalline cellulose, sodium carboxymethylcellulose, and magnesium stearate. (56) The pharmaceutical composition of (54), wherein the immediate release (IR) tablet comprises mannitol, crospovidone, and sodium stearyl fumarate. (57) A method of treating a subject with a disease or disorder, comprising: administering to the subject a therapeutically effective amount of the pharmaceutically acceptable salt of any one of (1) to (43). (58) A method of treating a subject with a disease or disorder associated with a serotonin 5-HT2 receptor, comprising: administering to the subject a therapeutically effective amount of the pharmaceutically acceptable salt of any one of (1) to (43). (59) The method of (58), wherein the disease or disorder is a neuropsychiatric disease or disorder or an inflammatory disease or disorder. (60) The method of (58), wherein the disease or disorder is a central nervous system (CNS) disorder. (61) The method of (60), wherein the central nervous system (CNS) disorder is at least one selected from the group consisting of major depressive disorder (MDD), treatment-resistant depression (TRD), post-traumatic stress disorder (PTSD), bipolar and related disorders, obsessivecompulsive disorder (OCD), generalized anxiety disorder (GAD), social anxiety disorder, a substance use disorder, an eating disorder, Alzheimer’s disease, cluster headache and migraine, attention deficit hyperactivity disorder (ADHD), pain and neuropathic pain, aphantasia, childhoodonset fluency disorder, major neurocognitive disorder, mild neurocognitive disorder, sexual dysfunction, suicidal ideation, suicidal behavior, major depressive disorder with suicidal ideation or suicidal behavior, melancholic depression, atypical depression, dysthymia, non-suicidal selfinjury disorder (NSSID), chronic fatigue syndrome, Lyme’s disease, gambling disorder, a paraphilic disorder, sexual dysfunction, peripheral neuropathy, and obesity. (62) The method of (60), wherein the central nervous system (CNS) disorder is major depressive disorder (MDD). (63) The method of (60), wherein the central nervous system (CNS) disorder is treatmentresistant depression (TRD). (64) The method of (60), wherein the central nervous system (CNS) disorder is generalized anxiety disorder (GAD). (65) The method of (60), wherein the central nervous system (CNS) disorder is social anxiety disorder. (66) The method of (60), wherein the central nervous system (CNS) disorder is obsessivecompulsive disorder (OCD). (67) The method of (60), wherein the central nervous system (CNS) disorder is a substance use disorder. (68) The method of (67), wherein the central nervous system (CNS) disorder is alcohol use disorder. (69) The method of (58), wherein the disease or disorder is an autonomic nervous system (ANS) condition. (70) The method of (58), wherein the disease or disorder is a pulmonary disorder. (71) The method of (58), wherein the disease or disorder is a cardiovascular disorder. (72) The method of any one of (58) to (71), wherein the pharmaceutically acceptable salt is administered orally to the subject. (73) The method of any one of (58) to (72), wherein the pharmaceutically acceptable salt is administered intraorally to the subject. (74) The method of any one of (58) to (71), wherein the pharmaceutically acceptable salt is administered transdermally to the subject. (75) The method of any one of (58) to (71), wherein the pharmaceutically acceptable salt is administered subcutaneously to the subject. (76) The method of any one of (58) to (75), wherein the pharmaceutically acceptable salt is administered at a psychedelic dose of about 0.083 mg / kg to about 1 mg / kg. (77) The method of (76), wherein the pharmaceutically acceptable salt is administered at the psychedelic dose once per week or less over a treatment course. (78) The method of any one of (57) to (75), wherein the pharmaceutically acceptable salt is administered at a sub-psychedelic dose of about 0.00001 mg / kg to less than about 0.083 mg / kg. (79) The method of (78), wherein the pharmaceutically acceptable salt is administered at the sub-psychedelic dose once per day or more over a treatment course. (80) A method for stabilizing the compound of Formula (I) comprising preparing the pharmaceutically acceptable salt of the compound of Formula (I) of any one of (1) to (43). (81) A method for decreasing time of therapeutic onset relative to a psilocybin-based drug, comprising: administering a therapeutically effective amount of the pharmaceutically acceptable salt of the compound of Formula (I) of any one of (1) to (43) to a subject in need thereof. (82) A method of reducing psychedelic side effects relative to a psilocybin-based drug, comprising: administering a therapeutically effective amount of the pharmaceutically acceptable salt of the compound of Formula (I) of any one of (1) to (43) to a subject in need thereof. (83) A method of decreasing duration of therapeutic effect relative to a psilocybin-based drug, comprising: administering a therapeutically effective amount of the pharmaceutically acceptable salt of the compound of Formula (I) of any one of (1) to (43) to a subject in need thereof. (84) A solution-phase composition, comprising: the pharmaceutically acceptable salt of the compound of Formula (I) of any one of (1) to (43), in solvated form. (85) The solution-phase composition of (84), which is an aqueous solution-phase composition comprising the pharmaceutically acceptable salt of the compound of Formula (I), in solvated form. (86) A crystalline polymorph of a compound of Formula (I), or a stereoisomer or a solvate thereof, R8 --"^9 r7 wherein: R2, R5, R6, and R? are independently selected from the group consisting of hydrogen or deuterium, Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, and Xi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium. (87) The crystalline polymorph of (86), which is a crystalline form of 3-(2-(bis(methyl-^3)amino)ethyl-1,1,2,2-1 / 4)-lH-indol-4-ol (1-3) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at difftaction angles (20 ± 0.2°) selected from 15 the group consisting of 7.582°, 8.395°, 9.647°, 10.444°, 11.319°, 12.614°, 13.372°, 14.222°, 15.157°, 16.524°, 16.787°, 17.693°, 19.468°, 19.699°, 20.901°, 21.132°, 21.859°, 22.547°, 23.699°, 24.630°, 25.034°, 25.264°, 26.867°, 27.399°, 27.929°, 28.219°, 28.871°, 29.430°, 30.120°, 30.675°, 31.373°, 32.365°, 33.880°, 34.418°, 34.792°, 35.884°, 36.254°, 37.156°, 38.200°, and 38.417°. (88) The crystalline polymorph of (86), which is a crystalline form of 3-(2-(bis(methyl-t / 3)amino)ethyl-l,l,2,2-c / 4)-l / 7-indol-4-ol (1-3) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 8.124°, 8.357°, 10.059°, 12.630°, 13.420°, 13.743°, 14.053°, 15.220°, 16.272°, 16.763°, 16.954°, 17.328°, 17.662°, 18.062°, 18.742°, 19.413°, 19.658°, 20.172°, 20.836°, 21.267°, 21.833°, 22.213°, 22.504°, 23.334°, 23.701°, 24.385°, 25.431°, 25.721°, 26.049°, 27.291°, 28.368°, 30.349°, 30.656°, 31.337°, 31.538°, 32.091°, 35.870°, 38.514°, and 41.361°. (89) The crystalline polymorph of (86), which is a crystalline form of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (1-7) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.563°, 8.375°, 12.626°, 13.383°, 15.211°, 16.753°, 17.671°, 19.668°, 21.112°, 21.863°, 22.201°, 22.560°, 23.711°, 24.592°, 25.415°, 26.820°, 27.357°, 27.921°, 28.228°, 29.253°, 30.653°, 31.364°, 32.401°, 33.797°, 34.445°, 39.867° (90) A pharmaceutical composition comprising the crystalline polymorph of any one of (86) to (89), and a pharmaceutically acceptable vehicle. (91) The pharmaceutical composition of (90), wherein the pharmaceutically acceptable vehicle comprises an acid. (92) The pharmaceutical composition of (91), wherein the acid is citric acid and / or tartaric acid. (93) A method of treating a subject with a disease or disorder associated with a serotonin 5-HT2 receptor, comprising: administering to the subject a therapeutically effective amount of the crystalline polymorph of any one of (86) to (89). (94) An amorphous compound of Formula (I), or a stereoisomer or a solvate thereof, wherein: R2, R5, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium, Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, and Xi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium. (95) The amorphous compound of (94), which is an amorphous form of3-(2-(bis(methyl-Jsjaminojethyl-1,1,2,2-( / 4)-l#-indol-4-ol (1-3), as determined by X-ray powder diffraction. (96) The amorphous compound of (94), which is an amorphous form of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (1-7), as determined by X-ray powder diffraction. (97) The amorphous compound of any one of (94) to (96), which has a glass transition temperature of about 26°C to about 30°C as determined by differential scanning calorimetry (DSC). (98) The amorphous compound of any one of (94) to (97), which is prepared by melting a crystalline form of the compound of Formula (I) to beyond a melting point of the crystalline form, and then rapidly cooling to a glass transition temperature. (99) A pharmaceutical composition comprising the amorphous compound of any one of (94) to (98), and a pharmaceutically acceptable vehicle. (100) A method of treating a subject with a disease or disorder associated with a serotonin 5-HT2 receptor, comprising: administering to the subj ect a therapeutically effective amount of the amorphous compound of any one of (94) to (98). (101) Use of the pharmaceutically acceptable salt of any one of (1) to (43), the pharmaceutical composition of any one of (44) to (56), the solution-phase composition of (84) or (85), the crystalline polymorph of any one of (86) to (89), the pharmaceutical composition of any one of (90) to (92), the amorphous compound of any one of (94) to (98), or the pharmaceutical composition of (99) for treating a subject with a disease or disorder associated with a serotonin 5-HT2 receptor. (102) The pharmaceutically acceptable salt of any one of (1) to (43), which is at least 10% more stable as both a solid and an aqueous solution, in terms of % (active) remaining after being subject to 40°C for 24 hours, compared to the compound of Formula (I) (free base) prepared in substantially the same way as a solid or aqueous solution. BRIEF DESCRIPTION OF THE DRAWINGS The forgoing paragraphs have been provided by way of general introduction and are not intended to limit the scope of the following claims. The described embodiments, together with further advantages, will be best understood by reference to the following detailed description when considered in conjunction with the accompanying drawings, wherein: Figs. 1A-1D show a synthetic route (Fig. 1A), a *H NMR spectrum (Figs. 1B-1C), and a high resolution mass spectrometry (HRMS) spectrum (Fig. ID) for compound 1-3 (PI-dio); Figs. 2A-2C show the X-ray powder diffraction (XRPD) pattern (pattern 1) of compound 1-3, with Figs. 2B and 2C being zoomed in and annotated; Figs. 3A-3D show the X-ray powder diffraction (XRPD) pattern of I-7a (pattern l)(Fig. 3A), with Fig. 3B being zoomed in and annotated, the XRPD pattern of 1-7 (Pl-Jo, free base)(pattem 1 )(Fig. 3C), and a comparison between the XRPD patterns of I-7a (benzenesulfonate salt) and 1-7 (Pl-do, free base)(pattem l)(Fig. 3D); Fig. 4 shows a differential scanning calorimetry (DSC) curve of I-7a; Fig. 5 shows a thermogravimetric analysis (TGA) curve of I-7a; Figs. 6A and 6B show a XH NMR spectrum of I-7a; Fig. 7 shows the ultra performance liquid chromatogram (UPLC) of I-7a; Fig. 8 shows a DVS isotherm plot of I-7a; Fig. 9 shows the XRPD patterns of 1-7a (pattern 1) pre- and post-DVS analysis; Fig. 10 shows the XRPD patterns of I-7a after storing solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample; Fig. 11 shows the XRPD patterns of I-7a after maturation in 12 different solvents; Fig. 12 shows the XRPD pattern of two different crystalline polymorphs of I-7b, pattern 1 (made from acetonitrile or THF), and pattern 2 (made from 1,4-dioxane); Fig. 13 shows the DSC curve of I-7b (polymorph of pattern 1); Fig. 14 shows the TGA curve of I-7b (polymorph of pattern 1); Figs. 15A-15B show the 1H NMR spectrum of I-7b (polymorph of pattern 1); Fig. 16 shows a DVS isotherm plot of I-7b (polymorph of pattern 1); Fig. 17 shows a DVS change in mass plot of I-7b (polymorph of pattern 1); Fig. 18 shows the XRPD patterns of I-7b (polymorph of pattern 1) after storing solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample, with samples ii), iii) and post DVS indicating a change in form to polymorph of pattern 3; Figs. 19A-19B show the DSC plots of I-7b (polymorph of pattern 1) pre-DVS (Fig. 19A) and post-DVS (Fig. 19B); Figs. 20A-20B show the TGA plots of I-7b (polymorph of pattern 1) pre-DVS (Fig. 20A) and post-DVS (Fig. 20B); Fig. 21 shows the XRPD patterns of I-7b (polymorph of pattern 1) after maturation in 12 different solvents; Fig. 22 shows the XRPD patterns of I-7b (amorphous) obtained from salt formation with 0.5 eq of L-tartaric acid from either 1,4-dioxane or THF; Fig. 23 shows the XRPD pattern of four different crystalline polymorphs of I-7c: a polymorph having pattern 1 (made from either 0.5 eq or 1 eq fumaric acid and THF), a polymorph having pattern 2 (made from 0.5 eq fumaric acid and acetonitrile), a polymorph having pattern 3 (made from either 0.5 eq or 1 eq fumaric acid in 1,4-dioxane), and a polymorph having pattern 4 (made from 1 eq fumaric acid in acetonitrile); Fig. 24 shows a DSC of I-7c (polymorph of pattern 4); Fig. 25 shows a TGA of I-7c (polymorph of pattern 4); Fig. 26 shows a DVS of I-7c (polymorph of pattern 4); Fig. 27 shows a DVS change in mass plot of I-7c (polymorph of pattern 4); Fig. 28 shows the XRPD pattern of I-7c pre-DVS (polymorph of pattern 5, obtained from scale-up using 1 eq fumaric acid in acetonitrile) and post-DVS (pattern 6); Figs. 29A-29B show the DSC plot of I-7c pre-DVS (Fig. 29A, polymorph 5, obtained from scale-up using 1 eq fumaric acid in acetonitrile) and post-DVS (Fig. 29B, pattern 6); Figs. 30A-30B show the TGA plot of I-7c pre-DVS (Fig. 30A, polymorph 5, obtained from scale-up using 1 eq fumaric acid in acetonitrile) and post-DVS (Fig. 3 0B, pattern 6); Fig. 31 shows the XRPD patterns of I-7c (polymorph of pattern 5) after maturation in 12 different solvents, forming polymorphs of patterns (P) 1, 6, 7, 8, 9, 10, and 11; Fig. 32 shows the XRPD pattern of two different crystalline polymorphs of I-7d: a polymorph having pattern 1 (made from 1,4-dioxane), and a polymorph having pattern 2 (made from THF / heptane); Fig. 33 shows the DSC curve of I-7d (polymorph of pattern 1); Fig. 34 shows the TGA plot of I-7d (polymorph of pattern 1); Fig. 35 shows the DSC curve of I-7d (polymorph of pattern 2); Fig. 36 shows the TGA curve of I-7d (polymorph of pattern 2); Fig. 37 shows the XRPD pattern of I-7e (amorphous); Figs. 38A-38B shows the NMR spectrum of I-7e; Fig. 39 shows the XRPD pattern of I-7f compared to free base; Fig. 40 shows the DSC curve of I-7f; Fig. 41 shows the TGA plot of I-7f; Fig. 42 shows the XRPD pattern of three different crystalline polymorphs of I-7g: a polymorph having pattern 1 (made from THF), a polymorph having pattern 2 (made from acetonitrile), a polymorph having pattern 3 (made from 1,4-dioxane); Fig. 43 shows the DSC curve of I-7g (polymorph of pattern 1); Fig. 44 shows the TGA plot of I-7g (polymorph of pattern 1); Fig. 45 shows the DSC curve of I-7g (polymorph of pattern 3); Fig. 46 shows the TGA plot of I-7g (polymorph of pattern 3); Fig. 47 shows the XRPD pattern of I-7h (polymorph of pattern 1) formed from either 1,4-dioxane or THF; Fig. 48 shows the DSC curve of I-7h (polymorph of pattern 1); Fig. 49 shows TGA plot of I-7h (polymorph of pattern 1); Fig. 50 shows the XRPD pattern of six different crystalline polymorphs of I-7i: a polymorph having pattern 1 (made from 0.5 eq oxalic acid and THF), a polymorph having pattern 2 (made from 1 eq oxalic acid and THF), a polymorph having pattern 3 (made from 0.5 eq oxalic acid and acetonitrile), a polymorph having pattern 4 (made from 1 eq oxalic acid and acetonitrile), a polymorph having pattern 5 (made from 0.5 eq oxalic acid and 1,4-dioxane), and a polymorph having pattern 6 (made from 1 eq oxalic acid and 1,4-dioxane); Fig. 51 shows the DSC curve of I-7i (polymorphs of patterns 1-6); Fig. 52 shows the TGA plot of I-7i (polymorphs of patterns 2-6); Figs. 53A-53B show the XRPD pattern of I-7j (polymorph of pattern 1), with Fig. 53B being zoomed in and annotated. Fig. 54 shows the TGA plot of I-7j (polymorph of pattern 1); Fig. 55 shows the DSC curve of I-7j (polymorph of pattern 1); Fig. 56 shows the XRPD patterns of I-7j (polymorph of pattern 1) after storing solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample; Fig. 57 shows the XRPD patterns of I-7j (polymorph of pattern 1) after maturation in 12 different solvents; Fig. 58 shows the DVS isotherm of I-7j (polymorph of pattern 1); Figs. 59A-59C show that no changes to I-7j (polymorph of pattern 1) took place after being subjected to DVS conditions (post-DVS) by XRPD (Fig. 59A, compared to pattern before DVS from material obtained from THF and acetonitrile) and by *H NMR (Figs. 59B and 59C); Fig. 60 shows the XRPD pattern of three different crystalline polymorphs of I-7k: a polymorph having pattern 1 (made from acetonitrile / TBME), a polymorph having pattern 2 (made from THF / heptane), and a polymorph having pattern 3 (made from 1,4-dioxane / heptane); Fig. 61 shows the DSC curve of three different crystalline polymorphs of I-7k; Fig. 62 shows the TGA plot of three different crystalline polymorphs of I-7k; Figs. 63A-63D show the XRPD pattern of I-3a (pattern 1) (Fig, 63A), zoomed in and annotated versions of the XRPD plot (Figs. 63B-63C), and a comparative XRPD plot of I-3a (pattern 1) to I-7a seeds (Fig. 63D); Figs. 64A-64B show a comparison of I-3a (pattern 1) to I-7a seeds by DSC (Fig. 64A) and TGA (Fig. 64B); Figs. 65A-65B shows the *H NMR spectrum of I-3a (pattern 1); Fig. 66 shows the XRPD pattern of I-3b (pattern 1, obtained from non-seeded experiments) compared to crystalline polymorphs of I-7b of pattern 1 (from THF) and pattern 2 (from 1,4-dioxane); Fig. 67 shows DSC curve of I-3b (pattern 1, obtained from non-seeded experiments) compared to crystalline polymorphs of I-7b of pattern 1 (from THF) and pattern 2 (from 1,4-dioxane); Fig. 68 shows the TGA plot of I-3b (pattern 1, obtained from non-seeded experiments) compared to crystalline polymorphs of I-7b of pattern 1 (from THF) and pattern 2 (from 1,4-dioxane); Figs. 69A-69B show the XRPD pattern of I-3b (pattern 2, obtained from seeded experiments), compared to the seeds of crystalline polymorph of I-7b of pattern 1, and the crystalline polymorph of I-3b of pattern 1 obtained from the non-seeded experiments (Fig. 69A), and the zoomed in and annotated XRPD of I-3b (pattern 2, obtained from seeded experiments)(Fig. 69B); Fig. 70 shows the DSC curve of I-3b (pattern 2); Fig. 71 shows the TGA plot of I-3b (pattern 2); Fig. 72 shows the XRPD pattern of I-3c (pattern 1, obtained from non-seeded experiments) to the crystalline polymorphs of I-7c of patterns 1 through 4; Fig. 73 shows the DSC curve of I-3c (pattern 1) compared to that of the polymorph patterns 1 through 4 of I-7c; Fig. 74 shows the TGA plot of I-3c (pattern 1) compared to that of the polymorph patterns 1 through 4 of I-7c; Fig. 75 shows the XRPD pattern of I-3c (pattern 2, obtained from seeded experiments) compared to crystalline polymorph of I-3c of pattern 1 obtained from the non-seeded experiments and the seeds of I-7c crystalline polymorph pattern 4; Fig. 76 shows the DSC curve of I-3c (pattern 2, obtained from seeded experiments) compared to crystalline polymorph of I-3c of pattern 1 obtained from the non-seeded experiments and the seeds of I-7c crystalline polymorph pattern 4; Fig. 77 shows the TGA plot of I-3c (pattern 2, obtained from seeded experiments) compared to crystalline polymorph of I-3c of pattern 1 obtained from the non-seeded experiments and the seeds of I-7c crystalline polymorph pattern 4; Figs. 78A-78E shows the XRPD pattern of I-3j (pattern 1) (Fig. 78A), a zoomed in and annotated version (Fig. 78B), a comparison of the XRPD pattern of I-3j (pattern 1) to that of the I-7j seed (Fig. 78C), a single crystal X-ray structure of I-3j (pattern 1) (Figs. 78D-78E); Figs. 79A-79B show the XH NMR spectrum of I-3j (pattern 1); Fig. 80 shows the DSC plot of I-3j (pattern 1) compared to I-7j (pattern 1); Fig. 81 shows the DVS isotherm plot of I-3j (pattern 1); Fig. 82 shows the DVS change in mass plot of I-3j (pattern 1); Fig. 83 shows the XRPD patterns of 1-3 j (polymorph of pattern 1) after storing solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample and post DVS sample; Fig. 84 shows the XRPD patterns of 1-3 j (polymorph of pattern 1) after maturation in 12 different solvents; Fig. 85 shows XRPD diffraction peaks of compound 1-3 (pattern 1) obtained from crash cooling and freeze-drying solutions of 1-3 (PI-Jw, free base) in 1,4-dioxane, t-BuOH, 1,4-dioxane / water, MeCN / water; Fig. 86 shows a DSC plot of compound 1-3 (PI-Jio, free base)(pattem 1); Fig. 87 shows an XRPD of the amorphous form of compound 1-3 (PI-Jio, free base) obtained from melt / crash cooling experiment (>185°C / 30°C) in DSC compared to the XRPD pattern of compound 1-3 (pattern 2) which resulted from the amorphous form crystallizing overnight upon standing; Fig. 88 shows the XRPD pattern of 1-3 (pattern 2) obtained from DSC scale-up experiments; Fig. 89 shows the annotated XRPD pattern of 1-3 (pattern 2) obtained from DSC scale-up experiments; Fig. 90 shows the XRPD pattern of I-3m (pattern 1) compared to diffraction patterns 1 and 2 of the free base 1-3; Fig. 91 shows the XRPD pattern of I-3n (pattern 1) compared to diffraction patterns 1 and 2 of the free base 1-3; Fig. 92 shows the XRPD pattern of I-3o (pattern 1) compared to diffraction patterns 1 and 2 of the free base 1-3; Fig. 93 shows the XRPD pattern of I-3p (pattern 1) compared to diffraction patterns 1 and 2 of the free base 1-3; Fig. 94 shows the XRPD pattern of two different polymorphs of I-3q (pattern 1 obtained from commercially available stearic acid, and pattern 2 obtained from desalting sodium stearate) compared to the diffraction patterns 1 and 2 of the free base 1-3; Fig. 95 shows the XRPD pattern of two different polymorphs of I-3r (pattern 1 obtained from desalting sodium oleate, and pattern 2 obtained from commercially available oleic acid) compared to the diffraction patterns 1 and 2 of the free base 1-3; Fig. 96 shows the XRPD pattern of I-3s (pattern 1) compared to diffraction patterns 1 and 2 of the free base 1-3; Fig. 97 shows the stability of 1-7 (PI-<7o) over 24 hours in 0.1 M solutions of acetic acid, with or without metal ions, compared to those solutions without acetic acid, at 40°C; Fig. 98 shows the stability of 1-7 (Pl-do) over 24 hours in 0.1 M solutions of ascorbic acid, with or without metal ions, compared to those solutions without ascorbic acid, at 40°C; Fig. 99 shows the stability of 1-7 (PI-<7o) over 24 hours in 0.1 M solutions of benzenesulfonic acid, with or without metal ions, compared to those solutions without benzenesulfonic acid, at 40°C; Fig. 100 shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1 M solutions of fumaric acid, with or without metal ions, compared to those solutions without fumaric acid, at 40°C; Fig. 101 shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1 M solutions of malonic acid, with or without metal ions, compared to those solutions without malonic acid, at 40°C; Fig. 102 shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1 M solutions of succinic acid, with or without metal ions, compared to those solutions without succinic acid, at 40°C; Fig. 103 shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1 M solutions of tartaric acid, with or without metal ions, compared to those solutions without tartaric acid, at 40°C; Fig. 104 shows the stability of 1-7 (Pl-Jo) over 24 hours in 0.1 M solutions of citric acid, with or without metal ions, compared to those solutions without citric acid, at 40°C; Fig. 105 shows the stability of 1-7 (PI-Jo) over 24 hours in dilute solutions of citric acid, with or without metal ions, compared to those solutions without citric acid, at 4°C; Fig. 106 shows the stability of 1-7 (PI-Jo) over 24 hours in dilute solutions of citric acid, with or without metal ions, compared to those solutions without citric acid, at 23°C; Fig. 107 shows the stability of 1-7 (PI-Jo) over 24 hours in dilute solutions of citric acid, with or without metal ions, compared to those solutions without citric acid, at 40°C; Figs. 108A-108C shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1M solutions of sodium citrate buffer, with or without metal ions, compared to those solutions without sodium citrate buffer, at 4°C (Fig. 108A), 23°C (Fig. 108B), 40°C (Fig. 108C); Fig. 109 shows the stability of 1-7 (PI-Jo) over 24 hours in 0.1M solutions of phosphate buffer (pH 6.0), phosphate buffer (pH 7.5), and sodium citrate buffer (6.0) at 40°C; Fig. 110 shows the long-term stability (up to 25 days) of 1-7 (Pl-Jo) in a sodium citrate buffer (0.1 M, pH6.01)at4°C and23°C; Fig. 111 shows the long-term stability (up to 25 days) of 1-7 (Pl-Jo) in a citric acid solution (0.1 M, pH 1.60)at4°C and 23°C; Fig. 112 shows the stability of 1-7 (PI-Jo) over 24 hours in 20 pM solutions of ethylenediaminetetraacetic acid (EDTA), with or without metal ions, compared to those solutions without ethylenediaminetetraacetic acid (EDTA), at 40°C; Fig. 113 shows the stability of 1-7 (PI-Jo) over 24 hours in 20 pM solutions of ascorbic acid, with or without metal ions, compared to those solutions without ascorbic acid, at 40°C; Fig. 114 shows the stability of 1-7 (PI-Jo) over 24 hours in 20 pM solutions of sodium metabisulfite, with or without metal ions, compared to those solutions without sodium metabisulfite, at 40°C; Fig. 115 shows the stability of 1-7 (Pl-Jo) over 24 hours in 20 pM solutions of L-cysteine, with or without metal ions, compared to those solutions without L-cysteine, at 40°C; Fig. 116 shows the stability of 1-7 (PI-t / o) over 24 hours in 20 pM solutions of propyl gallate, with or without metal ions, compared to those solutions without propyl gallate, at 40°C; Fig. 117 shows the stability of 1-7 (Pl-Jo) over 24 hours in 1% w / w solutions of CAVASOL® W7 HP, with or without metal ions, compared to those solutions without CAVASOL® W7 HP, at 40°C; Fig. 118 shows the stability of 1-7 (Pl-do) over 24 hours in 1% w / w solutions of CAVASOL® W7 M, with or without metal ions, compared to those solutions without CAVASOL® W7 M, at 40°C; Fig. 119 shows the stability of 1-7 (PI-Jo) over 24 hours in 1% w / w solutions of CAVITRON® W7 HP7, with or without metal ions, compared to those solutions without CAVITRON® W7 HP7, at 40°C; Fig. 120 shows the solubility of 1-3 (PI-Jio)(pattern 1), 1-7 (PI-Jo)(patteml), I-3j (pattern 1), I-7a (pattern 1), I-7b (pattern 1), I-7c (pattern 5), and I-7j (pattern 1) in FaSSGF (Fasted State Simulated Gastric Fluid)(pH 1.6), at 37°C for 2 and 6 hours; Fig. 121 shows the solubility of 1-3 (PI-Jio)(pattem 1), 1-7 (PI-Jo)(patteml), I-3j (pattern 1), I-7a (pattern 1), I-7b (pattern 1), I-7c (pattern 5), and I-7j (pattern 1) in water at room temperature for 2 and 6 hours; Fig. 122 shows the TGA plot of 1-7 (API) used in the ODT formulations; Fig. 123 show the DSC curve of 1-7 (API) used in the ODT formulations; Fig. 124 shows the XRPD pattern of 1-7 (pattern 1)(API) used in the ODT formulations; Fig. 125 shows the TGA plot of the ODT dosage form formed from batch la (SH24) formulated with the citrate salt of psilocin at pH 3.55; Fig. 126 shows the DSC curve of the ODT dosage form formed from batch la (SH24) formulated with the citrate salt of psilocin at pH 3.55; Fig. 127 shows the XRPD pattern of the ODT dosage form formed from batch la (SH24) formulated with the citrate salt of psilocin at pH 3.55; Fig. 128 shows the appearance of the ODT dosage form formed from batch la (SH24) formulated with the citrate salt of psilocin at pH 3.55; Fig. 129 shows the DSC plot of the ODT dosage form formed from batch lb (SH24) formulated with the citrate salt of psilocin at pH 4.50; Fig. 130 shows the XRPD pattern of the ODT dosage form formed from batch lb (SH24) formulated with the citrate salt of psilocin at pH 4.50; Fig. 131 shows the appearance of the ODT dosage form formed from batch lb (SH24) formulated with the citrate salt of psilocin at pH 4.50; Fig. 132 shows the DSC plot of the ODT dosage form formed from batch 1c (SH24) formulated with the citrate salt of psilocin at pH 7.56; Fig. 133 shows the XRPD pattern of the ODT dosage form formed from batch 1c (SH24) formulated with the citrate salt of psilocin at pH 7.56; Fig. 134 shows the appearance of the ODT dosage form formed from batch 1c (SH24) formulated with the citrate salt of psilocin at pH 7.56; Fig. 135 shows the DSC curve of the ODT dosage form formed from batch 2a (SH24) formulated with the tartrate salt of psilocin at pH 3.13; Fig. 136 shows the XRPD pattern of the ODT dosage form formed from batch 2a (SH24) formulated with the tartrate salt of psilocin at pH 3.13; Fig. 137 shows the appearance of the ODT dosage form formed from batch 2a (SH24) formulated with the tartrate salt of psilocin at pH 3.13; Fig. 138 shows the DSC plot of the ODT dosage form formed from batch 2b (SH24) formulated with the tartrate salt of psilocin at pH 4.33; Fig. 139 shows the XRPD pattern of the ODT dosage form formed from batch 2b (SH24) formulated with the tartrate salt of psilocin at pH 4.33; Fig. 140 shows the appearance of the ODT dosage form formed from batch 2b (SH24) formulated with the tartrate salt of psilocin at pH 4.33; Fig. 141 shows the DSC curve of the ODT dosage form formed from batch 2c (SH24) formulated with the tartrate salt of psilocin at pH 7.94; Fig. 142 shows the XRPD pattern of the ODT dosage form formed from batch 2c (SH24) formulated with the tartrate salt of psilocin at pH 7.94; Fig. 143 shows the TGA plot of the placebo ODT dosage form; Fig. 144 shows the DSC curve of the placebo ODT dosage form; Fig. 145 shows the XRPD pattern of the placebo ODT dosage form; Fig. 146 shows a plasma concentration-time curve of psilocybin dosed orally and intravenously in rats; Fig. 147 is a plasma concentration-time curve of PI-Jo + PI-Jio (Pl-tot) from co-dosing PI-Jo and PI-Jio orally and intravenously in rats; Fig. 148 is a plasma concentration-time curve comparing Pl-tot plasma levels after oral PI-Jo + PI-Jio and oral psilocybin in rats; Fig. 149 is a tissue concentration-time curve comparing brain and plasma psilocybin levels after intravenous dosing of psilocybin in rats; Fig. 150 is a tissue concentration-time curve comparing brain and plasma Pl-tot levels after intravenous co-dosing of PI-Jo and PI-Jio in rats; Fig. 151 is a brain concentration-time curve comparing brain PI levels after intravenous dosing of psilocybin and PI-tot levels after intravenous co-dosing of PI-Jo and PI-Jio in rats; Figs. 152A-152B show a plasma concentration-time curve following intravenous and oral administration of psilocin-Jio to dogs (Fig. 152A), and a bioavailability profile of psilocin-Jio to dogs of 91.3% (Fig. 152B); Figs. 153A-153B show the plasma concentration-time profiles for Pl-Jo after psilocybin dosing (Fig. 153A) and for PI-J / o after PI-J / o (Fig.l53B) with orally disintegrating tablets (ODT) and powder in capsule (PIC) dosage forms; Fig. 154 shows the exposure comparison between PI-Jo after psilocybin dosing and PI-J / o after PI-J / o dosing for both ODT and PIC dosage forms as assessed by Cmax; and Fig. 155 shows the exposure comparison between Pl-Jo after psilocybin dosing and PI-J / o after PI-J / o dosing for both ODT and PIC dosage forms as assessed by AUCinf. DETAILED DESCRIPTION In the following detailed description of the embodiments of the instant disclosure, numerous specific details are set forth in order to provide a thorough understanding of the disclosed embodiments. However, it will be obvious to one skilled in the art that the embodiments of this disclosure may be practiced without these specific details. In other instances, well known methods, procedures, components, and circuits have not been described in detail so as not to unnecessarily obscure aspects of the embodiments of the instant disclosure. Definitions Unless defined otherwise, all technical and scientific terms used herein have the same meaning as is commonly understood by one of skill in the art to which this disclosure belongs. When it is stated that a substituent or group “comprise(s) deuterium” or is “comprising deuterium,” it is to be understood that the substituent or group may itself be deuterium, or the substituent or group may contain at least one deuterium substitution in its chemical structure. For example, when substituent “-R” is defined to comprise deuterium, it is to be understood that -R may be -D (-deuterium), or a group such as -CD3 that is consistent with the other requirements set forth of -R. As used herein, the term “fatty” describes a compound with a long-chain (linear) hydrophobic portion made up of hydrogen and anywhere from 4 to 26 carbon atoms, which may be fully saturated or partially unsaturated. The phrases “pharmaceutically acceptable,” “physiologically acceptable,” and the like, are employed herein to refer to those compounds, materials, compositions, and / or dosage forms which are, within the scope of sound medical judgment, suitable for use in contact with the tissues of human beings without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit / risk ratio. When referencing salts, the phrases “pharmaceutically acceptable salt,” “physiologically acceptable salt,” and the like, means a salt which is acceptable for administration to a patient, such as a mammal (salts with counterions having acceptable mammalian safety for a given dosage regime). As is well known in the art, such salts can be derived from pharmaceutically acceptable inorganic or organic bases, by way of example, sodium, potassium, calcium, magnesium, ammonium, and tetraalkylammonium salts, and the like, and when the molecule contains a basic functionality, addition salts with inorganic acids, such as hydrochloride, hydrobromide, sulfate, sulfamate, phosphate, nitrate, perchlorate salts, and the like, and addition salts with organic acids, such as formate, tartrate, besylate, mesylate, acetate, maleate, malonate, oxalate, fumarate, benzoate, salicylate, succinate, oxalate, glycolate, hemi-oxalate, hemi-fumarate, propionate, stearate, lactate, citrate, ascorbate, pamoate, hydroxymaleate, phenylacetate, glutamate, 2-acetoxybenzoate, tosylate, ethanedisulfonate, isethionate salts, and the like. The term “salt thereof’ means a compound formed when a proton of an acid is replaced by a cation, such as a metal cation or an organic cation and the like. Where 29 applicable, the salt is a pharmaceutically acceptable salt, although this is not required for salts of intermediate compounds that are not intended for administration to a patient. By way of example, salts of the present compounds include those wherein the compound is protonated by an inorganic or organic acid to form a cation, with the conjugate base of the inorganic or organic acid as the anionic component of the salt. “Solvate” refers to a physical association of a compound or salt of the present disclosure with one or more solvent molecules, whether organic, inorganic, or a mixture of both. This physical association includes hydrogen bonding. In certain instances, the solvate will be capable of isolation, for example when one or more solvent molecules are incorporated in the crystal lattice of the crystalline solid. The solvent molecules in the solvate may be present in a regular arrangement and / or a non-ordered arrangement. The solvate may comprise either a stoichiometric or nonstoichiometric amount of the solvent molecules. “Solvate” encompasses both solution-phase and isolable solvates. Some examples of solvents include, but are not limited to, methanol, ethanol, isopropanol, N,N-dimethylformamide, tetrahydrofuran, dimethylsulfoxide, and water. When the solvent is water, the solvate formed is a hydrate (e.g., monohydrate, dihydrate, etc.). Exemplary solvates thus include, but are not limited to, hydrates, methanolates, ethanolates, isopropanolates, etc. Methods of solvation are generally known in the art. “Stereoisomer” and “stereoisomers” refer to compounds that have same atomic connectivity but different atomic arrangement in space. Stereoisomers include cis-trans isomers, E and Z isomers, enantiomers, and diastereomers. “Tautomer” refers to alternate forms of a molecule that differ only in electronic bonding of atoms and / or in the position of a proton, such as enol-keto and imine-enamine tautomers, or the tautomeric forms of heteroaryl groups containing a -N=C(H)-NH- ring atom arrangement, such as pyrazoles, imidazoles, benzimidazoles, triazoles, and tetrazoles. Other tautomeric ring atom arrangements are also possible. It will be appreciated that the compounds herein can exist in different salt, solvate, and stereoisomer forms, and the present disclosure is intended to include all permutations of salts, solvates and stereoisomers, such as a solvate of a pharmaceutically acceptable salt of a stereoisomer of the subject compound. As used herein, the term “steady” describes the stable or steady-state level of a molecule concentration, e g., concentration of any compound described herein. The term “stable,” “stability,” and the like, as used herein includes chemical stability and solid state (physical) stability. The term “chemical stability” means that the compound can be stored in an isolated form, or in the form of a formulation in which it is provided in admixture with for example, pharmaceutically acceptable carriers, diluents or adjuvants as described herein, under normal storage conditions, with little or no chemical degradation or decomposition. “Solid-state stability” means the compound can be stored in an isolated solid form, or the form of a solid formulation in which it is provided in admixture with, for example, pharmaceutically acceptable carriers, diluents or adjuvants as described herein, under normal storage conditions, with little or no solid-state transformation (eg., hydration, dehydration, solvatization, desolvatization, crystallization, recrystallization or solid-state phase transition). A “psilocybin-based” drug is any prodrug of a psilocin-type compound, such as an alkyl / aryl ester, an a-amino ester (e.g., an amino acid ester), a hemi-ester, a bis-ester, a phosphate ester, a sulfate ester, etc., that when administered releases psilocin or a deuterated analog thereof (e.g., a compound of Formula (I)) as the active component. A psilocybin-based drug includes psilocybin itself. As used herein, the term “composition” is equivalent to the term “formulation.” References to X-ray powder diffraction (XRPD) patterns of compounds / salts of the present disclosure being characterized by an X-ray powder diffraction pattern containing “at least three characteristic peaks” should be understood to include those compounds / salts characterized as having 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15 or more (including all) of the recited characteristic XRPD diffraction peaks. As used herein, the language “administration event” describes the administration of a subject a given dose, within any suitable window of time, e.g., less than about 60 minutes, 50, minutes, 40 minutes, 30 minutes, 20 minutes, 10 minutes, 5 minutes, or 2 minutes. The term “treating” or “treatment” as used herein means the treating or treatment of a disease or medical condition in a patient, such as a mammal (particularly a human) that includes: ameliorating the disease or medical condition, such as, eliminating or causing regression of the disease or medical condition in a patient; suppressing the disease or medical condition, for example by, slowing or arresting the development of the disease or medical condition in a patient; or alleviating one or more symptoms of the disease or medical condition in a patient. In an embodiment, prophylactic treatment can result in preventing the disease or medical condition from occurring, in a subject. A “patient” or “subject,” used interchangeably herein, can be any mammal including, for example, a human and non-human subjects. A patient or subject can have a condition to be treated or can be susceptible to a condition to be treated. As used herein, and unless otherwise specified, the terms “prevent,” “preventing” and “prevention” refer to the prevention of the onset, recurrence or spread of a disease, disorder, or condition, or of one or more symptoms thereof. The terms encompass the inhibition or reduction of a symptom of the particular disease, disorder, or condition. Subjects with familial history of a disease, disorder, or condition, in particular, are candidates for preventive regimens in certain embodiments. In addition, subjects who have a history of recurring symptoms are also potential candidates for the prevention. In this regard, the term “prevention” may be interchangeably used with the term “prophylactic treatment.” As used herein, and unless otherwise specified, the terms “manage,” “managing” and “management” refer to preventing or slowing the progression, spread or worsening of a disease, disorder, or condition, or of one or more symptoms thereof. Often, the beneficial effects that a subject derives from a prophylactic and / or therapeutic agent do not result in a cure of the disease, disorder, or condition. In this regard, the term “managing” encompasses treating a subject who had suffered from the particular disease, disorder, or condition in an attempt to prevent or minimize the recurrence of the disease, disorder, or condition. “Therapeutically effective amount” refers to an amount of a compound(s) or its salt form sufficient to treat a specified disorder or disease or one or more of its symptoms and / or to prevent the occurrence of the disease or disorder (prophylactically effective amount). As used herein, and unless otherwise specified, a “prophylactically effective amount” of an active agent, is an amount sufficient to prevent a disease, disorder, or condition, or prevent its recurrence. The term “prophylactically effective amount” can encompass an amount that improves overall prophylaxis or enhances the prophylactic efficacy of another prophylactic agent. The term “administration schedule” is a plan in which the type, amount, period, procedure, etc. of the drug in the drug treatment are shown in time series, and the dosage, administration method, administration order, administration date, and the like of each drug are indicated. The date specified to be administered is determined before the start of the drug administration. The 32 administration is continued by repeating the course with the set of administration schedules as “courses”. A “continuous” administration schedule means administration every day without interruption during the treatment course. If the administration schedule follows an “intermittent” administration schedule, then days of administration may be followed by “rest days” or days of non-administration of drug within the course. A “drug holiday” indicates that the drug is not administered in a predetermined administration schedule. For example, after undergoing several courses of treatment, a subject may be prescribed a regulated drug holiday as part of the administration schedule, e.g., prior to re-recommencing active treatment. The language “toxic spikes” is used herein to describe neurological spikes in concentration of any compound described herein that would produce side-effects of sedation or psychotomimetic effects, e.g., hallucination, dizziness, and nausea; which can not only have immediate repercussions, but also effect treatment compliance. In particular, side effects may become more pronounced at blood concentration levels of about 250, 300, 400, 500 ng / L or more. As used herein, and unless otherwise specified, a “neuropsychiatric disease or disorder” is a behavioral or psychological problem associated with a known neurological condition, and typically defined as a cluster of symptoms that co-exist. Examples of neuropsychiatric disorders include, but are not limited to, attention deficit disorder, attention deficit hyperactivity disorder, bipolar and manic disorders, depression or any combinations thereof. “Inflammatory conditions,” “inflammatory disease,” or “inflammatory disorder” as used herein, refers broadly to chronic or acute inflammatory diseases, including but are not limited to rheumatic diseases (e.g., rheumatoid arthritis, osteoarthritis, psoriatic arthritis) spondyloarthropathies (e g., ankylosing spondylitis, reactive arthritis, Reiter's syndrome), crystal arthropathies (e.g., gout, pseudogout, calcium pyrophosphate deposition disease), multiple sclerosis, Lyme disease, polymyalgia rheumatica; connective tissue diseases (e.g., systemic lupus erythematosus, systemic sclerosis, polymyositis, dermatomyositis, Sjogren's syndrome); vasculitides (e.g., polyarteritis nodosa, Wegener's granulomatosis, Churg-Strauss syndrome); inflammatory conditions including consequences of trauma or ischaemia, sarcoidosis; vascular diseases including atherosclerotic vascular disease, atherosclerosis, and vascular occlusive disease (e.g., atherosclerosis, ischaemic heart disease, myocardial infarction, stroke, peripheral vascular disease), and vascular stent restenosis; ocular diseases including uveitis, corneal disease, iritis, iridocyclitis, and cataracts. As used herein, the term “and / or” includes any and all combinations of one or more of the associated listed items. As used in the description herein and throughout the claims that follow, the meaning of “a”, “an”, and “the” includes plural reference as well as the singular reference unless the context clearly dictates otherwise. The term “about” in association with a numerical value means that the value varies up or down by 5%. For example, for a value of about 100, means 95 to 105 (or any value between 95 and 105). Compounds Disclosed herein is a compound of Formula (I), or a pharmaceutically acceptable salt, a polymorph, stereoisomer, or solvate thereof, R8 \l-—-R9 r7 wherein: R2, Rs, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium, Rs and R9 are independently selected from the group consisting of -CH3, -CH2D, -CHD2, and -CD3, and Xi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium. In some embodiments, R2, Rs, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium. In some embodiments, R2 is deuterium. In some embodiments, R2 is hydrogen. In some embodiments, Rs is deuterium. In some embodiments, Rs is hydrogen. In some embodiments, Re is deuterium. In some embodiments, Re is hydrogen. In some embodiments, R7 is deuterium. In some embodiments, R7 is hydrogen. R2, R5, Re, and R7 may be the same, for example, R2, R5, Re, and R7 may each be hydrogen, or alternatively, R2, R5, Re, and R7 may each be deuterium. In some embodiments, at least one of R2, Rs, Re, and R7 is deuterium. In some embodiments, at least two of R2, R5, Re, and R7 are deuterium. In some embodiments, at least three of R2, R5, Re, and R7 are deuterium. In some embodiments, Rs and R9 are independently selected from the group consisting of -CH3, -CH2D, -CHD2, and -CD3. Rs and R9 may be the same, or different. In some embodiments, Rs and R9 are the same. In some embodiments, Rs and R9 are independently selected from the group consisting of -CH3 and -CD3 In some embodiments, Rs and R9 are methyl (-CH3). In some embodiments, Rs and R9 are a partially deuterated methyl group, i.e., -CDH2 or -CD2H. In some embodiments, Rs and R9 are a fully deuterated methyl group (-CD3). In some embodiments, at least one of Rs and R9 is -CD3. In some embodiments, Xi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium. Xi and X2 may be the same, or different. In some embodiments, Xi and X2 are the same. In some embodiments, Xi and X2 are hydrogen. In some embodiments, Xi and X2 are deuterium. Yi and Y2 may be the same, or different. In some embodiments, Yi and Y2 are the same. In some embodiments, Yi and Y2 are hydrogen. In some embodiments, Yi and Y2 are deuterium. In some embodiments, Xi, X2, Yi, and Y2 are hydrogen. In some embodiments, Xi, X2, Yi, and Y2 are deuterium. In some embodiments, Xi, X2, Yi, Y2, R2, R5, Re, R7, Rs, and R9 are each hydrogen. In some embodiments, at least one of Xi, X2, Yi, Y2, R2, R5, Re, R7, Rs, and R9 comprises deuterium. In some embodiments, at least Xi, X2, Rs, and Ry comprise deuterium. In some embodiments, at least Xi, X2, Yi, Y2, Rs, and R9 comprise deuterium. In some embodiments, Xi, X2, Yi, and Y2 are deuterium, and Rs and R9 are a fully deuterated methyl group (-CD3). The compounds of Formula (I) may contain a stereogenic center. In such cases, the compounds may exist as different stereoisomeric forms, even though Formula (I) is drawn without reference to stereochemistry. Accordingly, the present disclosure includes all possible stereoisomers and includes not only racemic compounds but the individual enantiomers (enantiomerically pure compounds), individual diastereomers (diastereomerically pure compounds), and their non-racemic mixtures as well. When a compound is desired as a single enantiomer, such may be obtained by, e.g., stereospecific synthesis, as is known in the art. In some embodiments, the compounds described herein, e.g., compounds of Formula (I), are non-stereogenic. In some embodiments, the compounds described herein, e.g., compounds of Formula (I), are racemic. In some embodiments, the compounds described herein, e.g., compounds of Formula (I), are enantiomerically enriched (one enantiomer is present in a higher percentage), including enantiomerically pure. In some embodiments, the compounds described herein, e.g., compounds of Formula (I), are provided as a single diastereomer. In some embodiments, the compounds described herein, e.g., compounds of Formula (I), are provided as a mixture of diastereomers. When provided as a mixture of diastereomers, the mixtures may include equal mixtures, or mixtures which are enriched with a particular diastereomer (one diastereomer is present in a higher percentage than another). In some embodiments, the compound of Formula (I) is an agonist of a serotonin 5-HT2 receptor. In some embodiments, the compound of Formula (I) is an agonist of a serotonin 5-HT2A receptor. In some embodiments, the compound of Formula (I) is selected from the group consisting (1-6), (1-5), (1-8), The compound number, IUPAC name, and substituent listing for the above-identified compounds are provided in Table 1. Table 1. Exemplary compounds of Formula (I) Compound identifier and name Formula (I) X1,X2 Yi,Y2 r2 r5 r6 r7 Rs,R9 I-l 3-(2-(bis(methyl-e / 3)amino)ethyl-l,l,2,2-( / 4)-l / f-indol-2,5,6,7-t / 4-4-ol D,D D,D D D D D -CD3,-CD3 1-2 3-(2-(bis(methyl-e / 3)amino)ethyl-2,2- < / 2)-17 / -indol-2,5,6,7-rf4-4-ol D,D H,H D D D D -CD3,-CD3 1-3 3-(2-(bis(methyl-< / 3)amino)ethyl-l,l,2,2-<4)-17Aindol-4-ol D,D D,D H H H H -cd3,-cd3 1-4 3-(2-(bis(methyl-<73)amino)ethyl-2,2-t / 2)-l / 7-mdol-4-ol D,D H,H H H H H -cd3,-cd3 1-5 3 -(2-(dimethylamino)ethyl-1,1 l / f-indol-4-ol D,D D,D H H H H -ch3,-ch3 1-6 3-(2-(dimethylamino)ethyl-2, indol-4-ol D,D H,H H H H H -ch3,-ch3 1-7 3-(2-(dimethylamino)ethyl)-12f-indol-4-ol H,H H,H H H H H -CH3,-CH3 1-8 3"(2"(bis(methyl"J3)amino)ethyl)"lH-indol-4-ol H,H H,H H H H H -CD3,-CD3 1-9 3 -(2-(dimethylamino)ethyl-1,1 - J2)-1H-indol-4-ol H,H D,D H H H H -CH3,-CH3 1-10 3-(2-(bis(methyl-e / 3)amino)ethyl-1,1-< / 2)-lH-indol-4-ol H,H D,D H H H H -CD3,-CD3 In some embodiments, the compounds of the present disclosure are provided as a free base in crystalline form, e.g., as determined by XRPD. Accordingly, pharmaceutical compositions may be prepared from compounds of Formula (I) as a free base, in one or more polymorphic forms, and may be used for treatment as set forth herein. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-t / 4)-177-indol-2,5,6,7-J4-4-ol (1-1), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(bis(methyl-J3)amino)ethyl-2,2-<72)-l / / -indol-2,5,6,7-^4-4-01 (1-2), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(bis(methyl-J3)amino)ethyl-1,1,2,2-^)-l / f-indol-4-ol (1-3), as determined by X-ray powder diffraction. In some embodiments, 1-3 is a crystalline solid form (polymorph of pattern 1) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.582°, 8.395°, 9.647°, 10.444°, 11.319°, 12.614°, 13.372°, 14.222°, 15.157°, 16.524°, 16.787°, 17.693°, 19.468°, 19.699°, 20.901°, 21.132°, 21.859°, 22.547°, 23.699°, 24.630°, 25.034°, 25.264°, 26.867°, 27.399°, 27.929°, 28.219°, 28.871°, 29.430°, 30.120°, 30.675°, 31.373°, 32.365°, 33.880°, 34.418°, 34.792°, 35.884°, 36.254°, 37.156°, 38.200°, and 38.417°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 2A-2C. In some embodiments, 1-3 is a crystalline solid form (polymorph of pattern 2) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 8.124°, 8.357°, 10.059°, 12.630°, 13.420°, 13.743°, 14.053°, 15.220°, 16.272°, 16.763°, 16.954°, 17.328°, 17.662°, 18.062°, 18.742°, 19.413°, 19.658°, 20.172°, 20.836°, 21.267°, 21.833°, 22.213°, 22.504°, 23.334°, 23.701°, 24.385°, 25.431°, 25.721°, 26.049°, 27.291°, 28.368°, 30.349°, 30.656°, 31.337°, 31.538°, 32.091°, 35.870°, 38.514°, and 41.361°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 88-89. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(bis(methyl-J3)amino)ethyl-2,2-<72)-177-indol-4-ol (1-4), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(dimethylamino)ethyl-1,1,2,2-^)-l / f-indol-4-ol (1-5), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(dimethylamino)ethyl-2,2-( / 1)-l / f-indol-4-ol (1-6), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is a crystalline form of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (1-7), as determined by X-ray powder diffraction. In some embodiments, 1-7 is a crystalline solid form (polymorph of pattern 1) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.563°, 8.375°, 12.626°, 13.383°, 15.211°, 16.753°, 17.671°, 19.668°, 21.112°, 21.863°, 22.201°, 22.560°, 23.711°, 24.592°, 25.415°, 26.820°, 27.357°, 27.921°, 28.228°, 29.253°, 30.653°, 31.364°, 32.401°, 33.797°, 34.445°, 39.867°, as determined by XRPD using a CuKa radiation source, for example, as shown in Fig 3C. In some embodiments, the compounds of the present disclosure are provided as a free base in amorphous form, e g., as determined by XRPD. Accordingly, pharmaceutical compositions may 39 be prepared from compounds of Formula (I) as a free base, in one or more amorphic forms, and may be used for treatment as set forth herein. Numerous attempts to make an amorphous form of the compounds of the present disclosure proved unsuccessful, including crash cooling / freeze drying, fast evaporation from numerous organic solvents, and anti-solvent precipitation. Crash cooling / freeze drying and fast evaporation techniques each gave only crystalline material, while anti-solvent precipitation failed to produce solid material. After significant experimentation, it has been discovered that amorphous forms of the compounds of Formula (I), e.g., compound 1-3 (psilocin-4 / 10) can be prepared through a melt / crash cooling procedure. Briefly, crystalline free base material may be heated beyond its melting point, e.g., to at least 180°C, at least 181°C, at least 182°C, at least 183°C, at least 184°C, at least 185°C using DSC or similar technique, followed by rapid cooling to near the glass transition of the material, e.g., to about 26°C, about 27°C, about 28°C, about 29°C, about 30°C, as determined by differential scanning calorimetry (DSC). For example, it has been found that amorphous 1-3 (PI-4 / 10, free base) can be prepared by a melt / crash cooling procedure in DSC in which crystalline 1-3 is heated to beyond the melting point (to 185°C) and then rapidly cooled to 30°C (glass transition temperature of 27 °C). The amorphous nature of the compound of Formula (I) can be determined e.g., by XRPD. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-d4)-l / f-indol-2,5,6,7-J4-4-ol (1-1), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(bis(methyl-J3)amino)ethyl-2,2-t / 2)-l / f-indol-2,5,6,7-^4-4-01 (1-2), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-<74)-l / Z-indol-4-ol (1-3), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(bis(methyl-d3)amino)ethyl-2,2-4 / 2)-l#-indol-4-ol (1-4), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(dimethylamino)ethyl-1,1,2,2-4 / 4)-l / f-indol-4-ol (1-5), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(dimethylamino)ethyl-2,2-4 / 2)-l / f-indol-4-ol (1-6), as determined by X-ray powder diffraction. In some embodiments, the compound of Formula (I) is an amorphous form of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (1-7), as determined by X-ray powder diffraction. Such amorphous forms of the compounds of Formula (I) (free base) may be advantageous in terms of dissolution rates in water, compared to crystalline forms, thereby enabling rapid systemic absorption for quick therapeutic onset and a short duration of drug action. Further, in some embodiments, pharmaceutical compositions may be prepared which comprise the amorphous forms of the compounds of Formula (I) (free base). The pharmaceutical compositions of the present disclosure, such as those set forth herein, may act to stabilize the amorphous forms of the compounds of Formula (I), which tend to be unstable and have a tendency to crystallize. Accordingly, the pharmaceutical compositions can be used to stabilize and deliver these amorphous forms to subjects in need of treatment, e.g., for the treatment of a condition or disease associate with a serotonin 5-HT2 receptor. Salt forms Also disclosed herein is a pharmaceutically acceptable salt of the compound of Formula (I), or a pharmaceutically acceptable polymorph, stereoisomer, or solvate thereof. The acid used to form the pharmaceutically acceptable salt of the compound of Formula (I) may be a monoacid, a diacid, a triacid, a tetraacid, or may contain a higher number of acid groups. The acid groups may be, e.g., a carboxylic acid, a sulfonic acid, a phosphonic acid, or other acidic moieties containing at least one replaceable hydrogen atom. Examples of acids for use in the preparation of the pharmaceutically acceptable (acid addition) salts disclosed herein include, but are not limited to, acetic acid, 2,2-dichloroacetic acid, phenylacetic acid, acylated amino acids, alginic acid, ascorbic acid, L-aspartic acid, sulfonic acids (e.g., benzenesulfonic acid, camphorsulfonic acid, (+)-(1 S)-camphor-l O-sulfonic acid, ethane-l,2-disulfonic acid, ethanesulfonic acid, 2-hydroxy-ethanesulfonic acid, methanesulfonic acid, naphthalene-2-sulfonic acid, naphthalene-l,5-disulfonic acid, p-toluenesulfonic acid, ethanedisulfonic acid, etc.), benzoic acids (e.g., benzoic acid, 4-acetamidobenzoic acid, 2-acetoxybenzoic acid, salicylic acid, 4-amino-salicylic acid, gentisic acid, etc ), boric acid, (+)-camphoric acid, cinnamic acid, citric acid, cyclamic acid, cyclohexanesulfamic acid, dodecylsulfuric acid, formic acid, fumaric acid, galactaric acid, glucoheptonic acid, D-gluconic acid, D-glucuronic acid, L-glutamic acid, a-oxo-glutaric acid, glycolic acid, hippuric acid, hydrobromic acid, hydrochloric acid, hydroiodic acid, (+)-L-lactic acid, (—)-D-lactic acid, (±)-DL-lactic acid, lactobionic acid, maleic acid, malic acid, (—)-L-malic acid, (+)-D-malic acid, hydroxymaleic acid, malonic acid, (±)-DL-mandelic acid, 41 isethionic acid, l-hydroxy-2-naphthoic acid, nicotinic acid, nitric acid, orotic acid, oxalic acid, pamoic acid, perchloric acid, phosphoric acid, L-pyroglutamic acid, saccharic acid, succinic acid, sulfuric acid, sulfamic acid, tannic acid, tartaric acids (e.g., DL-tartaric acid, (+)-L-tartaric acid, (-)-D-tartaric acid), thiocyanic acid, propionic acid, valeric acid, and fatty acids (including fatty mono- and di- acids, e.g., adipic (hexandioic) acid, lauric (dodecanoic) acid, linoleic acid, myristic (tetradecanoic) acid, capric (decanoic) acid, stearic (octadecanoic) acid, oleic acid, caprylic (octanoic) acid, palmitic (hexadecenoic) acid, sebacic acid, undecylenic acid, caproic acid, etc.) Certain salts are preferred among the list above because they possess physical and pharmaceutical characteristics / properties which make them suitable for pharmaceutical preparation and administration. For example, preferred salt forms of the compounds disclosed herein (e.g., compounds of Formula (I)) are those that possess one or more of the following characteristics: are easy to prepare in high yield with a propensity towards salt formation; are stable and have well-defined physical properties such as crystallinity, lack of polymorphism, and high melting / enthalpy of fusion; have slight or no hygroscopicity; are free flowing, do not cohere / adhere to surfaces, and possess a regular morphology; have acceptable aqueous solubility and rate of dissolution for the intended dosage form; and / or are physiologically acceptable, e.g., do not cause excessive irritation. Crystallinity The pharmaceutically acceptable salt of the compound of Formula (I) may be crystalline or amorphous, as determined e g., by X-ray powder diffraction (XRPD). In some embodiments, the salt of the compound of Formula (I) is amorphous. Amorphous forms typically possess higher aqueous solubility and rates of dissolution compared to their crystalline counterparts, and thus may be well suited for quick acting dosage forms adapted to rapidly release the active agent, such as for orodispersible dosage forms (ODxs), immediate release (IR) dosage forms, and the like. In some embodiments, the salt of the compound of Formula (I) is crystalline. Crystalline forms are advantageous in terms of stability and providing well-defined physical properties, which is desirable for pharmaceutical preparation and administration. The salts of the compound of Formula (I) can be in a stable crystalline or amorphous form. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a percent crystallinity of at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95%, at least 99%, or at least 99.5%, and up to 100%, as determined by XRPD analysis. Preference is given to salt forms with high crystallinity, 42 as determined e.g., by discrete and sharp Bragg diffractions in the X-ray diffractograms. XRPD analyses can be carried out, e.g., on a Bruker AXS D2 diffractometer using CuKa radiation. The instrument may be equipped with a fine focus X-ray tube. The tube voltage and amperage can be set to 30 kV and 10 mA, respectively, and a 0-0 geometry can be used, using a LynxEye detector from 5-42 °20, with a step size of0.024 °20 and a collection time of 0.1 seconds per step. In terms of pharmaceutical production processes, advantageous salt forms of the compounds of Formula (I) are those that readily afford a solid material, either a crystalline solid or an amorphous solid, in acceptable yield without proceeding via an oil, and with favorable volume factors, making them suitable for mass production. Salts forms of the compound of Formula (I) can exist in different polymorphs (i.e., forms having a different crystal structure), however, preferred salt forms of the present disclosure are those which can be generated as a single crystalline form or single polymorph (including a single amorphous form), as determined by XRPD and / or differential scanning calorimetry (DSC). It is also generally desirable for the salts to be free flowing, not cohere / adhere to surfaces, and possess a regular morphology. Chemical / Solid-state Stability In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a melt onset of from about 90°C, from about 100°C, from about 110°C, from about 120°C, from about 130°C, from about 140°C, from about 150°C, from about 160°C, from about 170°C, from about 180°C, from about 190°C, and up to about 250°C, up to about 240°C, up to about 230°C, up to about 225°C, up to about 210°C, up to about 200°C, as determined by DSC. Pharmaceutically acceptable salts of the compound of Formula (I) may also be characterized as non-hygroscopic or slightly hygroscopic, preferably non-hygroscopic. The hygroscopicity may be measured herein by performing a moisture adsorption-desorption isotherm using a dynamic vapor sorption (DVS) analyzer with a starting exposure of 40% relative humidity (RH), increasing humidity up to 90% RH, decreasing humidity to 0% RH, increasing humidity to 90% RH, decreasing humidity to 0% RH, and finally increasing the humidity back to the starting 40% RH, and classified according to the following: non-hygroscopic: < 0.2%; slightly hygroscopic: > 0.2% and < 2%; hygroscopic: > 2% and < 15%; very hygroscopic: > 15%; deliquescent: sufficient water is absorbed to form a 43 liquid; all values measured as weight increase (w / w due to acquisition of water) at >90% RH and 25°C. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a weight increase at >90% RH of less than 1% w / w, less than 0.8% w / w, less than 0.6% w / w, less than 0.5% w / w, less than 0.4% w / w, less than 0.3% w / w, less than 0.2% w / w, less than 0.1% w / w, less than 0.08% w / w, less than 0.06% w / w, less than 0.05% w / w, less than 0.02% w / w, as determined by DVS. Dry powder samples of free base and salts can be maintained / stored in open or closed environments, such as in open or closed flasks / vials, under ambient or stress conditions e.g., 25°C / 90+% RH, 40°C / 75% RH, etc. without appreciable degradation or physical changes (e.g., changed forms, deliquesced, etc.). For example, dry powder samples of free base and salts forms disclosed herein may have a purity or form change of less than 10%, less than 5%, less than 1%, when stored under ambient conditions or stress conditions (e.g., increased temperature, e.g., 40°C, and / or humidity). Solution-phase samples of the free base and salts can be maintained / stored in open or closed environments, such as in open or closed flasks / vials, under ambient or stress conditions e.g., 25°C / 90+% RH, 40°C / 75% RH, etc. without appreciable degradation. Thus, in some embodiments, the present disclosure provides stable solution-phase compositions of salts of the compounds of Formula (I) (e.g., stable solvates of salt forms of compounds of Formula (I) which are in solvated form, preferably fully solvated form), which can be stored as a solution, such as in the form of an aqueous solution, an organic solvent solution, or a mixed aqueous-organic solvent solution, for prolonged periods of time without appreciable degradation or physical changes, such as oiling out of solution. Solvents which can be used to form the solution-phase compositions can be any one or more solvents set forth herein, e.g., water, ethanol, etc. In some embodiments, the solution-phase composition is an aqueous solution-phase composition comprising the pharmaceutically acceptable salt of the compound of Formula (I) solvated with water. The identification of stable solution-phase compositions of compounds of Formula (I) and their salts is advantageous at least because such compositions do not require use immediately after being prepared, such as within 5 minutes, within 4 minutes, within 3 minutes, within 2 minutes, within 1 minute, within 45 seconds, within 30 seconds, within 15 seconds, within 10 seconds of being prepared. Instead, the stable solution-phase compositions of the compounds of Formula (I) and 44 salts thereof described herein can be prepared in advance, when desired, optionally stored, and can be administered hours, days, or even weeks after being prepared, without materially effecting efficacy, e.g., without appreciable degradation of the psilocin or psilocin-type active. In some embodiments, aqueous solutions formed from the pharmaceutically acceptable salt of the compound of Formula (I) is characterized by increased stability compared to aqueous solutions that are prepared from the compound of Formula (I) (free base) but are otherwise substantially the same. For example, the pharmaceutically acceptable salt of the compound of Formula (I) may be at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70% more stable in aqueous solution subjected to 40°C for 24 hours, with or without the presence of metal ions, in terms of % (active) remaining, compared to aqueous solutions prepared with the compound of Formula (I) (free base) but are otherwise substantially the same. Such improved stability behavior can also be found in pharmaceutical compositions of the present disclosure. Samples can be pulled at pre-determined time-points and analyzed for stability, changes in form, etc. for example, by NMR, XRPD, HPLC with UV-visible multiple wavelength detector, UPLC, etc. Physiologically Acceptability Suitable salt forms of the compounds of Formula (I) are physiologically acceptable. Accordingly, preferred addition salts of the compound of Formula (I) are those formed with an organic acid, preferably an organic acid with a medium or mild acidity, for example an organic acid with a pKa in water of no less than -3.0, no less than -2.0, no less than -1.0, no less than 0, no less than 1.0, no less than 1.5, no less than 2.0, no less than 2.5, no less than 3.0, no less than 3.5, no less than 4.0, no less than 4.5, for example, from 3.0 to 6.5. Further, it may also be desirable to use acid addition salts that impart a pleasant taste profile (e.g., sweet, citrus flavored, etc.), although poor tasting salt forms (e.g., bitter, harsh, etc.) may still be acceptable depending on, for example, the route of administration and the optional use of taste masking agents such as sweetening agents, flavoring agents, etc. Solubility The aqueous solubility of the salt forms of the compounds of Formula (I) can be determined by equilibrating excess solid with 1 mL of water for 24 hours at 22° C. A 200 uL 45 aliquot can be centrifuged at 15,000 rpm for 15 minutes. The supernatant can be analyzed by HPLC and the solubility can be expressed as its free base equivalent (mg FB / mL). For example, pharmaceutically acceptable salts of compound of Formula (I) can be prepared and the solubility and solution pH can be measured. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a water solubility at 22°C of from about 1 mg / mL to about 400 mg / mL. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a water solubility of from about 1 mg / mL, from about 2 mg / mL, from about 3 mg / mL, from about 5 mg / mL, from about 10 mg / mL, from about 20 mg / mL, from about 30 mg / mL, from about 40 mg / mL, from about 50 mg / mL, from about 60 mg / mL, from about 70 mg / mL, from about 80 mg / mL, from about 90 mg / mL, from about 100 mg / mL, from about 110 mg / mL, from about 120 mg / mL, from about 130 mg / mL, from about 140 mg / mL, from about 150 mg / mL, and up to about 400 mg / mL, up to about 380 mg / mL, up to about 360 mg / mL, up to about 340 mg / mL, up to about 320 mg / mL, up to about 300 mg / mL, up to about 280 mg / mL, up to about 260 mg / mL, up to about 250 mg / mL. Several salt forms of the compounds described herein can exhibit the above solubilities, yielding a final water pH approximately between pH 3 to 6 without gelling. In some embodiments, the salt of the compound of Formula (I) has a water solubility from about 200 mg / mL to about 400 mg / mL. In some embodiments, the salt of the compound of Formula (I) has a water solubility from about 150 mg / mL to about 250 mg / mL. In some embodiments, the salt of the compound of Formula (I) has a water solubility of greater than about 1 mg / mL, 10 mg / mL, 20 mg / mL, 30 mg / mL, 40 mg / mL, 50 mg / mL, 60 mg / mL, 70 mg / mL, 80 mg / mL, 90 mg / mL, 100 mg / mL, 110 mg / mL, 120 mg / mL, 130 mg / mL, 140 mg / mL, or 150 mg / mL. In some embodiments, salt forms of the compounds of Formula (I) possess dissolution rates which enable rapid systemic absorption for quick therapeutic onset and a short duration of drug action. In some embodiments, the salt of the compound of Formula (I) is capable of dissolution in an aqueous medium below about pH 7.5, such as from pH 1-7, from pH 3-7, or from pH 4-7. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, a salicylate salt, an ascorbate salt, a hydrochloride salt, a maleate salt, a malate salt, a methanesulfonate salt, a 46 toluenesulfonate salt, a glucuronate salt, or a glutarate salt of the compound of Formula (I). In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a salt formed from a sulfonic acid (e.g., benzenesulfonic acid, camphorsulfonic acid, (+)-(1 S)-camphor-1 O-sulfonic acid, ethane-1,2-disulfonic acid, ethanesulfonic acid, 2-hydroxy-ethanesulfonic acid, methanesulfonic acid, naphthalene-2-sulfonic acid, naphthalene-l,5-disulfonic acid, p-toluenesulfonic acid, ethanedisulfonic acid, etc.). In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a salt formed from a benzoic acid (e.g., benzoic acid, 4-acetamidobenzoic acid, 2-acetoxybenzoic acid, salicylic acid, 4-amino-salicylic acid, etc ). In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a benzenesulfonate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a tartrate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a hemi-fumarate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is an acetate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a citrate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a malonate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a fumarate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a succinate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is an oxalate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a benzoate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a salicylate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is an ascorbate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a hydrochloride salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a maleate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a malate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a methanesulfonate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a toluenesulfonate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a glucuronate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a glutarate salt. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, or a salicylate salt of the compound of Formula (I), with a benzenesulfonate salt, a succinate salt, or a benzoate salt of the compound of Formula (I) being preferred, and with a benzenesulfonate salt or a benzoate salt of the compound of Formula (I) being particularly preferred. Exemplary pharmaceutically acceptable salt forms (i.e., addition salt forms) of the aboveidentified compounds are provided in Table 2. Table 2. Exemplary pharmaceutically acceptable salts of compounds of Formula (I) Salt form identifier Salt type of compound Salt form identifier Salt type of compound Lia Benzenesulfonate of LI L4g Fumarate of 1-4 Lib Tartrate of 1-1 L4h Succinate of 1-4 Lie Hemi-fumarate of LI L4i Oxalate of 1-4 Lid Acetate of LI L4j Benzoate of 1-4 Lie Citrate of LI L4k Salicylate of 1-4 Llf Malonate of LI L5a Benzenesulfonate of 1-5 Llg Fumarate of LI L5b Tartrate of 1-5 Llh Succinate of 1-1 L5c Hemi-fumarate of 1-5 Lli Oxalate of 1-1 L5d Acetate of 1-5 Ilj Benzoate of 1-1 L5e Citrate of 1-5 Ilk Salicylate of 1-1 L5f Malonate of 1-5 L2a Benzenesulfonate of 1-2 L5g Fumarate of 1-5 L2b Tartrate of 1-2 L5h Succinate of 1-5 L2c Hemi-fumarate of 1-2 L5i Oxalate of 1-5 L2d Acetate of 1-2 I-5j Benzoate of 1-5 L2e Citrate of 1-2 L5k Salicylate of 1-5 L2f Malonate of 1-2 L6a Benzenesulfonate of 1-6 L2g Fumarate of 1-2 L6b Tartrate of 1-6 L2h Succinate of 1-2 L6c Hemi-fumarate of 1-6 L2i Oxalate of 1-2 L6d Acetate of 1-6 I-2j Benzoate of 1-2 L6e Citrate of 1-6 L2k Salicylate of 1-2 L6f Malonate of 1-6 L3a Benzenesulfonate of 1-3 L6g Fumarate of 1-6 L3b Tartrate of 1-3 L6h Succinate of 1-6 L3c Hemi-fumarate of 1-3 L6i Oxalate of 1-6 L3d Acetate of 1-3 L6j Benzoate of 1-6 L3e Citrate of 1-3 L6k Salicylate of 1-6 L3f Malonate of 1-3 L7a Benzenesulfonate of 1-7 L3g Fumarate of 1-3 L7b Tartrate of 1-7 L3h Succinate of 1-3 L7c Hemi-fumarate of 1-7 L3i Oxalate of 1-3 L7d Acetate of 1-7 I-3j Benzoate of 1-3 L7e Citrate of 1-7 L3k Salicylate of 1-3 L7f Malonate of 1-7 L4a Benzenesulfonate of 1-4 L7g Fumarate of 1-7 L4b Tartrate of 1-4 L7h Succinate of 1-7 1-4 c Hemi-fumarate of 1-4 L7i Oxalate of 1-7 L4d Acetate of 1-4 I-7j Benzoate of 1-7 I-4e Citrate of 1-4 L7k Salicylate of 1-7 L4f Malonate of 1-4 Table 2 (continued) Salt form identifier Salt type of compound Salt form identifier Salt type of compound I-8a Benzenesulfonate of 1-8 I-lOa Benzenesulfonate of 1-10 I-8b Tartrate of 1-8 I-10b Tartrate of I-10 I-8c Hemi-fumarate of 1-8 I-10c Hemi-fumarate of 1-10 I-8d Acetate of 1-8 I-10d Acetate of I-10 I-8e Citrate of 1-8 I-10e Citrate of 1-10 I-8f Malonate of 1-8 I-10f Malonate of 1-10 I-8g Fumarate of 1-8 I-10g Fumarate of I-10 I-8h Succinate of 1-8 I-10h Succinate of 1-10 I-8i Oxalate of 1-8 I-10i Oxalate of 1-10 I-8j Benzoate of 1-8 I-10j Benzoate of 1-10 I-8k Salicylate of 1-8 I-10k Salicylate of 1-10 I-9a Benzenesulfonate of 1-9 I-9b Tartrate of 1-9 I-9c Hemi-fumarate of 1-9 I-9d Acetate of 1-9 I-9e Citrate of 1-9 I-9f Malonate of 1-9 I-9g Fumarate of 1-9 I-9h Succinate of 1-9 I-9i Oxalate of 1-9 I-9j Benzoate of 1-9 I-9k Salicylate of 1-9 In some embodiments, the pharmaceutically acceptable salt is a benzenesulfonate salt of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-d4)-l / f-indol-4-ol (I-3a). In some embodiments, salt I-3a is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.023°, l.lhT, 11.822°, 12.550°, 12.860°, 13.994°, 15.521°, 18.436°, 19.503°, 20.760°, 21.070°, 22.007°, 22.745°, 23.340°, 24.187°, 25.532°, 26.880°, 27.856°, 28.163°, 31.267°, 33.024°, 35.030°, 36.835°, 39.312°, 40.545°, and 40.988°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 63A-63D (pattern 1). In some embodiments, the pharmaceutically acceptable salt is a benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-l / f-indol-4-ol (I-7a). In some embodiments, salt I-7a is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.002°, 7.733°, 11.768°, 12.516°, 12.882°, 13.546°, 13.968°, 14.788°, 15.225°, 15.474°, 18.370°, 19.737°, 20.703°, 21.050°, 21.873°, 21.982°, 22.315°, 22.639°, 23.282°, 23.775°, 24.125°, 25.193°, 25.475°, 25.931°, 26.813°, 27.778°, 28.127°, 30.866°, 31.207°, 32.941°, 33.222°, 33.698°, 36.803°, 38.668°, and 39.289°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 3A-3B (pattern 1). In some embodiments, the pharmaceutically acceptable salt is a benzoate salt of 3-(2-(bis(methyl-d3)amino)ethyl-l, 1,2,2-^)-l / Z-indol-4-ol (I-3j). In some embodiments, salt 1-3 j is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 9.486°, 11.006°, 12.379°, 13.428°, 14.608°, 15.446°, 16.389°, 18.247°, 18.977°, 19.346°, 19.831°, 20.868°, 21.447°, 22.860°, 23.878°, 24.944°, 25.737°, 26.144°, 26.341°, 26.990°, 27.708°, 28.595°, 30.048°, 30.763°, 31.127°, 31.839°, 32.800°, 34.460°, 35.444°, 37.725°, and 38.597°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 78A-78C (pattern 1). In some embodiments, the pharmaceutically acceptable salt is a benzoate salt of 3-(2-(dimethylamino)ethyl)-l / Z-indol-4-ol (I-7j). In some embodiments, salt I-7j is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 9.492°, 11.011°, 12.391°, 13.440°, 14.609°, 15.432°, 16.394°, 18.259°, 18.967°, 19.356°, 19.827°, 20.843°, 21.476°, 22.062°, 22.805°, 23.862°, 24.963°, 25.734°, 26.170°, 26.992°, 27.738°, 28.593°, 30.073°, 30.746°, 31.041°, 31.799°, 32.794°, 33.551°, 34.480°, 35.430°, 37.685°, and 38.643°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 53A-53B (pattern 1). In some embodiments, the pharmaceutically acceptable salt is a citrate salt of 3-(2-(bis(methyl-J3)amino)ethyl-l, 1,2,2-^)-l / Z-indol-4-ol (I-3e). In some embodiments, salt I-3e is in the form of an amorphous solid as characterized by an X-ray powder diffraction (XRPD). In some embodiments, the pharmaceutically acceptable salt is a citrate salt of 3-(2-(dimethylamino)ethyl)-177-indol-4-ol (I-7e). In some embodiments, salt I-7e is in the form of an amorphous solid as characterized by an X-ray powder diffraction (XRPD), for example, as shown in Fig. 37. In some embodiments, the pharmaceutically acceptable salt is a tartrate salt of 3-(2-(bis(methyl-J3)amino)ethyl-1,1,2,2-4 / 4)-l / f-indol-4-ol (I-3b). In some embodiments, salt I-3b is in 51 a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0.2°) selected from the group consisting of 6.732°, 12.708°, 13.470°, 14.774°, 15.921°, 16.268°, 17.295°, 18.869°, 20.079°, 20.208°, 20.877°, 21.894°, 22.657°, 23.491°, 23.702°, 24.636°, 24.882°, 25.569°, 26.685°, 27.060°, 27.502°, 28.179°, 28.597°, 29.035°, 29.257°, 29.527°, 31.017°, 31.527°, 32.059°, 32.307°, 33.012°, 34.024°, 34.388°, 34.905°, 35.361°, 36.183°, 37.372°, 37.764°, 38.657°, 41.049°, as determined by XRPD using a CuKa radiation source, for example, as shown in Figs. 69A-69B (pattern 2). In some embodiments, the pharmaceutically acceptable salt is a tartrate salt of 3-(2-(dimethylamino)ethyl)-lK-indol-4-ol (I-7b). In some embodiments, salt I-7b is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0.2°) selected from the group consisting of 6.798°, 11.360°, 12.764°, 13.535°, 14.837°, 15.973°, 16.351°, 17.367°, 18.937°, 20.168°, 20.929°, 21.946°, 22.719°, 23.604°, 23.814°, 24.874°, 25.609°, 26.745°, 27.111°, 27.558°, 28.653°, 29.630°, 31.129°, 31.567°, 32.180°, 33.073°, 34.096°, 34.460°, 36.226°, 37.497°, 38.727°, and 41.126°, as determined by XRPD using a CuKa radiation source, for example, as shown in Fig. 12 (pattern 1). In some embodiments, salt I-7b is in a crystalline solid form of pattern 2 characterized by an X-ray powder diffraction as shown in Fig. 12. In some embodiments, the pharmaceutically acceptable salt is a hemi-fumarate salt of 3-(2-(dimethylamino)ethyl)-l / f-indol-4-ol (I-7c). In some embodiments, salt I-7c is in a crystalline solid form characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0,2°) selected from the group consisting of 8.483°, 8.733°, 11.080°, 11.351°, 11.622°, 12.615°, 13.258, 14.977°, 15.557°, 16.089°, 16.319°, 16.606°, 17.013°, 18.928°, 18.884°, 19.429°, 19.734°, 20.643°, 21.484°, 22.067°, 23.433°, 24.466°, 24.885°, 26.740°, 27.900°, 28.557°, 29.523°, 32.888°, 34.183°, and 36.808°, as determined by XRPD using a CuKa radiation source, for example, as shown in Fig. 28 (pattern 5). Without being bound to any particular theory, it is believed that the novel salts of the compounds of Formula (I) are stable and have a faster / quicker therapeutic onset, a shorter duration of drug action (i.e., short duration of therapeutic effect), and less variability in exposures than psilocybin-based drugs (e.g., psilocybin). In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is a fatty acid salt. The fatty acid used to make the fatty acid salt of the compound of Formula 52 (I) may be a fatty monoacid or a fatty diacid, and may contain a fatty hydrocarbon portion made up of hydrogen and anywhere from 4, from 6, from 8, from 10, from 12, from 14, from 16, and up to 26, up to 24, up to 22, up to 20, up to 18 carbon atoms, which may be fully saturated or partially unsaturated. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, a caprylate salt, a palmitate salt, a sebacate salt, an undecylenate salt, or a caproate salt of the compound of Formula (I). In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, or a caprylate salt of the compound of Formula (I), with a laurate salt, a linoleate salt, a caprate salt, or a caprylate salt of the compound of Formula (I) being preferred. Exemplary pharmaceutically acceptable fatty acid salt forms (i.e., addition salt forms) of the above-identified compounds are provided in Table 3. Table 3. Exemplary pharmaceutically acceptable fatty acid salts of compounds of Formula (I) Salt form identifier Salt type of compound Salt form identifier Salt type of compound Ill Adipate of LI 1-61 Adipate of 1-6 I-lm Laurate of 1-1 L6m Laurate of 1-6 Lin Linoleate of 1-1 L6n Linoleate of 1-6 1-10 Myristate of LI L6o Myristate of 1-6 Lip Caprate of 1-1 L6p Caprate of 1-6 Llq Stearate of 1-1 L6q Stearate of 1-6 Llr Oleate of LI L6r Oleate of 1-6 Lis Caprylate of 1-1 L6s Caprylate of 1-6 1-21 Adipate of 1-2 1-71 Adipate of 1-7 I-2m Laurate of 1-2 L7m Laurate of 1-7 L2n Linoleate of 1-2 L7n Linoleate of 1-7 L2o Myristate of 1-2 L7o Myristate of 1-7 L2p Caprate of 1-2 L7p Caprate of 1-7 L2q Stearate of 1-2 L7q Stearate of 1-7 L2r Oleate of 1-2 L7r Oleate of 1-7 L2s Caprylate of 1-2 L7s Caprylate of 1-7 L3I Adipate of 1-3 L8I Adipate of 1-8 L3m Laurate of 1-3 L8m Laurate of 1-8 L3n Linoleate of 1-3 L8n Linoleate of 1-8 L3o Myristate of 1-3 L8o Myristate of 1-8 L3p Caprate of 1-3 L8p Caprate of 1-8 L3q Stearate of 1-3 L8q Stearate of 1-8 L3r Oleate of 1-3 L8r Oleate of 1-8 L3s Caprylate of 1-3 L8s Caprylate of 1-8 1-41 Adipate of 1-4 1-91 Adipate of 1-9 I-4m Laurate of 1-4 I-9m Laurate of 1-9 I-4n Linoleate of 1-4 I-9n Linoleate of 1-9 1-4 o Myristate of 1-4 L9o Myristate of 1-9 L4p Caprate of 1-4 L9p Caprate of 1-9 L4q Stearate of 1-4 L9q Stearate of 1-9 L4r Oleate of 1-4 L9r Oleate of 1-9 L4s Caprylate of 1-4 L9s Caprylate of 1-9 1-51 Adipate of 1-5 1-101 Adipate of 1-10 L5m Laurate of 1-5 L10m Laurate of 1-10 L5n Linoleate of 1-5 LlOn Linoleate of 1-10 L5o Myristate of 1-5 LlOo Myristate of I-10 L5p Caprate of 1-5 L10p Caprate of I-10 L5q Stearate of 1-5 L10q Stearate of I-10 L5r Oleate of 1-5 L10r Oleate of 1-10 L5s Caprylate of 1-5 I-10s Caprylate of I-10 In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a solubility in corn oil at 22°C of from about 0.4 mg / mL, from about 0.5 mg / mL, from about 0.6 mg / mL, from about 0.7 mg / mL, from about 0.8 mg / mL, from about 0.9 mg / mL, from 54 about 1 mg / mL, and up to about 2 mg / mL, up to about 1.9 mg / mL, up to about 1.8 mg / mL, up to about 1.7 mg / mL, up to about 1.6 mg / mL, up to about 1.5 mg / mL, up to about 1.4 mg / mL, up to about 1.3 mg / mL, up to about 1.2 mg / mL. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a solubility in Crodamol® GTCC (medium chain glyceride, from Croda) at 22°C of from about 0.4 mg / mL, from about 0.6 mg / mL, from about 0.8 mg / mL, from about 1 mg / mL, from about 1.2 mg / mL, from about 1.4 mg / mL, from about 1.6 mg / mL, and up to about 4 mg / mL, up to about 3.8 mg / mL, up to about 3.6 mg / mL, up to about 3.4 mg / mL, up to about 3.2 mg / mL, up to about 3 mg / mL, up to about 2.8 mg / mL, up to about 2.6 mg / mL, up to about 2.4 mg / mL, up to about 2.2 mg / mL. In some embodiments, the pharmaceutically acceptable salt of the compound of Formula (I) has a solubility in Maisine® CC (mixture of unsaturated mono-, di-, and triglycerides, from Gattefosse) at 22°C of from about 0.8 mg / mL, from about 1 mg / mL, from about 1.2 mg / mL, from about 1.4 mg / mL, from about 1.6 mg / mL, from about 1.8 mg / mL, from about 2 mg / mL, and up to about 5 mg / mL, up to about 4.8 mg / mL, up to about 4.6 mg / mL, up to about 4.4 mg / mL, up to about 4.2 mg / mL, up to about 4 mg / mL, up to about 3.8 mg / mL, up to about 3.6 mg / mL, up to about 3.4 mg / mL, up to about 3.2 mg / mL, up to about 3 mg / mL, up to about 2.8 mg / mL, up to about 2.6 mg / mL, up to about 2.4 mg / mL, up to about 2.2 mg / mL. Owing to their relatively hydrophobic nature, fatty acid salts of the compounds of Formula (I) may be advantageous when used in medications adapted for a modified, controlled, slow, or extended release profile. As a result, the fatty acid salts of the compounds of Formula (I) may be well suited for routes of administration (e.g., subcutaneous, transdermal, etc.) and / or dosage forms adapted for providing low doses of API over extended periods of time, as may be the case for subpsychedelic dosing regimens. Non-limiting examples of such dosage forms include, but are not limited to, depots, patches including microneedle patches, liposomes, micelles, microspheres, nanosystems, or other controlled release devices, such as those set forth herein. Also disclosed herein is a method for stabilizing a compound of Formula (I). The method includes preparing a pharmaceutically acceptable salt of the compound of Formula (I). Also disclosed herein is a method for preparing a pharmaceutically acceptable salt of the compound of Formula (I). In some embodiments, the method includes: (a) suspending the free base of the compound of Formula (I) in a solvent or mixture of solvents; (b) contacting an acid with the compound of Formula (I) to provide a mixture; (c) optionally heating the mixture; (d) optionally cooling the mixture; and (e) isolating the salt. Various solvents may be used in the disclosed methods, including one or more protic solvents, one or more aprotic solvents, or mixtures thereof. In some embodiments, the solvent(s) used in the method of preparing the salt is / are a protic solvent(s). In some embodiments, the solvent used in the method of preparing the salt is selected from the group consisting of methanol, ethanol, propanol, isopropanol, butanol, 2-butanol, acetone, butanone, dioxanes (1,4-di oxane), water, tetrahydrofuran (THF), acetonitrile (MeCN), ether solvents (e.g., t-butylmethyl ether (TBME)), hexane, heptane, octane, and combinations thereof. In some embodiments, the solvent is ethanol. In some embodiments, the solvent is 1,4-dioxane. In some embodiments, the solvent is acetonitrile. In some embodiments, the solvent is tetrahydrofuran. Suitable acids for use in the preparation of pharmaceutically acceptable acid addition salts may include those described heretofore. The acid may be an inorganic acid such as hydrochloric acid, or an organic acid, with organic acids being preferred. In some embodiments, the acid is an organic acid selected from the group consisting of ascorbic acid, citric acid, fumaric acid, maleic acid, malonic acid, (—)-L-malic acid, (+)-L-tartaric acid, methanesulfonic acid, benzenesulfonic acid, toluenesulfonic acid, benzoic acid, salicylic acid, succinic acid, oxalic acid, D-glucuronic acid, glutaric acid salt, and acetic acid. In some embodiments, the acid is an organic acid selected from the group consisting of benzenesulfonic acid, (+)-L-tartaric acid, fumaric acid, acetic acid, citric acid, malonic acid, succinic acid, oxalic acid, benzoic acid, and salicylic acid, with benzenesulfonic acid, succinic acid, and benzoic acid being preferred. In some embodiments, the acid is a fatty acid, such as adipic (hexandioic) acid, lauric (dodecanoic) acid, linoleic acid, myristic (tetradecanoic) acid, capric (decanoic) acid, stearic (octadecanoic) acid, oleic acid, caprylic (octanoic) acid, palmitic (hexadecenoic) acid, sebacic acid, undecylenic acid, caproic acid, etc., with particular mention being made to adipic (hexandioic) acid, lauric (dodecanoic) acid, linoleic acid, myristic (tetradecanoic) acid, capric (decanoic) acid, stearic (octadecanoic) acid, oleic acid, and caprylic (octanoic) acid. In some embodiments, a stoichiometric (or superstoichiometric) quantity of the acid is contacted with the compound of Formula (I). In some embodiments, a sub-stoichiometric (eg., 0.5 molar equivalents) quantity of the acid is contacted with the compound of Formula (I). The use of sub-stoichiometric quantities of the acid may be desirable when, for example, the acid contains at least two acidic protons (e g., two or more carboxylic acid groups) and the target salt is a hemiacid salt. In some embodiments, the mixture is heated, e.g., refluxed, prior to cooling. In some embodiments, the mixture is cooled and the salt is precipitated out of the solution. In some embodiments, the salt is precipitated out of solution in crystalline form. In some embodiments, the salt is precipitated out of solution in amorphous form. Isolation of the salt may be performed by various well-known isolation techniques, such as filtration, decantation, and the like. In some embodiments, the isolating step includes filtering the mixture. After isolation, additional crystallization and / or recrystallization steps may also optionally be performed, if desired, for example to increase purity, crystallinity, etc. Pharmaceutical compositions Also disclosed herein is a pharmaceutical composition comprising a compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, and a pharmaceutically acceptable vehicle. The pharmaceutical compositions may contain one, or more than one, compound, salt form, polymorph, and / or solvate of the present disclosure. “Pharmaceutically acceptable vehicles” may be vehicles approved by a regulatory agency of the Federal or a state government or listed in the U.S. Pharmacopeia or other generally recognized pharmacopeia for use in mammals, such as humans. The term “vehicle” refers to a diluent, adjuvant, excipient, or carrier with which a compound or salt thereof of the present disclosure is formulated for administration to a mammal. Such pharmaceutical vehicles can be liquids, such as water and oils, including those of petroleum, animal, vegetable or synthetic origin, such as peanut oil, soybean oil, mineral oil, sesame oil and the like. The pharmaceutical vehicles can be water, saline, gum acacia, gelatin, starch paste, talc, keratin, colloidal silica, urea, and the like. In addition, auxiliary, stabilizing, solubilizing, thickening, lubricating, coloring agents, sweetening agents, and other pharmaceutical additives may be included in the disclosed compositions, for example those set forth hereinafter. The pharmaceutical vehicle can include an acid, such as those described heretofore for use in forming the pharmaceutically acceptable salt forms of the present disclosure, with specific mention being made to citric acid and / or tartaric acid. The pharmaceutical composition may comprise a single compound of Formula (I), or a pharmaceutically acceptable salt, a polymorph, stereoisomer, or solvate thereof, or a mixture of compounds of Formula (I), in either free base or salt form, including one or more polymorphs of such materials. The pharmaceutical composition may be formed from an isotopologue mixture of the disclosed compounds. In some embodiments, a subject compound of Formula (I) may be present in the pharmaceutical composition at a purity of at least 50% by weight, at least 60% by weight, at least 70% by weight, at least 80% by weight, at least 90% by weight, at least 95% by weight, at least 99% by weight, based on a total weight of isotopologues of the compound of Formula (I) present in the pharmaceutical composition. For example, a pharmaceutical composition formulated with a salt form of psilocin d-10 (compound 1-3; 3-(2-(bis(methyl-Jsjaminojethyl-1,1,2,2-^4)-l#-indol-4-ol), as the subject compound, may additionally contain isotopologues of the subject compound, e.g., psilocin d-9, psilocin d-8, etc., as free-base or salt forms, polymorphs, stereoisomers, solvates, or mixtures thereof. In some embodiments, the composition is substantially free of other isotopologues of the compound, in either free base or salt form, e.g., the composition has less than 20, 15, 10, 9, 8, 7, 6, 5, 4, 3, 2 or 1 or 0.5 mole percent of other isotopologues of the compound. In some embodiments, any position in the compound having deuterium has a minimum deuterium incorporation of at least 10 atom %, at least 20 atom %, at least 25 atom %, at least 30 atom %, at least 40 atom %, at least 45 atom %, at least 50 atom %, at least 60 atom %, at least 70 atom %, at least 80 atom %, at least 90 atom %, at least 95 atom %, at least 99 atom % at the site of deuteration. The pharmaceutical composition may be formulated with an enantiomerically pure compound of the present disclosure, e.g., a compound of Formula (I), or a racemic mixture of the compounds. As described herein, a racemic compound of Formula (I) may contain about 50% of the R- and S-stereoisomers based on a molar ratio (about 48 to about 52 mol %, or about a 1:1 ratio)) of one of the isomers. In some embodiments, a composition, medicament, or method of treatment may involve combining separately produced compounds of the R- and S-stereoisomers in an approximately equal molar ratio (e g., about 48 to 52%). In some embodiments, a medicament or pharmaceutical composition may contain a mixture of separate compounds of the R- and S-58 stereoisomers in different ratios. In some embodiments, the pharmaceutical composition contains an excess (greater than 50%) of the R-enantiomer. Suitable molar ratios of R / S may be from about 1.5:1, 2:1, 3:1, 4:1, 5:1, 10:1, or higher. In some embodiments, a pharmaceutical composition may contain an excess of the S-enantiomer, with the ratios provided for R / S reversed. Other suitable amounts of R / S may be selected. For example, the R-enantiomer may be enriched, e.g., may be present in amounts of at least about 55% to 100%, or at least 65%, at least 75%, at least 80%, at least 85%, at least 90%, about 95%, about 98%, or 100%. In other embodiments, the S-enantiomer may be enriched, e.g., in amounts of at least about 55% to 100%, or at least 65%, at least 75%, at least 80%, at least 85%, at least 90%, about 95%, about 98%, or 100%. Ratios between all these exemplary embodiments as well as greater than and less than them while still within the disclosure, all are included. Compositions may contain a mixture of the racemate and a separate compound of Formula (I), or a pharmaceutically acceptable salt, a polymorph, stereoisomer, or solvate thereof. The pharmaceutical composition may be formulated with one or more polymorphs of the compounds of Formula (I) and / or their salt forms, including crystalline and / or amorphous polymorphs of the compounds or salts thereof. Pharmaceutical compositions can take the form of capsules, tablets, pills, pellets, lozenges, powders, granules, syrups, elixirs, solutions, suspensions, emulsions, suppositories, or sustained-release formulations thereof, or any other form suitable for administration to a mammal. In some instances, the pharmaceutical compositions are formulated for administration in accordance with routine procedures as a pharmaceutical composition adapted for oral or intravenous administration to humans. Examples of suitable pharmaceutical vehicles and methods for formulation thereof are described in Remington: The Science and Practice of Pharmacy, Alfonso R. Gennaro ed., Mack Publishing Co. Easton, Pa., 19th ed., 1995, Chapters 86, 87, 88, 91, and 92, incorporated herein by reference. The choice of vehicle will be determined in part by the particular compound, salt form, as well as by the particular method used to administer the composition. Accordingly, there is a wide variety of suitable formulations of the subject pharmaceutical compositions. Pharmaceutical compositions may be generally provided herein which comprise about 0.1 to about 1000 mg, about 1 to about 500 mg, about 2 to about 100 mg, about 1 mg, about 2 mg, about 3 mg, about 5 mg, about 10 mg, about 20 mg, about 30 mg, about 40 mg, about 50 mg, about 100 mg, about 500 mg of one or more compounds as disclosed herein, in either free base or salt 59 form, as active pharmaceutical ingredient (API). The quantity of compound of Formula (I) (on active basis) in a unit dose preparation may be varied or adjusted within the above ranges as deemed appropriate using sound medical judgment, according to the particular application, administration route, potency of the active component, etc. The composition can, if desired, also contain other compatible therapeutic agents. The pharmaceutical compositions disclosed herein may be administered at once, or multiple times at intervals of time. It is understood that the precise dosage and duration of treatment may vary with the age, weight, and condition of the patient being treated, and may be determined empirically using known testing protocols or by extrapolation from in vivo or in vitro test or diagnostic data. It is further understood that for any particular individual, specific dosage regimens should be adjusted over time according to the individual need and the professional judgment of the person administering or supervising the administration of the formulations. In the case wherein the patient's condition does not improve, upon the doctor's discretion the compounds may be administered chronically, that is, for an extended period of time, including throughout the duration of the patient's life in order to ameliorate or otherwise control or limit the symptoms of the patient's disease or condition. In the case wherein the patient's status does improve, upon the doctor's discretion the compounds may be given continuously or temporarily suspended for a certain length of time (i.e., a “drug holiday”). Once improvement of the patient's conditions has occurred, a maintenance dose is administered if necessary. Subsequently, the dosage or the frequency of administration, or both, can be reduced, as a function of the symptoms, to a level at which the improved disorder is retained. Patients can, however, require intermittent treatment on a long-term basis upon any recurrence of symptoms. Pharmaceutical compositions comprising a compound disclosed herein may be formulated in various dosage forms, such as those for oral, parenteral, and topical administration. The pharmaceutical compositions may also be formulated as a modified release dosage form, including delayed-, extended-, prolonged-, sustained-, pulsatile-, controlled-, accelerated-, fast-, targeted-, programmed-release, and gastric retention dosage forms. These dosage forms can be prepared according to conventional methods and techniques known to those skilled in the art 60 (see, Remington: The Science and Practice of Pharmacy, supra; Modified-Release Drug Delivery Technology, Rathbone et al., Eds., Drugs and the Pharmaceutical Science, Marcel Dekker, Inc.: New York, N.Y., 2002; Vol. 126). Any of the pharmaceutical compositions described herein can comprise (as the active component) at least one of compounds of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. A. Oral Administration The pharmaceutical compositions disclosed herein may be provided in solid, semisolid, or liquid dosage forms for oral administration. As used herein, oral administration includes gastric (enteral) delivery, for example whereby the medication is taken by mouth and swallowed, as well as intraoral administration such as through the mucosal linings of the oral cavity, e.g., buccal, lingual, and sublingual administration. Suitable oral dosage forms include, but are not limited to, tablets, capsules, pills, troches, lozenges, pastilles, cachets, pellets, medicated chewing gum, granules, bulk powders, effervescent or non-effervescent powders or granules, solutions, emulsions, suspensions, solutions, wafers, films, sprinkles, elixirs, and syrups. In addition to the active ingredient(s), the pharmaceutical compositions may contain one or more pharmaceutically acceptable vehicles (e.g., carriers or excipients), including, but not limited to, binders, fillers, diluents, disintegrants, wetting agents, lubricants, glidants, coloring agents, dye-migration inhibitors, sweetening agents, preservatives, antioxidants, lyoprotectants, stabilizing agents, solubilizing agents, complexing agents, and flavoring agents. In some embodiments, pharmaceutical compositions of the present disclosure may be in orodispersible dosage forms (ODxs), including orally disintegrating tablets (ODTs) (also sometimes referred to as fast disintegrating tablets, orodispersible tablets, or fast dispersible tablets) or orodispersible films (ODFs) (or wafers). Such dosage forms may be particularly advantageous in the present disclosure as they allow for pre-gastric absorption of the compounds / salts herein, e.g., when administered intraorally through the mucosal linings of the oral cavity, e.g., buccal, lingual, and sublingual administration, for increased bioavailability and faster onset compared to oral administration through the gastrointestinal tract. Orally disintegrating tablets can be prepared by different techniques, such as freeze drying (lyophilization), molding, spray drying, mass extrusion or compressing. Preferably, the orally disintegrating tablets are prepared by lyophilization. In some embodiments, orally disintegrating 61 tablet refers to forms which disintegrate in less than about 90 seconds, in less than about 60 seconds, in less than about 30 seconds, in less than about 20, in less than about 10 seconds, in less than about 5 seconds, or in less than about 2 seconds after being received in the oral cavity. In some embodiments, orally disintegrating tablet refers to forms which dissolve in less than about 90 seconds, in less than about 60 seconds, or in less than about 30 seconds after being received in the oral cavity. In some embodiments, orally disintegrating tablet refers to forms which disperse in less than about 90 seconds, in less than about 60 seconds, in less than about 30 seconds, in less than about 20, in less than about 10 seconds, in less than about 5 seconds, or in less than about 2 seconds after being received in the oral cavity. In some embodiments, the pharmaceutical compositions are in the form of orodispersible dosage forms, such as oral disintegrating tablets (ODTs), having a disintegration time according to the United States Phamacopeia (USP) disintegration test <701> of not more than about 30 seconds, not more than about 20, not more than about 10 seconds, not more than about 5 seconds, not more than about 2 seconds. Orodispersible dosage forms having longer disintegration times according to the United States Phamacopeia (USP) disintegration test <701>, such as when adapted for extended release, for example on the order of 30 minutes or less, 20 minutes or less, 10 minutes or less, 5 minutes or less, 4 minutes or less, 3 minutes or less, 2 minutes or less, are also contemplated. In some embodiments, the pharmaceutical compositions are in the form of lyophilized orodispersible dosage forms, such as lyopholized ODTs. In some embodiments, the lyophilized orodispersible dosage forms (e g., lyophilized ODTs) are created by creating a porous matrix by subliming the water from pre-frozen aqueous formulation of the drug containing matrix-forming agents and other vehicles such as those set forth herein, e g., one or more lyoprotectants, preservatives, antioxidants, stabilizing agents, solubilizing agents, flavoring agents, etc. In some embodiments, the orodispersible dosage forms comprise two component frameworks of a lyophilized matrix system that work together to ensure the development of a successful formulation. In some embodiments, the first component is a water-soluble polymer such as gelatin, dextran, alginate, and maltodextrin. This component maintains the shape and provides mechanical strength to the dosage form (binder). In some embodiments, the second constituent is a matrix-supporting / disintegration-enhancing agent such as sucrose, lactose, mannitol, xylitol, microcrystalline cellulose, calcium diphosphate, and / or starch, which acts by cementing the porous framework, provided by the water-soluble polymer and accelerates the disintegration of the 62 orodispersible dosage forms. In some embodiments, the lyophilized orodispersible dosage form (e.g., lyophilized ODT) includes gelatin and mannitol. In some embodiments, the lyophilized orodispersible dosage form (e.g., lyophilized ODT) includes gelatin, mannitol, and one or more of a lyoprotectant, a preservative, an antioxidant, a stabilizing agent, a solubilizing agent, a flavoring agent, etc., with particular mention being made to citric acid. A non-limiting example of an ODT formulation is Zydis® orally dispersible tablets (available from Catalent). In some embodiments, the ODT formulation (e.g., Zydis® orally dispersible tablets) includes one or more water-soluble polymers, such as gelatin, one or more matrix materials, fillers, or diluents, such as mannitol, a compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, and optionally a lyoprotectant, a preservative, an antioxidant, a stabilizing agent, a solubilizing agent, and / or a flavoring agent. In some embodiments, the ODT formulation (e.g., Zydis® orally dispersible tablets) includes gelatin, mannitol, a compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, and citric acid and / or tartaric acid. In some embodiments, the pharmaceutical compositions are in the form of lyophilized orodispersible films (ODFs) (or wafers). In some embodiments, the pharmaceutical compositions are in the form of lyophilized ODFs protected for the long-term storage by a specialty packaging excluding moisture, oxygen, and light. In some embodiments, the lyophilized ODFs are created by creating a porous matrix by subliming the water from pre-frozen aqueous formulation of the drug containing matrix-forming agents and other vehicles such as those set forth herein, e.g., one or more of a lyoprotectant, a preservative, an antioxidant, a stabilizing agent, a solubilizing agent, a flavoring agent, etc. In some embodiments, the lyophilized ODF includes a thin water-soluble film matrix. In some embodiments, the ODFs comprise two component frameworks of a lyophilized matrix system that work together to ensure the development of a successful formulation. In some embodiments, the first component is water-soluble polymers such as gelatin, dextran, alginate, and maltodextrin. This component maintains the shape and provides mechanical strength to the film / wafer (binder). In some embodiments, the second constituent is matrix-supporting / disintegration-enhancing agents such as sucrose and mannitol, which acts by cementing the porous framework, provided by the water-soluble polymer and accelerates the disintegration of the wafer. In some embodiments, the lyophilized ODFs include gelatin and mannitol. In some embodiments, the lyophilized ODFs include gelatin, mannitol, and one or more of a lyoprotectant, a preservative, an antioxidant, a stabilizing agent, a solubilizing agent, a flavoring agent, etc., with particular mention being made to citric acid. In some embodiments, the ODF (or wafer) can comprise a monolayer, bilayer, or trilayer. In some embodiments, the monolayer ODF contains an active agent and one or more pharmaceutically acceptable vehicles (e.g., carrier or excipients). In some embodiments, the bilayer ODF contains one or more excipients, such as a solubilizing agent, in a first layer and an active agent in the second layer. This configuration allows the active agent to be stored separately from the excipients and can increase the stability of the active agent and optionally increase the shelf life of the composition compared to the case where the excipients and the active agent were contained in a single layer. For tri-layer ODFs, each of the layers may be different or two of the layers, such as the upper and lower layers, may have substantially the same composition. In some embodiments, the lower and upper layers surround a core layer containing the active agent. In some embodiments, the lower and upper layers may contain one or more excipients, such as a solubilizing agent. In some embodiments, the lower and upper layers have the same composition. Alternatively, the lower and upper layers may contain different excipients or different amounts of the same excipient. The core layer typically contains the active agent, optionally with one or more excipients. In some embodiments, in addition to the active ingredient(s), the pharmaceutical compositions in orodispersible dosage forms (ODxs) may contain one or more pharmaceutically acceptable vehicles (e.g., carriers or excipients). For example, in some embodiments, pharmaceutical compositions in orodispersible dosage forms include one or more of pharmaceutically acceptable a lyoprotectant, a preservative, an antioxidant, a stabilizing agent, a solubilizing agent, a flavoring agent, etc. Examples of pharmaceutically acceptable lyoprotectants include, but are not limited to, disaccharides such as sucrose and trehalose, anionic polymers such as sulfobutylether-P-cyclodextrin (SBECD) and hyaluronic acid, and hydroxylated cyclodextrins. Examples of pharmaceutically acceptable preservatives include, but are not limited to, glycerin, methyl and propylparaben, benzoic acid, sodium benzoate and alcohol. Examples of pharmaceutically acceptable antioxidants, which may act to further enhance stability of the composition, include: (1) water soluble antioxidants, such as ascorbic acid, cysteine or salts thereof (cysteine hydrochloride), sodium bisulfate, sodium metabisulfite, sodium sulfite 64 and the like; (2) oil-soluble antioxidants, such as ascorbyl palmitate, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), lecithin, propyl gallate, alpha-tocopherol, and the like; and (3) metal chelating agents, such as citric acid, ethylenediamine tetraacetic acid (EDTA), sorbitol, tartaric acid, phosphoric acid, and the like. Examples of pharmaceutically acceptable stabilizing agents include, but are not limited to, fatty acids, fatty alcohols, alcohols, long chain fatty acid esters, long chain ethers, hydrophilic derivatives of fatty acids, polyvinyl pyrrolidones, polyvinyl ethers, polyvinyl alcohols, hydrocarbons, hydrophobic polymers, moisture-absorbing polymers, glycerol, methionine, monothioglycerol, ascorbic acid, citric acid, polysorbate, arginine, cyclodextrins, microcrystalline cellulose, modified celluloses (e g., carboxymethylcellulose, sodium salt), sorbitol, and cellulose gel. Examples of pharmaceutically acceptable solubilizing agents (or dissolution aids) include, but are not limited to, citric acid, hydroxypropyl cellulose, hydroxypropylmethylcellulose, sodium stearyl fumarate, methacrylic acid copolymer LD, methylcellulose, sodium lauryl sulfate, polyoxyl 40 stearate, purified shellac, sodium dehydroacetate, fumaric acid, DL-malic acid, L-ascorbyl stearate, L-asparagine acid, adipic acid, aminoalkyl methacrylate copolymer E, propylene glycol alginate, casein, casein sodium, a carboxyvinyl polymer, carboxymethylethylcellulose, powdered agar, guar gum, succinic acid, copolyvidone, cellulose acetate phthalate, tartaric acid, dioctylsodium sulfosuccinate, zein, powdered skim milk, sorbitan trioleate, lactic acid, aluminum lactate, ascorbyl palmitate, hydroxyethylmethylcellulose, hydroxypropylmethylcelluloseacetate succinate, polyoxyethylene (105) polyoxypropylene (5) glycol, polyoxyethylene hydrogenated castor oil 60, polyoxyl 35 castor oil, poly(sodium 4-styrenesulfonate), polyvinylacetaldiethylamino acetate, polyvinyl alcohol, maleic acid, methacrylic acid copolymer S, lauromacrogol, sulfuric acid, aluminum sulfate, phosphoric acid, calcium dihydrogen phosphate, sodium dodecylbenzenesulfonate, a vinyl pyrrolidone-vinyl acetate copolymer, sodium lauroyl sarcosinate, acetyl tryptophan, sodium methyl sulfate, sodium ethyl sulfate, sodium butyl sulfate, sodium octyl sulfate, sodium decyl sulfate, sodium tetradecyl sulfate, sodium hexadecyl sulfate, and sodium octadecyl sulfate. Of these, in some embodiments, such as in ODT formulation, citric acid is preferred. Flavoring agents include natural flavors extracted from plants, such as fruits, and synthetic blends of compounds which produce a pleasant taste sensation or taste masking effect. Examples 65 of flavoring agents include, but are not limited to, aspartame, saccharin (as sodium, potassium or calcium saccharin), cyclamate (as a sodium, potassium or calcium salt), sucralose, acesulfame-K, thaumatin, neohisperidin, dihydrochalcone, ammoniated glycyrrhizin, dextrose, maltodextrin, fructose, levulose, sucrose, glucose, wild orange peel, citric acid, tartaric acid, oil of wintergreen, oil of peppermint, methyl salicylate, oil of spearmint, oil of sassafras, oil of clove, cinnamon, anethole, menthol, thymol, eugenol, eucalyptol, lemon, lime, and lemon-lime. Cyclodextrins such as a-cyclodextrin, P-cyclodextrin, y-cyclodextrin, methyl-P-cyclodextrin, hydroxyethyl p-cyclodextrin, hydroxypropyl-P-cyclodextrin, hydroxypropyl y-cyclodextrin, sulfated P-cyclodextrin, sulfated a-cyclodextrin, sulfobutyl ether P-cyclodextrin, or other solubilized derivatives can also be advantageously used to enhance delivery of compositions described herein. Disclosed herein are pharmaceutical compositions in modified release dosage forms, which comprise a compound as disclosed herein and one or more release controlling excipients or carriers as described herein. Suitable modified release dosage vehicles include, but are not limited to, hydrophilic or hydrophobic matrix devices, water-soluble separating layer coatings, enteric coatings, osmotic devices, multiparticulate devices, and combinations thereof. The pharmaceutical compositions may also comprise non-release controlling excipients or carriers. Further disclosed herein are pharmaceutical compositions in enteric coated dosage forms, which comprise a compound as disclosed herein and one or more release controlling excipients or carriers for use in an enteric coated dosage form. The pharmaceutical compositions may also comprise non-release controlling excipients or carriers. Further disclosed herein are pharmaceutical compositions in effervescent dosage forms, which comprise a compound as disclosed herein and one or more release controlling excipients or carriers for use in an effervescent dosage form. The pharmaceutical compositions may also comprise non-release controlling excipients or carriers. Additionally disclosed are pharmaceutical compositions in a dosage form that has an instant releasing component and at least one delayed releasing component, and is capable of giving a discontinuous release of the compound in the form of at least two consecutive pulses separated in time from about 0.1 up to about 24 hours (e g., about 0.1, 0.5, 1, 2, 4, 6, 8, 10, 12, 14, 16, 18, 10, 22, or 24 hours). The pharmaceutical compositions comprise a compound as disclosed herein and one or more release controlling and non-release controlling excipients or carriers, such as those 66 excipients or carriers suitable for a disruptable semipermeable membrane and as swellable substances. Disclosed herein also are pharmaceutical compositions in a dosage form for oral administration to a subject, which comprise a compound, salt, or solvate as disclosed herein and one or more pharmaceutically acceptable vehicles (e g., excipients or carriers), enclosed in an intermediate reactive layer comprising a gastric juice-resistant polymeric layered material partially neutralized with alkali and having cation exchange capacity and a gastric juice-resistant outer layer. Pharmaceutical compositions adapted for oral administration, e.g., via compressed tablets, may be formulated with various vehicles such as those set forth herein. Examples of suitable vehicles may include, but are not limited to, binders, fillers, diluents, disintegrants, wetting agents, lubricants, glidants, coloring agents, dye-migration inhibitors, sweetening agents, preservatives, antioxidants, stabilizing agents, solubilizing agents, and flavoring agents. Binders or granulators impart cohesiveness to a tablet to ensure the tablet remains intact after compression. Suitable binders or granulators include, but are not limited to, starches, such as corn starch, potato starch, and pre-gelatinized starch (e.g., STARCH 1500); gelatin; sugars, such as sucrose, glucose, dextrose, molasses, and lactose; natural and synthetic gums, such as acacia, alginic acid, alginates, extract of Irish moss, Panwar gum, ghatti gum, mucilage of isabgol husks, carboxymethylcellulose, methylcellulose, polyvinylpyrrolidone (PVP), Veegum, larch arabogalactan, powdered tragacanth, and guar gum; celluloses, such as ethyl cellulose, cellulose acetate, carboxymethyl cellulose calcium, sodium carboxymethyl cellulose, methyl cellulose, hydroxyethylcellulose (HEC), hydroxypropylcellulose (HPC), hydroxypropyl methyl cellulose (HPMC); microcrystalline celluloses, such as AVICEL-PH-101, AVICEL-PH-103, AVICEL RC-581, AVICEL-PH-105 (FMC Corp., Marcus Hook, Pa ); and mixtures thereof. Suitable fillers include, but are not limited to, talc, calcium carbonate, microcrystalline cellulose, powdered cellulose, dextrates, kaolin, mannitol, silicic acid, sorbitol, starch, pre-gelatinized starch, and mixtures thereof. The binder or filler may be present from about 50 to about 99% by weight in the pharmaceutical compositions disclosed herein. Suitable diluents include, but are not limited to, dicalcium phosphate, calcium sulfate, lactose, sorbitol, sucrose, inositol, cellulose, kaolin, mannitol, sodium chloride, dry starch, and powdered sugar. Certain diluents, such as mannitol, lactose, sorbitol, sucrose, and inositol, when 67 present in sufficient quantity, can impart properties to some compressed tablets that permit disintegration in the mouth by chewing. Such compressed tablets can be used as chewable tablets. Suitable disintegrants include, but are not limited to, agar; bentonite; celluloses, such as methylcellulose and carboxymethylcellulose; wood products; natural sponge; cation-exchange resins; alginic acid; gums, such as guar gum and Veegum HV; citrus pulp; cross-linked celluloses, such as croscarmellose; cross-linked polymers, such as crospovidone; cross-linked starches; calcium carbonate; microcrystalline cellulose, such as sodium starch glycolate; polacrilin potassium; starches, such as corn starch, potato starch, tapioca starch, and pre-gelatinized starch; clays; aligns; and mixtures thereof. The amount of disintegrant in the pharmaceutical compositions disclosed herein varies upon the type of formulation, and is readily discernible to those of ordinary skill in the art. The pharmaceutical compositions disclosed herein may contain from about 0.5 to about 15% or from about 1 to about 5% by weight of a disintegrant. Suitable lubricants include, but are not limited to, calcium stearate; magnesium stearate; mineral oil; light mineral oil; glycerin; sorbitol; mannitol; glycols, such as glycerol behenate and polyethylene glycol (PEG); stearic acid; sodium lauryl sulfate; sodium stearyl fumarate; talc; hydrogenated vegetable oil, including peanut oil, cottonseed oil, sunflower oil, sesame oil, olive oil, com oil, and soybean oil; zinc stearate; ethyl oleate; ethyl laureate; agar; starch; lycopodium; silica or silica gels, such as AEROSIL® 200 (W.R. Grace Co., Baltimore, Md.) and CAB-O-SIL® (Cabot Co. of Boston, Mass.); and mixtures thereof. The pharmaceutical compositions disclosed herein may contain about 0.1 to about 5% by weight of a lubricant. Suitable glidants include colloidal silicon dioxide, CAB-O-SIL® (Cabot Co. of Boston, Mass ), and asbestos-free talc. Coloring agents include any of the approved, certified, water soluble FD&C dyes, and water insoluble FD&C dyes suspended on alumina hydrate, and color lakes and mixtures thereof. A color lake is the combination by adsorption of a water-soluble dye to a hydrous oxide of a heavy metal, resulting in an insoluble form of the dye. Sweetening agents include sucrose, lactose, mannitol, syrups, glycerin, and artificial sweeteners, such as saccharin and aspartame. Suitable emulsifying agents include gelatin, acacia, tragacanth, bentonite, and surfactants, such as polyoxyethylene sorbitan monooleate (TWEEN® 20), polyoxyethylene sorbitan monooleate 80 (TWEEN® 80), and triethanolamine oleate. Suspending and dispersing agents include sodium carboxymethylcellulose, pectin, tragacanth, Veegum, acacia, sodium carbomethyl cellulose, hydroxypropyl methylcellulose, and polyvinylpyrolidone. Preservatives include glycerin, methyl and propylparaben, benzoic add, sodium benzoate and alcohol. Wetting agents include propylene glycol monostearate, sorbitan monooleate, diethylene glycol monolaurate, and polyoxyethylene lauryl ether. Solvents include glycerin, sorbitol, ethyl alcohol, and syrup. Examples of non-aqueous liquids utilized in emulsions include mineral oil and cottonseed oil. Organic acids include citric and tartaric acid. Sources of carbon dioxide include sodium bicarbonate and sodium carbonate. It should be understood that many vehicles (carriers, excipients, etc.) may serve several functions, even within the same formulation. Particular mention is made to pharmaceutical compositions herein containing citric acid, which may play multiple roles as a stabilizing agent, e g., to stabilize the psilocin compound of the present disclosure in free base or salt form, as a solubilizing agent to provide fast dissolution of the active for rapid onset, etc., particularly for dosage forms adapted for rapid onset and a shorter duration of drug action, such as orodispersible dosage forms (e g., ODTs and ODFs). The pharmaceutical compositions herein may be in the form of compressed tablets, tablet triturates, chewable lozenges, rapidly dissolving tablets, multiple compressed tablets, or entericcoating tablets, sugar-coated, or film-coated tablets. Enteric-coated tablets are compressed tablets coated with substances that resist the action of stomach acid but dissolve or disintegrate in the intestine, thus protecting the active ingredients from the acidic environment of the stomach. Enteric-coatings include, but are not limited to, fatty acids, fats, phenylsalicylate, waxes, shellac, ammoniated shellac, and cellulose acetate phthalates. Sugar-coated tablets are compressed tablets surrounded by a sugar coating, which may be beneficial in covering up objectionable tastes or odors and in protecting the tablets from oxidation. Film-coated tablets are compressed tablets that are covered with a thin layer or film of a water-soluble material. Film coatings include, but are not limited to, hydroxyethylcellulose, sodium carboxymethylcellulose, polyethylene glycol 4000, and cellulose acetate phthalate. Film coating imparts the same general characteristics as sugar coating. Multiple compressed tablets are compressed tablets made by more than one compression cycle, including layered tablets, and press-coated or dry-coated tablets. The tablet dosage forms may be prepared from the active ingredient in powdered, crystalline, or granular forms, alone or in combination with one or more vehicles (e.g., carriers or excipients) described herein, including binders, disintegrants, controlled-release polymers, lubricants, diluents, and / or colorants. Flavoring and sweetening agents are especially useful in the formation of chewable tablets and lozenges. The dosage form may be an immediate release (IR) dosage form, examples of which include, but are not limited to, an immediate release (IR) tablets or an immediate release (IR) capsule. In addition to the API, dosage forms adapted for immediate release may include one or more pharmaceutically acceptable vehicles which readily disperse, dissolve, or otherwise breakdown in the gastric environment so as not to delay or prolong dissolution / absorption of the API. Examples of pharmaceutically acceptable vehicles for immediate release dosage forms include, but are not limited to, one or more binders / granulators, matrix materials, fillers, diluents, disintegrants, dispersing agents, solubilizing agents, lubricants, and / or performance modifiers. In some embodiments, the immediate release (IR) dosage form is an immediate release (IR) tablet comprising one or more of microcrystalline cellulose, sodium carboxymethylcellulose, magnesium stearate, mannitol, crospovidone, and sodium stearyl fumarate. In some embodiments, the immediate release (IR) dosage form comprises microcrystalline cellulose, sodium carboxymethylcellulose, and magnesium stearate. In some embodiments, the immediate release (IR) dosage form comprises mannitol, crospovidone, and sodium stearyl fumarate. The pharmaceutical compositions disclosed herein may be disclosed as soft or hard capsules, which can be made from gelatin, methylcellulose, starch, or calcium alginate. The hard gelatin capsule, also known as dry-filled capsule (DFC) or powder in capsule (PIC), consists of two sections, one slipping over the other, thus completely enclosing the active ingredient. The soft elastic capsule (SEC) is a soft, globular shell, such as a gelatin shell, which is plasticized by the addition of glycerin, sorbitol, or a similar polyol. The soft gelatin shells may contain a preservative to prevent the growth of microorganisms. Suitable preservatives are those as described herein, including methyl- and propyl-parabens, and sorbic acid. The liquid, semisolid, and solid dosage forms disclosed herein may be encapsulated in a capsule. Suitable liquid and semisolid dosage forms include solutions and suspensions in propylene carbonate, vegetable oils, or triglycerides. The capsules may also be coated as known by those of skill in the art in order to modify or sustain dissolution of the active ingredient. In some embodiments, the pharmaceutical compositions are in the form of immediate-release capsules for oral administration, and may further comprise cellulose, iron oxides, lactose, magnesium stearate, and sodium starch glycolate. In some embodiments, the pharmaceutical compositions are in the form of delayed-release capsules for oral administration, and may further comprise cellulose, ethylcellulose, gelatin, hypromellose, iron oxide, and titanium dioxide. In some embodiments, the pharmaceutical compositions are in the form of enteric coated delayed-release tablets for oral administration, and may further comprise carnauba wax, crospovidone, diacetylated monoglycerides, ethylcellulose, hydroxypropyl cellulose, hypromellose phthalate, magnesium stearate, mannitol, sodium hydroxide, sodium stearyl fumarate, talc, titanium dioxide, and yellow ferric oxide. In some embodiments, the pharmaceutical compositions are in the form of enteric coated delayed-release tablets for oral administration, and may further comprise calcium stearate, crospovidone, hydroxypropyl methylcellulose, iron oxide, mannitol, methacrylic acid copolymer, polysorbate 80, povidone, propylene glycol, sodium carbonate, sodium lauryl sulfate, titanium dioxide, and triethyl citrate. The pharmaceutical compositions disclosed herein may be disclosed in liquid and semisolid dosage forms, including emulsions, solutions, suspensions, elixirs, and syrups. An emulsion is a two-phase system, in which one liquid is dispersed in the form of small globules throughout another liquid, which can be oil-in-water or water-in-oil. Emulsions may include a pharmaceutically acceptable non-aqueous liquids or solvent, emulsifying agent, and preservative. Suspensions may include a pharmaceutically acceptable suspending agent and preservative. Aqueous alcoholic solutions may include a pharmaceutically acceptable acetal, such as a di(lower alkyl) acetal of a lower alkyl aldehyde (the term “lower” means an alkyl having between 1 and 6 carbon atoms), e.g., acetaldehyde diethyl acetal; and a water-miscible solvent having one or more hydroxyl groups, such as propylene glycol and ethanol. Elixirs are clear, sweetened, and hydroalcoholic solutions. Syrups are concentrated aqueous solutions of a sugar, for example, sucrose, and may also contain a preservative. For a liquid dosage form, for example, a solution in a polyethylene glycol may be diluted with a sufficient quantity of a pharmaceutically acceptable liquid carrier, e.g., water, to be measured conveniently for administration. Other useful liquid and semisolid dosage forms include, but are not limited to, those containing the active ingredient(s) disclosed herein, and a dialkylated mono- or poly-alkylene glycol, including, 1,2-dimethoxymethane, diglyme, triglyme, tetraglyme, polyethylene glycol-350-dimethyl ether, polyethylene glycol-550-dimethyl ether, polyethylene glycol-750-dimethyl ether, wherein 350, 550, and 750 refer to the approximate average molecular weight of the polyethylene glycol. These formulations may further comprise one or more antioxidants, such as butylated hydroxytoluene (BHT), butylated hydroxyanisole (BHA), propyl gallate, vitamin E, hydroquinone, hydroxycoumarins, ethanolamine, lecithin, cephalin, ascorbic acid, malic acid, sorbitol, phosphoric acid, bisulfite, sodium metabisulfite, thiodipropionic acid and its esters, and dithiocarbamates. In some embodiments, examples of pharmaceutically acceptable antioxidants include:      (1) water soluble antioxidants, such as ascorbic acid, cysteine hydrochloride, sodium bisulfate, sodium metabisulfite, sodium sulfite and the like; (2) oil-soluble antioxidants, such as ascorbyl palmitate, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), lecithin, propyl gallate, alpha-tocopherol, and the like; and (3) metal chelating agents, such as citric acid, ethylenediamine tetraacetic acid (EDTA), sorbitol, tartaric acid, phosphoric acid, and the like. Cyclodextrins such as a-cyclodextrin, P-cyclodextrin, y-cyclodextrin, methyl-p-cyclodextrin, hydroxyethyl p-cyclodextrin, hydroxypropyl-P-cyclodextrin, hydroxypropyl y-cyclodextrin, sulfated P-cyclodextrin, sulfated a-cyclodextrin, sulfobutyl ether P-cyclodextrin, or other solubilized derivatives can also be advantageously used to enhance delivery of compositions described herein. The pharmaceutical compositions disclosed herein for oral administration may be also disclosed in the forms of liposomes, micelles, microspheres, or nanosystems. The pharmaceutical compositions disclosed herein may be disclosed as non-effervescent or effervescent, granules and powders, to be reconstituted into a liquid dosage form. Pharmaceutically acceptable carriers and excipients used in the non-effervescent granules or powders may include diluents, sweeteners, and wetting agents. Pharmaceutically acceptable carriers and excipients used in the effervescent granules or powders may include organic acids and a source of carbon dioxide. Coloring and flavoring agents can be used in all of the above dosage forms. The pharmaceutical compositions disclosed herein may be co-formulated with other active ingredients which do not impair the desired therapeutic action, or with substances that supplement the desired action, such as drotrecogin-a, and hydrocortisone. • B. Parenteral Administration The pharmaceutical compositions disclosed herein may be administered parenterally by injection, infusion, or implantation, for local or systemic administration. Parenteral administration, as used herein, includes, but is not limited to, intravenous, intraarterial, intraperitoneal, intrathecal, intraventricular, intraurethral, intrastemal, intracranial, intramuscular, intrasynovial, and subcutaneous administration. The pharmaceutical compositions disclosed herein may be formulated in any dosage forms that are suitable for parenteral administration, including solutions, suspensions, emulsions, micelles, liposomes, microspheres, nanosystems, and solid forms suitable for solutions or suspensions in liquid prior to injection. Such dosage forms can be prepared according to conventional methods known to those skilled in the art of pharmaceutical science (see, Remington: The Science and Practice of Pharmacy, supra). The pharmaceutical compositions intended for parenteral administration may include one or more pharmaceutically acceptable vehicles (e g., carriers and excipients), including, but not limited to, aqueous vehicles, water-miscible vehicles, non-aqueous vehicles, antimicrobial agents or preservatives against the growth of microorganisms, stabilizers, solubility enhancers, isotonic agents, buffering agents, antioxidants, local anesthetics, suspending and dispersing agents, wetting or emulsifying agents, complexing agents, sequestering or chelating agents, cryoprotectants, lyoprotectants, thickening agents, pH adjusting agents, and inert gases. Suitable aqueous vehicles include, but are not limited to, water, saline, physiological saline or phosphate buffered saline (PBS), sodium chloride injection, Ringers injection, isotonic dextrose injection, sterile water injection, dextrose and lactated Ringers injection. Non-aqueous vehicles include, but are not limited to, fixed oils of vegetable origin, castor oil, com oil, cottonseed oil, olive oil, peanut oil, peppermint oil, safflower oil, sesame oil, soybean oil, hydrogenated vegetable oils, hydrogenated soybean oil, and medium-chain triglycerides of coconut oil, and palm seed oil. Water-miscible vehicles include, but are not limited to, ethanol, 1,3-butanediol, liquid polyethylene glycol (e g., polyethylene glycol 300 and polyethylene glycol 400), propylene glycol, glycerin, N-methyl-2-pyrrolidone, dimethylacetamide, and dimethylsulfoxide. Suitable antimicrobial agents or preservatives include, but are not limited to, phenols, cresols, mercurials, benzyl alcohol, chlorobutanol, methyl and propyl p-hydroxybenzates, thimerosal, benzalkonium chloride, benzethonium chloride, methyl- and propyl-parabens, and sorbic acid. Suitable isotonic agents include, but are not limited to, sodium chloride, glycerin, and dextrose. Suitable buffering agents include, but are not limited to, phosphate and citrate. Suitable antioxidants are those as described herein, including bisulfite and sodium metabisulfite. Suitable local anesthetics include, but are not limited to, procaine hydrochloride. Suitable suspending and dispersing agents are those as described herein, including sodium carboxymethylcelluose, hydroxypropyl methylcellulose, and polyvinylpyrrolidone. Suitable emulsifying agents include those described herein, including polyoxyethylene sorbitan monolaurate, polyoxyethylene sorbitan monooleate 80, and triethanolamine oleate. Suitable sequestering or chelating agents include, but are not limited to EDTA. Suitable pH adjusting agents include, but are not limited to, sodium hydroxide, hydrochloric acid, citric acid, and lactic acid. Suitable complexing agents include, but are not limited to, cyclodextrins, including a-cyclodextrin, 0-cyclodextrin, methyl-0-cyclodextrin, hydroxypropyl-3-cyclodextrin / hydroxypropyl-P-cyclodextrin,    sulfobutyl ether-0-cyclodextrin, and sulfobutylether 7-O-cyclodextrin (CAPTISOL®, CyDex, Lenexa, Kans.). The pharmaceutical compositions disclosed herein may be formulated for single or multiple dosage administration. The single dosage formulations are packaged in an ampule, a vial, or a syringe. The multiple dosage parenteral formulations must contain an antimicrobial agent at bacteriostatic or fungistatic concentrations. All parenteral formulations must be sterile, as known and practiced in the art. In some embodiments, the pharmaceutical compositions are disclosed as ready-to-use sterile solutions. In some embodiments, the pharmaceutical compositions are disclosed as sterile dry soluble products, including lyophilized powders and hypodermic tablets, to be reconstituted with a vehicle prior to use. In some embodiments, the pharmaceutical compositions are disclosed as ready-to-use sterile suspensions. In some embodiments, the pharmaceutical compositions are disclosed as sterile dry insoluble products to be reconstituted with a vehicle prior to use. In some embodiments, the pharmaceutical compositions are disclosed as ready-to-use sterile emulsions. The pharmaceutical compositions may be formulated as a suspension, solid, semi-solid, or thixotropic liquid, for administration as an implanted depot. In some embodiments, the pharmaceutical compositions disclosed herein are dispersed in a solid inner matrix, which is 74 surrounded by an outer polymeric membrane that is insoluble in body fluids but allows the active ingredient in the pharmaceutical compositions diffuse through. Fatty acid salts of the compounds of Formula (I) may be well-suited for such dosage forms. Suitable inner matrixes include polymethylmethacrylate, polybutylmethacrylate, plasticized or unplasticized polyvinylchloride, plasticized nylon, plasticized polyethyleneterephthalate, natural rubber, polyisoprene, polyisobutylene, polybutadiene, polyethylene, ethylene-vinylacetate copolymers, silicone rubbers, polydimethylsiloxanes, silicone carbonate copolymers, hydrophilic polymers, such as hydrogels of esters of acrylic and methacrylic acid, collagen, cross-linked polyvinylalcohol, and cross-linked partially hydrolyzed polyvinyl acetate. Suitable outer polymeric membranes include polyethylene, polypropylene, ethylene / propylene copolymers, ethylene / ethyl acrylate copolymers, ethylene / vinylacetate copolymers, silicone rubbers, polydimethyl siloxanes, neoprene rubber, chlorinated polyethylene, polyvinylchloride, vinylchloride copolymers with vinyl acetate, vinylidene chloride, ethylene and propylene, ionomer polyethylene terephthalate, butyl rubber epichlorohydrin rubbers, ethylene / vinyl alcohol copolymer, ethylene / vinyl acetate / vinyl alcohol terpolymer, and ethylene / vinyloxyethanol copolymer. C. Topical Administration The pharmaceutical compositions disclosed herein may be administered topically to the skin, orifices, or mucosa. Topical administration, as described herein, includes, but is not limited to, (intra)dermal, conjuctival, intracorneal, intraocular, ophthalmic, auricular, transdermal, nasal, vaginal, uretheral, respiratory, and rectal administration. The pharmaceutical compositions disclosed herein may be formulated in any dosage forms that are suitable for topical administration for local or systemic effect, including emulsions, solutions, suspensions, creams, gels, hydrogels, ointments, dusting powders, dressings, elixirs, lotions, suspensions, tinctures, pastes, foams, films, aerosols, irrigations, sprays, suppositories, bandages, dermal patches. The topical formulation of the pharmaceutical compositions disclosed herein may also comprise liposomes, micelles, microspheres, nanosystems, and mixtures thereof. Pharmaceutically acceptable vehicles (e.g., carriers and excipients) suitable for use in the topical formulations disclosed herein include, but are not limited to, aqueous vehicles, water-75 miscible vehicles, non-aqueous vehicles, antimicrobial agents or preservatives against the growth of microorganisms, stabilizers, solubility enhancers, isotonic agents, buffering agents, antioxidants, local anesthetics, suspending and dispersing agents, wetting or emulsifying agents, complexing agents, sequestering or chelating agents, penetration enhancers, cryoprotectants, lyoprotectants, thickening agents, and inert gases. The pharmaceutical compositions may also be administered topically by electroporation, iontophoresis, phonophoresis, sonophoresis and microneedle or needle-free injection, such as POWDERJECT™ (Chiron Corp., Emeryville, Calif.), and BIOJECT™ (Bioject Medical Technologies Inc., Tualatin, Oreg ). The pharmaceutical compositions disclosed herein may be disclosed in the forms of ointments, creams, and gels. Suitable ointment vehicles include oleaginous or hydrocarbon vehicles, including such as lard, benzoinated lard, olive oil, cottonseed oil, and other oils, white petrolatum; emulsifiable or absorption vehicles, such as hydrophilic petrolatum, hydroxystearin sulfate, and anhydrous lanolin; water-removable vehicles, such as hydrophilic ointment; water-soluble ointment vehicles, including polyethylene glycols of varying molecular weight; emulsion vehicles, either water-in-oil (W / O) emulsions or oil-in-water (O / W) emulsions, including cetyl alcohol, glyceryl monostearate, lanolin, and stearic acid (see, Remington: The Science and Practice of Pharmacy, supra). These vehicles are emollient but generally require addition of antioxidants and preservatives. Suitable cream base can be oil-in-water or water-in-oil. Cream vehicles may be water-washable, and contain an oil phase, an emulsifier, and an aqueous phase. The oil phase is also called the “internal” phase, which is generally comprised of petrolatum and a fatty alcohol such as cetyl or stearyl alcohol. The aqueous phase usually, although not necessarily, exceeds the oil phase in volume, and generally contains a humectant. The emulsifier in a cream formulation may be a nonionic, anionic, cationic, or amphoteric surfactant. Gels are semisolid, suspension-type systems. Single-phase gels contain organic macromolecules distributed substantially uniformly throughout the liquid carrier. Suitable gelling agents include crosslinked acrylic acid polymers, such as carbomers, carboxypolyalkylenes, Carbopol®; hydrophilic polymers, such as polyethylene oxides, polyoxyethylenepolyoxypropylene copolymers, and polyvinylalcohol; cellulosic polymers, such as hydroxypropyl cellulose, hydroxy ethyl cellulose, hydroxypropyl methylcellulose, hydroxypropyl methylcellulose 76 phthalate, and methylcellulose; gums, such as tragacanth and xanthan gum; sodium alginate; and gelatin. In order to prepare a uniform gel, dispersing agents such as alcohol or glycerin can be added, or the gelling agent can be dispersed by trituration, mechanical mixing, and / or stirring. The pharmaceutical compositions disclosed herein may be administered rectally, urethrally, vaginally, or perivaginally in the forms of suppositories, pessaries, bougies, poultices or cataplasm, pastes, powders, dressings, creams, plasters, contraceptives, ointments, solutions, emulsions, suspensions, tampons, gels, foams, sprays, or enemas. These dosage forms can be manufactured using conventional processes as described in Remington: The Science and Practice of Pharmacy, supra. Rectal, urethral, and vaginal suppositories are solid bodies for insertion into body orifices, which are solid at ordinary temperatures but melt or soften at body temperature to release the active ingredient(s) inside the orifices. Pharmaceutically acceptable carriers utilized in rectal and vaginal suppositories include bases or vehicles, such as stiffening agents, which produce a melting point in the proximity of body temperature, when formulated with the pharmaceutical compositions disclosed herein; and antioxidants as described herein, including bisulfite and sodium metabisulfite. Suitable vehicles include, but are not limited to, cocoa butter (theobroma oil), glycerin-gelatin, carbowax (polyoxyethylene glycol), spermaceti, paraffin, white and yellow wax, and appropriate mixtures of mono-, di- and triglycerides of fatty acids, hydrogels, such as polyvinyl alcohol, hydroxyethyl methacrylate, polyacrylic acid; glycerinated gelatin. Combinations of the various vehicles may be used. Rectal and vaginal suppositories may be prepared by the compressed method or molding. The typical weight of a rectal and vaginal suppository is about 2 to about 3 g. The pharmaceutical compositions disclosed herein may be administered ophthalmically in the forms of solutions, suspensions, ointments, emulsions, gel-forming solutions, powders for solutions, gels, ocular inserts, and implants. The pharmaceutical compositions disclosed herein may be administered intranasally or by inhalation to the respiratory tract. The pharmaceutical compositions may be disclosed in the form of an aerosol or solution for delivery using a pressurized container, pump, spray, atomizer, such as an atomizer using electrohydrodynamics to produce a fine mist, or nebulizer, alone or in combination with a suitable propellant, such as 1,1,1,2-tetrafluoroethane or 1,1,1,2,3,3,3-heptafluoropropane. The pharmaceutical compositions may also be disclosed as a dry powder for 77 insufflation, alone or in combination with an inert carrier such as lactose or phospholipids; and nasal drops. For intranasal use, the powder may comprise a bioadhesive agent, including chitosan or cyclodextrin. Solutions or suspensions for use in a pressurized container, pump, spray, atomizer, or nebulizer may be formulated to contain ethanol, aqueous ethanol, or a suitable alternative agent for dispersing, solubilizing, or extending release of the active ingredient disclosed herein, a propellant as solvent; and / or an surfactant, such as sorbitan trioleate, oleic acid, or an oligolactic acid. The pharmaceutical compositions disclosed herein may be micronized to a size suitable for delivery by inhalation, such as about 50 micrometers or less, or about 10 micrometers or less. Particles of such sizes may be prepared using a comminuting method known to those skilled in the art, such as spiral jet milling, fluid bed jet milling, supercritical fluid processing to form nanoparticles, high pressure homogenization, or spray drying. Capsules, blisters and cartridges for use in an inhaler or insufflator may be formulated to contain a powder mix of the pharmaceutical compositions disclosed herein; a suitable powder base, such as lactose or starch; and a performance modifier, such as 1-leucine, mannitol, or magnesium stearate. The lactose may be anhydrous or in the form of the monohydrate. Other suitable excipients or carriers include dextran, glucose, maltose, sorbitol, xylitol, fructose, sucrose, and trehalose. The pharmaceutical compositions disclosed herein for inhaled / intranasal administration may further comprise a suitable flavor, such as menthol and levomenthol, or sweeteners, such as saccharin or saccharin sodium. The pharmaceutical compositions disclosed herein for topical administration may be formulated to be immediate release or modified release, including delayed-, sustained-, pulsed-, controlled-, targeted, and programmed release. D. Modified Release The pharmaceutical compositions disclosed herein may be formulated as a modified release dosage form. As used herein, the term “modified release” refers to a dosage form in which the rate or place of release of the active ingredient(s) is different from that of an immediate dosage form when administered by the same route. The pharmaceutical compositions in modified release dosage forms can be prepared using a variety of modified release devices and methods known to those skilled in the art, including, but not limited to, matrix controlled release devices, osmotic 78 controlled release devices, multiparticulate controlled release devices, ion-exchange resins, enteric coatings, multilayered coatings, microspheres, liposomes, and combinations thereof. The release rate of the active ingredient(s) can also be modified by varying the particle sizes and polymorphism of the active ingredient(s). 1. Matrix Controlled Release Devices The pharmaceutical compositions disclosed herein in a modified release dosage form may be fabricated using a matrix controlled release device known to those skilled in the art (see, Takada et al in “Encyclopedia of Controlled Drug Delivery,” Vol. 2, Mathiowitz ed., Wiley, 1999). In one embodiment, the pharmaceutical compositions disclosed herein in a modified release dosage form is formulated using an erodible matrix device, which is water-swellable, erodible, or soluble polymers, including synthetic polymers, and naturally occurring polymers and derivatives, such as polysaccharides and proteins. Materials useful in forming an erodible matrix include, but are not limited to, chitin, chitosan, dextran, and pullulan; gum agar, gum arabic, gum karaya, locust bean gum, gum tragacanth, carrageenans, gum ghatti, guar gum, xanthan gum, and scleroglucan; starches, such as dextrin and maltodextrin; hydrophilic colloids, such as pectin; phosphatides, such as lecithin; alginates; propylene glycol alginate; gelatin; collagen; and cellulosics, such as ethyl cellulose (EC), methylethyl cellulose (MEC), carboxymethyl cellulose (CMC), CMEC, hydroxyethyl cellulose (HEC), hydroxypropyl cellulose (HPC), cellulose acetate (CA), cellulose propionate (CP), cellulose butyrate (CB), cellulose acetate butyrate (CAB), CAP, CAT, hydroxypropyl methyl cellulose (HPMC), HPMCP, HPMCAS, hydroxypropyl methyl cellulose acetate trimellitate (HPMCAT), and ethylhydroxy ethylcellulose (EHEC); polyvinyl pyrrolidone; polyvinyl alcohol; polyvinyl acetate; glycerol fatty acid esters; polyacrylamide; polyacrylic acid; copolymers of ethacrylic acid or methacrylic acid (EUDRAGIT®, Rohm America, Inc., Piscataway, N.J.); poly(2-hydroxyethyl-methacrylate); polylactides; copolymers of L-glutamic acid and ethyl-L-glutamate; degradable lactic acid-glycolic acid copolymers; poly-D-(-)-3-hydroxybutyric acid; and other acrylic acid derivatives, such as homopolymers and copolymers of butylmethacrylate, methylmethacrylate, ethylmethacrylate, ethylacrylate, (2-dimethylaminoethyl)methacrylate, and (trimethylaminoethyl)methacrylate chloride. In further embodiments, the pharmaceutical compositions are formulated with a non-erodible matrix device. The active ingredient(s) is dissolved or dispersed in an inert matrix and is 79 released primarily by diffusion through the inert matrix once administered. Materials suitable for use as a non-erodible matrix device included, but are not limited to, insoluble plastics, such as polyethylene, polypropylene, polyisoprene, polyisobutylene, polybutadiene, polymethylmethacrylate, polybutylmethacrylate, chlorinated polyethylene, polyvinylchloride, methyl acrylate-methyl methacrylate copolymers, ethylene-vinylacetate copolymers, ethylene / propylene copolymers, ethylene / ethyl acrylate copolymers, vinylchloride copolymers with vinyl acetate, vinylidene chloride, ethylene and propylene, ionomer polyethylene terephthalate, butyl rubber epichlorohydrin rubbers, ethylene / vinyl alcohol copolymer, ethylene / vinyl acetate / vinyl alcohol terpolymer, and ethylene / vinyloxyethanol copolymer, polyvinyl chloride, plasticized nylon, plasticized polyethyleneterephthalate, natural rubber, silicone rubbers, polydimethylsiloxanes, silicone carbonate copolymers, and; hydrophilic polymers, such as ethyl cellulose, cellulose acetate, crospovidone, and cross-linked partially hydrolyzed polyvinyl acetate, and fatty compounds, such as carnauba wax, microcrystalline wax, and triglycerides. In a matrix controlled release system, the desired release kinetics can be controlled, for example, via the polymer type employed, the polymer viscosity, the particle sizes of the polymer and / or the active ingredient(s), the ratio of the active ingredient(s) versus the polymer, and other excipients or carriers in the compositions. The pharmaceutical compositions disclosed herein in a modified release dosage form may be prepared by methods known to those skilled in the art, including direct compression, dry or wet granulation followed by compression, melt-granulation followed by compression. 2. Osmotic Controlled Release Devices The pharmaceutical compositions disclosed herein in a modified release dosage form may be fabricated using an osmotic controlled release device, including one-chamber system, two-chamber system, asymmetric membrane technology (AMT), and extruding core system (ECS). In general, such devices have at least two components: (a) the core which contains the active ingredient(s); and (b) a semipermeable membrane with at least one delivery port, which encapsulates the core. The semipermeable membrane controls the influx of water to the core from an aqueous environment of use so as to cause drug release by extrusion through the delivery port(s). In addition to the active ingredient(s), the core of the osmotic device optionally includes an osmotic agent, which creates a driving force for transport of water from the environment of use into the core of the device. One class of osmotic agents water-swell able hydrophilic polymers, which are also referred to as “osmopolymers” and “hydrogels,” including, but not limited to, hydrophilic vinyl and acrylic polymers, polysaccharides such as calcium alginate, polyethylene oxide (PEO), polyethylene glycol (PEG), polypropylene glycol (PPG), poly(2-hydroxyethyl methacrylate), poly(acrylic) acid, poly(methacrylic) acid, polyvinylpyrrolidone (PVP), crosslinked PVP, polyvinyl alcohol (PVA), PVA / PVP copolymers, PVA / PVP copolymers with hydrophobic monomers such as methyl methacrylate and vinyl acetate, hydrophilic polyurethanes containing large PEO blocks, sodium croscarmellose, carrageenan, hydroxyethyl cellulose (HEC), hydroxypropyl cellulose (HPC), hydroxypropyl methyl cellulose (HPMC), carboxymethyl cellulose (CMC) and carboxyethyl, cellulose (CEC), sodium alginate, polycarbophil, gelatin, xanthan gum, and sodium starch glycolate. The other class of osmotic agents are osmogens, which are capable of imbibing water to affect an osmotic pressure gradient across the barrier of the surrounding coating. Suitable osmogens include, but are not limited to, inorganic salts, such as magnesium sulfate, magnesium chloride, calcium chloride, sodium chloride, lithium chloride, potassium sulfate, potassium phosphates, sodium carbonate, sodium sulfite, lithium sulfate, potassium chloride, and sodium sulfate; sugars, such as dextrose, fructose, glucose, inositol, lactose, maltose, mannitol, raffinose, sorbitol, sucrose, trehalose, and xylitol, organic acids, such as ascorbic acid, benzoic acid, fumaric acid, citric acid, maleic acid, sebacic acid, sorbic acid, adipic acid, edetic acid, glutamic acid, p-toluenesulfonic acid, succinic acid, and tartaric acid; urea; and mixtures thereof. Osmotic agents of different dissolution rates may be employed to influence how rapidly the active ingredient(s) is initially delivered from the dosage form. For example, amorphous sugars, such as Mannogeme EZ (SPI Pharma, Lewes, Del.) can be used to provide faster delivery during the first couple of hours to promptly produce the desired therapeutic effect, and gradually and continually release of the remaining amount to maintain the desired level of therapeutic or prophylactic effect over an extended period of time. In this case, the active ingredient(s) is released at such a rate to replace the amount of the active ingredient metabolized and excreted. The core may also include a wide variety of other excipients and carriers as described herein to enhance the performance of the dosage form or to promote stability or processing. Materials useful in forming the semipermeable membrane include various grades of acrylics, vinyls, ethers, polyamides, polyesters, and cellulosic derivatives that are water-permeable and water-insoluble at physiologically relevant pHs, or are susceptible to being rendered water-insoluble by chemical alteration, such as crosslinking. Examples of suitable polymers useful in forming the coating, include plasticized, unplasticized, and reinforced cellulose acetate (CA), cellulose diacetate, cellulose triacetate, CA propionate, cellulose nitrate, cellulose acetate butyrate (CAB), CA ethyl carbamate, CAP, CA methyl carbamate, CA succinate, cellulose acetate trimellitate (CAT), CA dimethyl amino acetate, CA ethyl carbonate, CA chloroacetate, CA ethyl oxalate, CA methyl sulfonate, CA butyl sulfonate, CA p-toluene sulfonate, agar acetate, amylose triacetate, beta glucan acetate, beta glucan triacetate, acetaldehyde dimethyl acetate, triacetate of locust bean gum, hydroxylated ethyl ene-vinylacetate, EC, PEG, PPG, PEG / PPG copolymers, PVP, HEC, HPC, CMC, CMEC, HPMC, HPMCP, HPMCAS, HPMCAT, poly(acrylic) acids and esters and poly-(methacrylic) acids and esters and copolymers thereof, starch, dextran, dextrin, chitosan, collagen, gelatin, polyalkenes, polyethers, polysulfones, polyethersulfones, polystyrenes, polyvinyl halides, polyvinyl esters and ethers, natural waxes, and synthetic waxes. Semipermeable membrane may also be a hydrophobic microporous membrane, wherein the pores are substantially fdled with a gas and are not wetted by the aqueous medium but are permeable to water vapor, as disclosed in U.S. Pat. No. 5,798,119. Such hydrophobic but watervapor permeable membrane are typically composed of hydrophobic polymers such as poly alkenes, polyethylene, polypropylene, polytetrafluoroethylene, polyacrylic acid derivatives, polyethers, polysulfones, polyethersulfones, polystyrenes, polyvinyl halides, polyvinylidene fluoride, polyvinyl esters and ethers, natural waxes, and synthetic waxes. The delivery port(s) on the semipermeable membrane may be formed post-coating by mechanical or laser drilling. Delivery port(s) may also be formed in situ by erosion of a plug of water-soluble material or by rupture of a thinner portion of the membrane over an indentation in the core. In addition, delivery ports may be formed during coating process, as in the case of asymmetric membrane coatings of the type disclosed in U.S. Pat. Nos. 5,612,059 and 5,698,220. The total amount of the active ingredient(s) released and the release rate can substantially by modulated via the thickness and porosity of the semipermeable membrane, the composition of the core, and the number, size, and position of the delivery ports. The pharmaceutical compositions in an osmotic controlled-release dosage form may further comprise additional conventional excipients or carriers as described herein to promote performance or processing of the composition. The osmotic controlled-release dosage forms can be prepared according to conventional methods and techniques known to those skilled in the art (see, Remington: The Science and Practice of Pharmacy, supra; Santus and Baker, J. Controlled Release 1995, 35, 1-21; Verma et al., Drug Development and Industrial Pharmacy 2000, 26, 695-708; Verma et al., J. Controlled Release 2002, 79, 7-27). In some embodiments, the pharmaceutical compositions disclosed herein are formulated as AMT controlled-release dosage forms, which comprises an asymmetric osmotic membrane that coats a core comprising the active ingredient(s) and other pharmaceutically acceptable vehicles (e.g., excipients or carriers). The AMT controlled-release dosage forms can be prepared according to conventional methods and techniques known to those skilled in the art, including direct compression, dry granulation, wet granulation, and a dip-coating method. In some embodiments, the pharmaceutical compositions disclosed herein are formulated as ESC controlled-release dosage form, which comprises an osmotic membrane that coats a core comprising the active ingredient(s), a hydroxylethyl cellulose, and other pharmaceutically acceptable excipients or carriers. 3. Multiparticulate Controlled Release Devices The pharmaceutical compositions disclosed herein in a modified release dosage form may be fabricated a multiparticulate controlled release device, which comprises a multiplicity of particles, granules, or pellets, ranging from about 10 pm to about 3 mm, about 50 m to about 2.5 mm, or from about 100 m to about 1 mm in diameter. Such multiparticulates may be made by the processes know to those skilled in the art, including wet- and dry-granulation, extrusion / spheronization, roller-compaction, melt-congealing, and by spray-coating seed cores. See, for example, Multiparticulate Oral Drug Delivery, Marcel Dekker: 1994; and Pharmaceutical Pelletization Technology, Marcel Dekker: 1989. Other excipients or carriers as described herein may be blended with the pharmaceutical compositions to aid in processing and forming the multiparticulates. The resulting particles may themselves constitute the multiparticulate device or may be coated by various film-forming materials, such as enteric polymers, water-swellable, and water-soluble polymers. The multiparticulates can be further processed as a capsule or a tablet. 4. Targeted Delivery The pharmaceutical compositions disclosed herein may also be formulated to be targeted to a particular tissue, receptor, or other area of the body of the subject to be treated, including liposome-, resealed erythrocyte-, and antibody-based delivery systems. Any of the delivery devices above, e.g., controlled release device, implant, patch, pump, depot, etc., can be optionally manufactured with smart technology enabling remote activation of the drug delivery. The remote activation can be performed via computer or mobile app. To ensure security, the remote activation device can be password encoded. This technology enables a healthcare provider to perform telehealth sessions with a patient, during which the healthcare provider can remotely activate and administer the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, via the desired delivery device while supervising the patient on the televisit. Pharmacokinetics In some embodiments, the pharmacologic half-life (Tl / 2) of the compound of Formula (I), when administered orally to a subject via the pharmaceutical composition disclosed herein, is less than 180 minutes, less than 160 minutes, less than 140 minutes, less than 120 minutes. In some embodiments, the time for the compound of Formula (I) to reach the maximum serum concentration (Tmax), after being administered orally to a subject via the pharmaceutical composition disclosed herein, is less than 180 minutes, less than 160 minutes, less than 140 minutes, less than 120 minutes, less than 100 minutes, less than 80 minutes, less than 60 minutes, less than 50 minutes, less than 40 minutes, less than 30 minutes. In some embodiments, the time for the compound of Formula (I) to reach the maximum serum concentration (Tmax), after being administered orally to a subject via an orally disintegrating tablet (ODT) dosage form is at least 20% lower, at least 25% lower, at least 30% lower, at least 35% lower, at least 40% lower, at least 45% lower, or at least 50% lower than oral administration of the same compound of Formula (I) via a powder in capsule (PIC) dosage form. In some embodiments, oral administration of the pharmaceutical composition disclosed herein comprising the compound of Formula (I) provides a maximum serum concentration (Cmax) of the compound of Formula (I) which is at least 20% higher, at least 40% higher, at least 60% higher, at least 80% higher, at least 100% higher, at least 120% higher, at least 130% higher than oral administration of psilocybin in substantially the same dosage form. In some embodiments, oral administration of the pharmaceutical composition disclosed herein comprising the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, provides an exposure of the compound of Formula (I)— represented as area under the concentration time curve from the time of dosing to the time of last measurable concentration (AUClast) or area under the concentration time curve from the time of dosing extrapolated to infinity (AUCINF obs)—which is at least 50% higher, at least 70% higher, at least 90% higher, at least 100% higher, at least 120% higher, at least 140% higher, at least 160% higher, at least 170% higher than oral administration of psilocybin in substantially the same dosage form. In some embodiments, the volume of distribution of the compound of Formula (I) observed (VzFobs) after being administered orally to a subject is at least 20% lower, at least 25% lower, at least 30% lower, at least 35% lower, at least 40% lower, at least 45% lower, at least 50% lower, at least 55% lower, at least 60% lower, than oral administration of psilocybin in substantially the same dosage form. In some embodiments, the clearance of the compound of Formula (I) observed (CI F obs; mL / kg / hr) after being administered orally to a subject via the pharmaceutical composition disclosed herein, is from 1,500, from 1,600, from 1,700, from 1,800, from 1,900, from 2,000, from 2,100, from 2,200, from 2,300, from 2,400, and up to 3,500, to 3,400, to 3,300, to 3,200, to 3,100, to 3,000, to 2,900, to 2,800, to 2,700, to 2,600 mL / kg / hr. In some embodiments, the pharmaceutical composition has an onset of therapeutic action of 60 minutes or less, 50 minutes or less, 40 minutes or less, 30 minutes or less, 20 minutes or less, 10 minutes or less, or 5 minutes or less. In some embodiments, the pharmaceutical composition has an acute effects duration of 240 minutes or less, 180 minutes or less, 120 minutes or less, 60 minutes or less, 50 minutes or less, 40 minutes or less, 30 minutes or less, 20 minutes or less, 10 85 minutes or less, or 5 minutes or less. In some embodiments, the pharmaceutical composition has a drug dissolution time of 120 seconds or less, 90 seconds or less, 60 seconds or less, 50 seconds or less, 40 seconds or less, 30 seconds or less, 20 seconds or less, 10 seconds or less, or 5 seconds or less. Stabilized compositions In some embodiments, pharmaceutical compositions are provided which include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, in a stabilized form with a pharmaceutically acceptable vehicle. For example, an amorphous form of the compound of Formula (I) may be stabilized in the disclosed pharmaceutical compositions. In some embodiments, formulations of the compound of Formula (I) in which the compound of Formula (I) exists stably in amorphous form may be accomplished, for example, by immobilizing the compound within a matrix formed by a polymer, e.g., as a solid dispersion or solid molecular complex of the compound of Formula (I) and a polymer. Provided are solid dispersions and solid molecular complexes that include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. For example, the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, may be dispersed within a matrix formed by a polymer in its solid state such that it is immobilized in its amorphous form. In some embodiments, the polymer may prevent intramolecular hydrogen bonding or weak dispersion forces between two or more drug molecules of the compound of Formula (I). In some embodiments, the solid dispersion provides for a large surface area, thus further allowing for improved dissolution and bioavailability of the compound of Formula (I). In some embodiments, a solid dispersion or solid molecular complex includes a therapeutically effective amount of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, is present in the solid dispersion in an amount of from about 1% to about 50%, by weight; or from about 10% to about 40% by weight; or from about 20% to about 35% by weight; or from about 25% to about 30% by weight. In related embodiments, a polymer is present in the solid dispersion in an amount of from about 0% to about 50% by weight; or from about 5% to about 60% by weight; or from 10% to about 70% by weight. In some embodiments, a polymer is present in the solid dispersion in an amount greater than about 10% by 86 weight; or greater than about 20% by weight; or greater than about 30% by weight; or greater than about 40% by weight; or greater than about 50% by weight. In some embodiments, the solid dispersion is about 30% by weight of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, and about 70% by weight polymer. The solid dispersion may comprise the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof dispersed in a non-ionic polymer. This may be accomplished by, for example, melting the polymer and dissolving the compound in the polymer and then cooling the mixture. The resulting solid dispersion may comprise the compound dispersed in the polymer in amorphous form. A solid dispersion may be formed by dispersing the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof in an ionic polymer. Such solid dispersion may result in increased stability of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. This may be accomplished by various means, including the methods described above for use in forming a dispersion in a non-ionic polymer. Because ionic polymers have pH dependent solubility in aqueous systems, the resulting solid dispersion of the compound of Formula (I) and the polymer may be stable at low pH in the stomach and release the compound of Formula (I) in the intestine at higher pH. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof in such solid dispersions with an ionic polymer may thus be less capable of separating from the polymer and may be immobilized by the polymer in its amorphous form. Examples of such ionic polymers include, but are not limited to, hydroxypropylmethyl cellulose acetate succinate (HPMC-AS), hydroxypropylmethyl cellulose phthalate (HPMCP), and methacrylic acid copolymers. In some embodiments, a polymer is used that is capable of immobilizing the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof so that it exists primarily in one particular polymorph, e g., an amorphous form, for an extended period of time. In some embodiments, the polymer may be linear, branched, or crosslinked. In some embodiments, the polymer may be a homopolymer or copolymer. In some embodiments, the polymer may be a synthetic polymer derived from vinyl, acrylate, methacrylate, urethane, ester and oxide monomers. In some embodiments, the polymer can be a derivative of naturally occurring polymers such as polysaccharides (e.g. chitin, chitosan, dextran and pullulan; gum agar, gum 87 arabic, gum karaya, locust bean gum, gum tragacanth, carrageenans, gum ghatti, guar gum, xanthan gum and scleroglucan), starches (e.g. dextrin and maltodextrin), hydrophilic colloids (e.g. pectin), phosphatides (e.g. lecithin), alginates (e.g. ammonium alginate, sodium, potassium or calcium alginate, propylene glycol alginate), gelatin, collagen, and cellulose polymers. In some embodiments, the cellulose polymer is selected from the group consisting of ethyl cellulose (EC), methylethyl cellulose (MEC), carboxymethyl cellulose (CMC), CMEC, hydroxyethyl cellulose (HEC), hydroxypropyl cellulose (HPC), cellulose acetate (CA), cellulose propionate (CP), cellulose butyrate (CB), cellulose acetate butyrate (CAB), CAP, CAT, hydroxypropyl methyl cellulose (HPMC), HPMCP, HPMCAS, hydroxypropyl methyl cellulose acetate trimellitate (HPMCAT), and ethylhydroxy ethylcellulose (EHEC). In some embodiments, the polymer may be selected from the group consisting of gelatin, polyvinyl alcohol, polyvinylpyrrolidone, pullulan, and the cellulose polymers already disclosed herein. In some embodiments, the cellulose polymer comprises various grades of low viscosity, e.g., MW less than or equal to 50,000 daltons. In some embodiments, the composition can include solid dispersions and solid molecular complexes that include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof dispersed within a matrix formed by gelatin. In some embodiments, the composition can include solid dispersions and solid molecular complexes that include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof dispersed within a matrix formed by gelatin and a non-reducing sugar, e.g., mannitol. In some embodiments, the composition can include solid dispersions and solid molecular complexes that include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof dispersed within a matrix formed by a cellulose polymer described herein. In some embodiments, the composition can include solid dispersions and solid molecular complexes that include the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof dispersed within a matrix formed by a cellulose polymer described herein and polyvinylpyrrolidone. In some embodiments, the ratio of the amount by weight of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof within the solid complex to the amount by weight of the polymer therein is from about 1:9 to about 1:1. In some embodiments, the ratio of the amount by weight of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, within the solid 88 complex to the amount by weight of the polymer therein is from about 2:8 to about 4:6. In some embodiments, the ratio of the amount by weight of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof within the solid complex to the amount by weight of the polymer therein is about 3:7. In some embodiments, the composition can further include solubilizing agents for the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. Solubilizing agents include those set forth herein, such as citric acid, sodium phosphate, and natural amino acids. Other solubilizing agents include, but are not limited to, acacia, cholesterol, diethanolamine (adjunct), glyceryl monostearate, lanolin alcohols, mono- and di-glycerides, monoethanolamine (adjunct), lecithin, oleic acid (adjunct), oleyl alcohol (stabilizer), poloxamer, polyoxyethylene 50 stearate, polyoxyl 35 castor oil, polyoxyl 40 hydrogenated castor oil, polyoxyl 10 oleyl ether, polyoxyl 20 cetostearyl ether, polyoxyl 40 stearate, polysorbate 20, polysorbate 40, polysorbate 60, polysorbate 80, diacetate, monostearate, sodium lauryl sulfate, sodium stearate, sorbitan monolaurate, sorbitan monooleate, sorbitan monopalmitate, sorbitan monostearate, stearic acid, trolamine, and emulsifying wax. Various additives can be mixed, ground or granulated with the solid dispersion as described herein to form a material suitable for the above dosage forms. Potentially beneficial additives may fall generally into the following classes: other matrix materials or diluents, surface active agents, drug complexing agents or solubilizers, fillers, disintegrants, binders, lubricants, and pH modifiers (e.g., acids, bases, or buffers). Examples of other matrix materials, fillers, or diluents include lactose, mannitol, xylitol, microcrystalline cellulose, calcium diphosphate, and starch. Examples of surface active agents include sodium lauryl sulfate and polysorbate 80. Examples of drug complexing agents or solubilizers include the polyethylene glycols, caffeine, xanthene, gentisic acid and cylodextrins. Examples of disintegrants include sodium starch gycolate, sodium alginate, carboxymethyl cellulose sodium, methyl cellulose, and croscarmellose sodium. Examples of binders include methyl cellulose, microcrystalline cellulose, starch, and gums such as guar gum, and tragacanth. Examples of lubricants include magnesium stearate and calcium stearate. Examples of pH modifiers include acids such as citric acid, acetic acid, ascorbic acid, lactic acid, aspartic acid, succinic acid, phosphoric acid, and the like; bases such as sodium acetate, potassium acetate, calcium oxide, magnesium oxide, trisodium phosphate, sodium hydroxide, calcium hydroxide, aluminum hydroxide, and the like, and buffers generally comprising mixtures of acids and the salts of said acids. The composition may, in addition to the solid dispersion or solid molecular complex, also comprise therapeutically inert, inorganic or organic vehicles, such as those set forth herein. Therapeutic applications and methods Also disclosed is a method of treating a subject with a disease or disorder comprising administering to the subject a therapeutically effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof. In some embodiments, the disease or disorder is associated with a serotonin 5-HT2 receptor. The dosage and frequency (single or multiple doses) of the compounds herein administered can vary depending upon a variety of factors, including, but not limited to, the salt form / compound / polymorph to be administered; the disease / condition being treated; route of administration; size, age, sex, health, body weight, body mass index, and diet of the recipient; nature and extent of symptoms of the disease being treated; presence of other diseases or other health-related problems; kind of concurrent treatment; and complications from any disease or treatment regimen. Other therapeutic regimens or agents can be used in conjunction with the methods and compounds / salt forms disclosed herein. Therapeutically effective amounts for use in humans may be determined from animal models. For example, a dose for humans can be formulated to achieve a concentration that has been found to be effective in animals. The dosage in humans can be adjusted by monitoring response to the treatment and adjusting the dosage upwards or downwards. Dosages may be varied depending upon the requirements of the subject and the compound, salt form, and / or polymorph being employed. The dose administered to a subject, in the context of the pharmaceutical compositions presented herein, should be sufficient to affect a beneficial therapeutic response in the subject over time. The size of the dose also will be determined by the existence, nature, and extent of any adverse side effects. Generally, treatment is initiated with smaller dosages, which are less than the optimum dose of the compound. Thereafter, the dosage is increased by small increments until the optimum effect under circumstances is reached. Dosage amounts and intervals can be adjusted individually to provide levels of the administered compounds effective for the particular clinical indication being treated. This will provide a therapeutic regimen that is commensurate with the severity of the individual’s disease state. Routes of administration may include oral routes (e.g., enteral / gastric delivery, intraoral administration such buccal, lingual, and sublingual routes), parenteral routes (e.g., intravenous, intraarterial, intraperitoneal, intrathecal, intraventricular, intraurethral, intrastemal, intracranial, intramuscular, intrasynovial, and subcutaneous administration), and topical routes (e.g., (intra)dermal, conjuctival, intracorneal, intraocular, ophthalmic, auricular, transdermal, nasal, vaginal, uretheral, respiratory, and rectal administration), or others sufficient to affect a beneficial therapeutic response. Administration may follow a continuous administration schedule, or an intermittent administration schedule. The administration schedule may be varied depending on the drug employed, the condition being treated, the administration route, etc. For example, administration may be performed once a day (QD), or in divided dosages throughout the day, such as 2-times a day (BID), 3-times a day (TID), 4-times a day (QID), or more. In some embodiments administration may be performed nightly (QHS). In some embodiments, the compounds / pharmaceutical compositions may be administered as needed (PRN). Administration may also be performed on a weekly basis, e g., once a week, twice a week, three times a week, four times a week, every other week, or other administration schedules deemed appropriate using sound medical judgement. The dosing can be continuous (7 days of administration in a week) or intermittent, for example, depending on the pharmacokinetics and a particular subject’s clearance / accumulation of the drug. If intermittently, the schedule may be, for example, 4 days of administration and 3 days off (rest days) in a week or any other intermittent dosing schedule deemed appropriate using sound medical judgement. The dosing whether continuous or intermittent is continued for a particular treatment course, typically at least a 28-day cycle (1 month), which can be repeated with or without a drug holiday. Longer or shorter courses can also be used such as 14 days, 18 days, 21 days, 24 days, 35 days, 42 days, 48 days, or longer, or any range therebetween. The course may be repeated without a drug holiday or with a drug holiday depending upon the subject. Other schedules are possible depending upon the presence or absence of adverse events, response to the treatment, patient convenience, and the like. In some embodiments, the use of compositions of the disclosure may be used as a standalone therapy. In some embodiments, the use of compositions of the disclosure may be used as an adjuvant / combination therapy. Utilizing the teachings provided herein, an effective prophylactic or therapeutic treatment regimen can be planned that does not cause substantial toxicity or adverse side effects (e.g., caused by sedative or psychotomimetic toxic spikes in plasma concentration of any of the compounds Formula (I)), and yet is entirely effective to treat the clinical symptoms demonstrated by the particular patient. This planning should involve the careful choice of active compound and salt form by considering factors such as compound potency, relative bioavailability, patient body weight, presence and severity of adverse side effects, preferred mode of administration, and the toxicity profile of the selected agent. A therapeutically effective dose of the compounds, salt forms, polymorphs, solvates, compositions, disclosed herein may vary depending on the variety of factors described above, but is typically that which provides the compound of Formula (I) in an amount of about 0.00001 mg to about 10 mg per kilogram body weight of the recipient per day, or any range in between, e.g., about 0.00001 mg / kg, about 0.00005 mg / kg, about 0.0001 mg / kg, about 0.0005 mg / kg, about 0.001 mg / kg, about 0.005 mg / kg, about 0.01 mg / kg, about 0.05 mg / kg, about 0.1 mg / kg, about 0.2 mg / kg, about 0.3 mg / kg, about 0.4 mg / kg, about 0.5 mg / kg, about 0.6 mg / kg, about 0.7 mg / kg, about 0.8 mg / kg, about 0.9 mg / kg, about 1.0 mg / kg, about 2.0 mg / kg, about 3.0 mg / kg, about 4.0 mg / kg, about 5.0 mg / kg, about 6.0 mg / kg, about 7.0 mg / kg, about 8.0 mg / kg, about 9.0 mg / kg, about 10.0 mg / kg of the compound of Formula (I) (active). The compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, may be administered at a psychedelic dose. For example, when administered by mouth, the dose range for a psychedelic dosing may range from about 0.083 mg / kg, about 0.09 mg / kg, about 0.1 mg / kg, about 0.15 mg / kg, about 0.2 mg / kg, about 0.25 mg / kg, about 0.3 mg / kg, about 0.35 mg / kg, about 0.4 mg / kg, about 0.45 mg / kg, about 0.5 mg / kg, and up to about 1 mg / kg, about 0.95 mg / kg, about 0.9 mg / kg, about 0.85 mg / kg, about 0.8 mg / kg, about 0.75 mg / kg, about 0.7 mg / kg, about 0.65 mg / kg, about 0.6 mg / kg, about 0.55 mg / kg of the compound of Formula (I) (active). Typically, psychedelic doses are administered once by mouth, with the possibility of repeat doses at least one week apart. In some instances, no more than 5 doses are given in any one course of treatment. Courses can be repeated as necessary, with or without a drug holiday. Such acute treatment regimens may be accompanied by psychotherapy, 92 before, during, and / or after the psychedelic dose. These treatments are appropriate for a variety of mental health disorders disclosed herein, examples of which include, but are not limited to, major depressive disorder (MDD), therapy resistant depression (TRD), anxiety disorders, and substance use disorders (e.g., alcohol use disorder, opioid use disorder, amphetamine use disorder, nicotine use disorder, smoking, and cocaine use disorder). The compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, may be administered at serotonergic, but sub-psychoactive concentrations to achieve durable therapeutic benefits, with decreased toxicity, and may thus be suitable for microdosing. For example, when administered by mouth, the dose range for subpsychedelic dosing may range from about 0.00001 mg / kg, about 0.00005 mg / kg, about 0.0001 mg / kg, about 0.0005 mg / kg, about 0.001 mg / kg, about 0.005 mg / kg, about 0.006 mg / kg, about 0.008 mg / kg, about 0.009 mg / kg, about 0.01 mg / kg, and less than about 0.083 mg / kg, about 0.08 mg / kg, about 0.075 mg / kg, about 0.07 mg / kg, about 0.06 mg / kg, about 0.05 mg / kg, about 0.04 mg / kg, about 0.03 mg / kg, about 0.02 mg / kg of the compound of Formula (I) (active). Typically, sub-psychedelic doses are administered orally up to every day, for a treatment course (e.g., 1 month). However, there is no limitation on the number of doses at sub-psychedelic doses—dosing can be less frequent or more frequent as deemed appropriate. Courses can be repeated as necessary, with or without a drug holiday. Sub-psychedelic dosing can also be carried out, for example, by transdermal delivery, subcutaneous administration, etc., via modified, controlled, slow, or extended release dosage forms, including, but not limited to, depot dosage forms, implants, patches, and pumps, which can be optionally remotely controlled. Here, doses would achieve similar blood levels as low oral dosing, but would nevertheless be sub-psychedelic. Sub-psychedelic doses can be used, e.g., for the chronic treatment a variety of diseases or disorders disclosed herein, examples of which include, but are not limited to, inflammation, pain and neuroinflammation. In such settings where chronic administration is performed over extended periods of time, the stabilized forms of the compounds provided in the present disclosure become increasingly valuable. The subjects treated herein may have a disease or disorder associated with a serotonin 5-HT2 receptor. In some embodiments, the disease or disorder is a neuropsychiatric disease or disorder or an inflammatory disease or disorder. In some embodiments, the neuropsychiatric disease or disorder is not schizophrenia or cognitive deficits in schizophrenia. In some embodiments, the disease or disorder is a central nervous system (CNS) disorder, including, but not limited to, major depressive disorder (MDD), treatment-resistant depression (TRD), post-traumatic stress disorder (PTSD), bipolar and related disorders (including, but not limited to, bipolar I disorder, bipolar II disorder, cyclothymic disorder), obsessive-compulsive disorder (OCD), generalized anxiety disorder (GAD), social anxiety disorder, substance use disorders (including, but not limited to, alcohol use disorder, opioid use disorder, amphetamine use disorder, nicotine use disorder, smoking, and cocaine use disorder), eating disorders (including, but not limited to anorexia nervosa, bulimia nervosa, binge-eating disorder, etc.), Alzheimer’s disease, cluster headache and migraine, attention deficit hyperactivity disorder (ADHD), pain and neuropathic pain, aphantasia, childhood-onset fluency disorder, major neurocognitive disorder, mild neurocognitive disorder, sexual dysfunction, suicidal ideation, suicidal behavior, major depressive disorder with suicidal ideation or suicidal behavior, melancholic depression, atypical depression, dysthymia, non-suicidal self-injury disorder (NSSID), chronic fatigue syndrome, Lyme’s disease, gambling disorder, paraphilic disorders (including, but not limited to, pedophilic disorder, exhibitionistic disorder, voyeuristic disorder, fetishistic disorder, sexual masochism or sadism disorder, and transvestic disorder, etc.), sexual dysfunction (e.g., low libido), peripheral neuropathy, and obesity. In some embodiments, the disease or disorder is major depressive disorder (MDD). In some embodiments, the disease or disorder is treatment-resistant depression (TRD). In some embodiments, the disease or disorder is anxiety, e.g., generalized anxiety disorder (GAD) or social anxiety disorder. In some embodiments, the disease or disorder is obsessive-compulsive disorder (OCD). In some embodiments, the disease or disorder is cancer related depression and anxiety. In some embodiments, the disease or disorder is headaches (e.g., cluster headache, migraine, etc.). In some embodiments, the disease or disorder is alcohol use disorder. In some embodiments, the disease or disorder is smoking disorder and the therapy is used for smoking cessation. In some embodiments, the disease or disorder includes conditions of the autonomic nervous system (ANS). In some embodiments, the disease or disorder includes pulmonary disorders including asthma and chronic obstructive pulmonary disorder (COPD). In some embodiments, the disease or disorder includes cardiovascular disorders including atherosclerosis. The administering physician can provide a method of treatment that is prophylactic or therapeutic by adjusting the amount and timing of any of the compounds / salt forms described herein on the basis of observations of one or more symptoms of the disorder or condition being treated. In some embodiments, the subject is a mammal. In some embodiments, the mammal is a human. Also disclosed herein is a method for decreasing time of therapeutic onset relative to a psilocybin-based drug comprising administering a therapeutically effective amount of a compound as disclosed herein (i.e., the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof) to a patient in need thereof. Also disclosed herein is a method of reducing psychedelic side effects relative to a psilocybin-based drug comprising administering a therapeutically effective amount of a compound as disclosed herein (i.e., the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof) to a patient in need thereof. The terms “hallucinogenic side effects” and “psychedelic side effects” are used in the present disclosure interchangeably to refer to unwanted and / or unintended secondary effects caused by the administration of a medicament to an individual resulting in subjective experiences being qualitatively different from those of ordinary consciousness. These experiences can include derealization, depersonalization, hallucinations and / or sensory distortions in the visual, auditory, olfactory, tactile, proprioceptive and / or interoceptive spheres and / or any other perceptual modifications, and / or any other substantial subjective changes in cognition, memory, emotion and consciousness. In some embodiments, the administration of the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof causes no hallucinogenic and / or psychedelic side effects and / or less hallucinogenic and / or psychedelic side effects relative to a psilocybin-based drug. In some embodiments, the administration of the 95 compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof, alleviates, reduces, removes, and / or eliminates the hallucinogenic and / or psychedelic side effects caused by a psilocybin-based drug. Also disclosed herein is a method of reducing dose related side-effects, e.g., nausea, relative to treatment with a psilocybin-based drug, comprising administering a therapeutically effective amount of a compound as disclosed herein (i.e., the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof) to a subject in need thereof The compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof has better brain penetration (i.e., a higher brain:plasma ratio) than that obtained from administration of psilocybin. As a result, the effective dosing for the compounds of the present disclosure can be lowered, thereby reducing dose related side effects such as nausea. Also disclosed herein is a method of decreasing duration of therapeutic effect relative to a psilocybin-based drug comprising administering a therapeutically effective amount of a compound as disclosed herein (i.e., the compound of Formula (I), or a pharmaceutically acceptable salt, polymorph, stereoisomer, or solvate thereof) to a patient in need thereof. Generally, a duration of therapeutic effect for a psilocybin-based drug is about 6-8 hours. In some embodiments, the duration of therapeutic effect of the compound of Formula (I) is less than the duration of therapeutic effect for a psilocybin-based drug. In some embodiments, the duration of therapeutic effect of the compound of Formula (I) is 7, 6, 5, 4, 3, 2, 1 hour or less, or 60, 50, 40, 30, 20, 10, 5 minutes or less. In some embodiments, the duration of therapeutic effect of the compound of Formula (I) is less than the duration of therapeutic effect of a psilocybin cased drug by 7, 6, 5, 4, 3, 2, 1 hour or less, or 60, 50, 40, 30, 20, 10, 5 minutes or less. EXAMPLES I. Analytical Methods Differential scanning calorimetry (DSC) DSC data were collected on a Mettler DSC 3+ equipped with a 34 position auto-sampler. The instrument was calibrated for energy and temperature using certified indium. Typically 0.5-3 mg of each sample, in apin-holed aluminum pan, was heated at 10 °C.min'1 from 30 °C to 300 °C. A nitrogen purge at 50 mL.min4 was maintained over the sample. STARe v!5.00 was used for 96 instrument control and data processing. X-ray powder diffraction (XRPD) X-Ray Powder Diffraction patterns were collected on a Bruker AXS D2 diffractometer using CuKa radiation (30 kV, 10 mA), 0-0 geometry, using a LynxEye detector from 5-42 °20. The software used for data collection was DIFFRAC.SUITE and the data were analysed and presented using DIFFRAC EVA v 5. The details of the data collection are: • Angular range: 5 to 42 °20 • Step size: 0.024 °20 • Collection time: 0.1 seconds per step. Samples were run under ambient conditions and prepared as flat plate specimens using powder as received without grinding. Approximately 1-2 mg of the sample was lightly pressed on a silicon wafer to obtain a flat surface. Gravimetric Vapor Sorption (GVS)ZDynamic vapor sorption (DVS) Sorption isotherms were obtained using a SMS DVS Intrinsic moisture sorption analyzer, controlled by SMS Analysis Suite software. The sample temperature was maintained at 25 °C throughout. The humidity was controlled by mixing streams of dry and wet nitrogen, with a total flow rate of 200 mL.min1. Relative humidity (RH) was measured by a calibrated Rotronic probe (dynamic range of 1.0-100 %RH), located near the sample. Weight change (mass relaxation) of the sample as a function of %RH was constantly monitored by the microbalance (accuracy ±0.005 mg) 5-20 mg of sample was placed in a pre- tared stainless steel mesh basket under ambient conditions. The sample was loaded and unloaded at 40 %RH and 25 °C (typical room conditions). A moisture sorption isotherm was performed as outlined below. The standard isotherm was performed at 25 °C using 10 %RH intervals over a 0-90 %RH range. The sample was recovered after completion of the isotherm and in some cases re-analyzed by XRPD. Parameters used during GVS / DVS acquisition are presented in Table 4. Table 4 Parameter Value RH Profile - Cycle 1 40-90, 90-0,0-40 RH Profile - Cycle 2 40-90, 90-0,0-40 Intervals (%RH) 10 Flow rate (mL.min'1) 200 Temperature (°C) 25 Stability (°C.min'1) 0.2 Sorption Time (hours) 6 hour time out Nuclear Magnetic Resonance (NMR) Solution phase *H NMR Spectra were obtained using a Bruker AVIIIHD NMR spectrometer, fitted with a 5mm PABBO probe operating at 400.1326 MHz. Samples were prepared in d6-DMSO, unless otherwise stated and referenced using a TMS internal standard. Thermogravimetric Analysis (TGA) TGA data were collected on a Mettler TGA 2 equipped with a 34 position auto-sampler. The instrument was temperature calibrated using certified isatherm and nickel. Typically 5-30 mg of each sample was loaded into a pin-holed aluminum pan and heated at 10 °C.min'1 from 30 °C to 400 °C. A nitrogen purge at 50 mL.min'1 was maintained over the sample. STARe vl5.00 was used for instrument control and data processing. Ultra Performance Liquid Chromatography (UPLC) Purity analysis was performed on a Waters Acquity system equipped with a diode array detector and MicroMass ZQ mass spectrometer using MassLynx software. The UPLC method parameters used for chemical purity analysis are presented in Table 5. Table 5 Sample Preparation: 0.2-0.5mg.mL'1 in DMSO Column: BEH C18 1.7 pm 100 x 2.1 mm Column Temperature (°C): 40 Injection (pL): 2 Detection: Wavelength, Bandwidth (nm) : UV Diode array 200-500 nm Phase A: 0.1% formic acid in water Phase B: 0.1% formic acid in acetonitrile Flow Rate (mL.mirT1) 0.4 Timetable: Time (min) % Phase A % Phase B 0 97 3 0.4 97 3 6.5 55 45 7.0 55 45 7.5 95 5 8.0 95 5 High Resolution Mass Spectrometry (HRMS) andMS / MS Samples were dissolved in acetonitrile:water (50:50) at 2 mg / mL and examined by LC-MS under the following conditions listed in Tables 6-8. Table 6 Instrumentation: Waters Xevo G2 QTOF with Acquity LC system Injection Volume (p.L): 1 Column: Acquity UPLC HSS T3 1.8 gm 50 x 2.1 mm Mobile Phase: A) HPLC Grade Water + 0.1% Formic Acid B) Acetonitrile + 0.1% Formic Acid Mobile Phase Gradient: Time (min) Flow (mL / min) %A %B Curve Initial 0.600 98.0 2.0 1.00 0.600 98.0 2.0 6 8.00 0.600 2.0 98.0 6 9.00 0.600 2.0 98.0 6 9.10 0.600 98.0 2.0 6 10.00 0.600 98.0 2.0 6 Table 7 Time Method Ionisation Polarity ESI + Analyser Mode Resolution mode Capillary 0.7 kV Sampling Cone 35 V Extraction Cone 4 V Source temperature 100°C Desolvation temperature 500°C Cone Gas Flow 50 L.hr’1 Desolvation Gas Flow 900 L.hr’1 Lockspray Analyte Leucine Enkephalin Capillary 3 kV Collision Energy OFF Table 8 Scanning Conditions Start Mass (Da): 50 End Mass (Da): 1200 Scan Time (s): 0.1 Set Mass (Da): [M+H]+ Collision Energy (V): Ramp: 10-30 n. Compounds and Salt Forms Example 1 (free base) 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-t / 4)-lH-indol-4-ol (1-3; psilocin-Jio; Pl-t / io) Compound 3-(2-(bis(methyl-t / 3)amino)ethyl-l,l,2,2-d4)-l / / -indol-4-ol (1-3; PI-dio) was synthesized according to Fig. 1A. 4-acetoxyindole was acylated using oxalyl chloride producing intermediate B as a yellow solid. Treatment of intermediate B with dimethyl-de-amine (Cambridge Isotopes Labs, Tewksbury, MA) resulted in amidation and de-acetylation to form intermediate C, which was then reduced by LiAlD4 to form compound 1-3 (free base). The structure of the final product with deuterium enrichment over 90% was confirmed by JH NMR (Figs. IB-IC) and HRMS (Fig. ID). The tentative structure of molecular ion observed in HRMS is presented in Table 9. Table 9 Compound Ion Observed Proposed Formula Calculated Mass Tentative Structure Error (mDa) Psilocin-dio 215.19629 C12H7D1oN20+ 215.1963 [M+H]+ -0.01 X-ray powder diffraction (XRPD) pattern of 1-3 indicates the material is crystalline, with diffraction peaks of pattern 1 (Fig. 2A). Figs. 2B and 2C show the zoomed in and annotated XRPD patterns of 1-3. Table 10 shows the XRPD peak listing for 1-3 (pattern 1). Table 10 Name Caption (display) Angle d Value Net Intensity Rei. Intensity Peak #1 7.582 0 7.582295 11.65008 861.3094 0.007792 Peak #2 8.395 0 8.394759 10.52429 110533.8 1.000000 Peak #3 9.647 0 9.646576 9.161201 269.5037 0.002438 Peak #4 10.444 0 10.44383 8.46358 84.23746 0.000762 Peak #5 11.319 0 11.3193 7.81087 32.57419 0.000295 Peak #6 12.614 0 12.61394 7.011955 432.8757 0.003916 Peak #7 13.372 0 13.3719 6.616152 84.5412 0.000765 Peak #8 14.222 ° 14.22235 6.222384 21.97205 0.000199 Peak #9 15.157° 15.15702 5.840713 744.3998 0.006735 Peak #10 16.524 ° 16.52404 5.360464 654.2328 0.005919 Peak #11 16.787° 16.78656 5.277219 74073.52 0.670143 Peak #12 17.693 ° 17.69319 5.008796 284.0384 0.002570 Peak #13 19.468 ° 19.46828 4.555921 423.9552 0.003836 Peak #14 19.699 ° 19.69928 4.503015 1017.259 0,009203 Peak #15 20.901 ° 20.90102 4.246741 389.4514 0.003523 Peak #16 21.132 0 21.13205 4.200831 679.8422 0.006151 Peak #17 21.859 0 21.85903 4.062737 85.95354 0.000778 Peak #18 22.547 0 22.54694 3.940314 67.01072 0.000606 Peak #19 23.699 0 23.6988 3.751339 942.5151 0.008527 Peak #20 24.630 ° 24.62965 3.611631 30.55703 0.000276 Peak #21 25.034 ° 25.03401 3.554202 51.79423 0.000469 Peak #22 25.264 ° 25.2645 3.522297 638.7632 0.005779 Peak #23 26.867 ° 26.86674 3.315764 360.7947 0.003264 Peak #24 27.399 ° 27.39855 3.252601 28.91455 0.000262 Peak #25 27.929 ° 27.92929 3.191985 54.06995 0.000489 Peak #26 28.219 ° 28.21871 3.159902 20.70195 0.000187 Peak #27 28.871 ° 28.87078 3.089999 43.83303 0.000397 Peak #28 29.430 0 29.42954 3.03259 73.03846 0.000661 Peak #29 30.120 0 30.11959 2.964665 34.19807 0.000309 Peak #30 30.675 0 30.67536 2.912207 207.2589 0.001875 Peak #31 31.373 0 31.37339 2.848986 91.50857 0.000828 Peak #32 32.365 0 32.36467 2.763953 54.7266 0.000495 Peak #33 33.880 ° 33.88012 2.643708 132.8692 0.001202 Peak #34 34.418 ° 34.41825 2.603594 19.10025 0.000173 Peak #35 34.792 ° 34.7921 2.576469 20.48885 0.000185 Peak #36 35.884 ° 35.88435 2.500512 136.4738 0.001235 Peak #37 36.254 ° 36.25361 2.475885 28.93899 0.000262 Peak #38 37.156 ° 37.15607 2.417796 31.10832 0.000281 Peak #39 38.200 ° 38.20009 2.354083 34.23606 0.000310 Peak #40 38.417° 38.41659 2.341313 52.08007 0,000471 3-(2-(dimethylamino)ethyl)-l / f-indol-4-ol (I-7 / psilocin / psilocin-t / o / PI-^o) Compound 1-7 (Pl-db, free base) used in the below examples was characterized by X-ray powder diffraction (XRPD) as having an XRPD pattern of pattern 1 (see Fig. 3C). Table 11 shows the XRPD peak listing for 1-7 (pattern 1). Table 11. Caption (display) Angle d Value Net Intensity Rei. Intensity 7.563 ° 7.563431 11.67909 44.11061 0.00672 8.375 ° 8.374504 10.5497 6563.628 1 12.626 ° 12.62642 7.005054 208.3727 0.031747 13.383 ° 13.38263 6.610871 185.4812 0.028259 15.211 ° 15.21114 5.820052 265.2301 0.040409 16.753 ° 16.75303 5.287707 3690.068 0.562199 17.671 ° 17.67111 5.015004 304.343 0.046368 19.668 ° 19.66817 4.510068 2602.091 0.396441 21.112° 21.11224 4.204728 864.1647 0.13166 21.863 ° 21.86267 4.062068 148.0073 0.02255 22.201 ° 22.20094 4.000934 80.56883 0.012275 22.560 ° 22.56038 3.937997 103.738 0.015805 23.711 ° 23.71067 3.749489 1043.58 0.158994 24.592 ° 24.59193 3.617084 48.51187 0.007391 25.415 ° 25.41542 3.501722 60.87042 0.009274 26.820 ° 26.81979 3.321463 226.2585 0.034472 27.357° 27.35734 3.257406 63.70338 0.009706 27.921 ° 27.92109 3.192905 111.1571 0.016935 28.228 ° 28.22797 3.158886 18.08015 0.002755 29.253 ° 29.25296 3.050493 70.03584 0.01067 30.653 ° 30.65323 2.914259 174.6236 0.026605 31.364° 31.3638 2.849835 103.4405 0.01576 32.401 ° 32.40136 2.760907 58.739 0.008949 33.797° 33.79747 2.649983 17.68047 0.002694 34.445 ° 34.44516 2.601622 29.53493 0.0045 39.867° 39.86696 2.259415 40.48755 0.006168 Example 2 Synthesis of benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-lK-indol-4-ol (I-7a)(benzenesulfonate salt of I-7 / psilocin / psilocin-Jo / PI-t / o) Compound 1-7 (PI-do, free base)(10 mM) was dissolved in acetonitrile and treated with a solution of benzenesulfonic acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-7a (mono-benzenesulfonate salt of PI-do). As shown in Fig. 3 A, the X-ray powder diffraction (XRPD) pattern of I-7a indicates one crystalline polymorph was produced (pattern 1) having high crystallinity. Fig. 3B shows the zoomed in and annotated XRPD patterns of I-7a. Fig. 3C shows the XRPD pattern of 1-7 (Pl-do, free base)(pattem 1), and Fig. 3D shows a comparison between the XRPD patterns of I-7a (benzenesulfonate salt) and 1-7 (Pl-do, free base)(pattem 1). Table 12 shows the XRPD peak listing for I-7a (pattern 1). Table 12 Name Caption (display) Angle d Value Net Intensity Rei. Intensity Peak #1 7.002 0 7.00186 12.61448 24.92258 0.001100 Peak #2 7.733 0 7.732948 11.42345 1731.93 0.076457 Peak #3 11.768 0 11.76836 7.513811 77.21395 0.003409 Peak #4 12.516 0 12.51581 7.066712 92.23495 0.004072 Peak #5 12.882 0 12.88182 6.866737 12.68317 0.000560 Peak #6 13.546 0 13.54551 6.531741 57.04026 0.002518 Peak #7 13.968 0 13.96827 6.334989 229.514 0.010132 Peak #8 14.788 ° 14.78807 5.985592 86.10961 0.003801 Peak #9 15.225 ° 15.22511 5.814743 194.4308 0.008583 Peak #10 15.474 ° 15.47401 5.721769 22652.34 1.000000 Peak #11 18.370 ° 18.37028 4.825681 815.8047 0.036014 Peak #12 19.737° 19.73692 4.494512 37.58994 0.001659 Peak #13 20.703 ° 20.7033 4.286849 116.4809 0.005142 Peak #14 21.050 0 21.04972 4.217076 68.59189 0.003028 Peak #15 21.873 0 21.87293 4.060185 33.76218 0.001490 Peak #16 21.982 0 21.98196 4.040294 270.1723 0.011927 Peak #17 22.315 0 22.31468 3.980798 55.64486 0.002456 Peak #18 22.639 0 22.63877 3.924538 158.6271 0.007003 Peak #19 23.282 0 23.28249 3.817467 2953.931 0.130403 Peak #20 23.775 0 23.77462 3.739549 179.0302 0.007903 Peak #21 24.125 ° 24.12521 3.685993 150.6518 0.006651 Peak #22 25.193 ° 25.19252 3.532198 48.53237 0.002142 Peak #23 25.475 ° 25.47532 3.493623 141.9634 0.006267 Peak #24 25.931 ° 25.93118 3.433232 49.37065 0.002179 Peak #25 26.813 ° 26.81276 3.322318 61.6441 0.002721 Peak #26 27.778 ° 27.77834 3.208987 27.04133 0.001194 Peak #27 28.127° 28.12704 3.169992 28.03019 0.001237 Peak #28 30.866 0 30.86559 2.89469 52.91717 0.002336 Peak #29 31.207° 31.20687 2.863808 2039.447 0.090033 Peak #30 32.941 0 32.94133 2.716873 58.67304 0.002590 Peak #31 33.222 0 33.22205 2.694555 36.2762 0.001601 Peak #32 33.698 ° 33.69811 2.657569 31.60854 0.001395 Peak #33 36.803 ° 36.80291 2.440182 40.07982 0.001769 Peak #34 38.668 ° 38.66787 2.326675 22.73825 0.001004 Peak #35 39.289 ° 39.28912 2.291304 227.1359 0.010027 The DSC curve of I-7a is shown in Fig. 4 and it is evident that the salt has a high melt onset (159.10°C) and peak (161.68°C). Equally, no events were observed prior to the melt endotherm, indicating the absence of multiple physical forms in the sample, and also no conversion of physical forms prior to the melt. The thermogravimetric analysis (TGA) curve of I-7a is shown in Fig. 5 showed 95% mass remaining at 301 °C at a heating rate of 10°C / min. Figs. 6A and 6B show a *H NMR spectrum of I-7a, which indicates protonation and 1 molar equivalent of benzenesulfonate. The UPLC chromatogram of 1-7a (Fig. 7) indicates a purity including counterion of 99.2%. DVS isotherm plot of I-7a is shown in Fig. 8. There is no significant hygroscopicity and the acquisition of water was very low, even on exposure to elevated relative humidities (RH) of >90% RH, with a 0.08% mass increase over 0-90% RH range (second sorption cycle). The change in mass was low over the typical range of ambient relative humidities, and there was no evidence of physical form conversion throughout the cycle. This isotherm plot represents advantageous behavior for pharmaceutical development purposes. Fig. 9 shows the XRPD pattern of I-7a after being subjected to the DVS conditions above (post-DVS) compared to the XRPD pattern before DVS (Pre-DVS), indicating that no changes to the crystal structure took place. There was also no loss of purity following DVS analysis according to *H NMR and UPLC. The storage stability of I-7a was also assessed by storing the solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample by XRPD. The results are presented in Fig. 10, which showed no change in form by XRPD post storage. There was also no loss of purity post storage for any of i) to iii) according to *H NMR and UPLC. The benzenesulfonate salt (I-7a) was also subjected to maturation in 12 different solvents Briefly, 12 portions of I-7a (each ca.10 mg) were weighed into amber glass vials and treated with the following 12 solvents: TBME, acetone, chloroform, THF, ethyl acetate, ethanol, acetonitrile, heptane, water, toluene, 2-methoxyethanol, and benzyl alcohol. The resulting slurries were subjected to maturation with thermal cycling between room temperature and 50 °C (4 hours at each condition) for 3 days. Solids were then analysed by XRPD. All samples were isolated as solids and retained their initial crystalline form according to XRPD analysis (Fig. 11). Example 3 Synthesis of tartrate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7b)(tartrate salt of I-7 / psilocin / psilocin-<Zo / PI-<io) L-tartaric acid salt (1 eq). Compound 1-7 (Pl-t / o, free base)(10 mM) was dissolved in 1,4-dioxane, acetonitrile, or THF and treated with a solution of L-tartaric acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-7b (as a mono-L-tartrate salt of Pl-do). As shown in Fig. 12, the X-ray powder diffraction (XRPD) pattern indicates that two different crystalline polymorphs of I-7b were formed: a polymorph having pattern 1 (made from acetonitrile or THF), and a polymorph having pattern 2 (made from 1,4-dioxane). The XRPD peak listing of I-7b (pattern 1) is provided in Table 13. Table 13 Caption (display) Angle d Value Net Intensity ReL Intensity 6.798 ° 6.798303 12.99172 81.18942 0.038823 11.360° 11.36046 7.782664 38.20749 0.01827 12.764 ° 12.76448 6.929597 187.3042 0.089565 13.535 ° 13.53549 6.536554 359.2127 0.171768 14.837° 14.83685 5.966021 518.4961 0.247934 15.973 ° 15.97262 5.544258 221.2755 0.105809 16.351 ° 16.35057 5.416944 88.56068 0.042348 17.367° 17.36715 5.102086 2091.27 1 18.937° 18.93699 4.682525 859.745 0.411111 20.168 ° 20.16842 4.399317 729.6246 0.348891 20.929 ° 20.92882 4.241163 299.6507 0.143287 21.946 ° 21.94606 4.046822 686.9625 0.328491 22.719° 22.71909 3.910844 1124.994 0.537948 23.604 ° 23.6036 3.766255 214.5516 0.102594 23.814° 23.81428 3.733409 211.4754 0.101123 24.874 ° 24.87359 3.57676 376.8852 0.180218 25.609 ° 25.60921 3.475661 285.7198 0.136625 26.745 ° 26.74474 3.330612 251.1225 0.120081 27.111 ° 27.11058 3.286493 138.8324 0.066387 27.558 ° 27.55802 3.23414 68.66545 0.032834 28.653 ° 28.65312 3.112975 232.9794 0.111406 29.630 ° 29.63035 3.012493 176.5445 0.08442 31.129° 31.12856 2.870833 132.7006 0.063455 31.567° 31.56692 2.831959 106.4913 0.050922 32.180° 32.18027 2.779369 100.1601 0.047894 33.073 ° 33.0727 2.706382 58.33579 0.027895 34.096 ° 34.09647 2.627426 68.95352 0.032972 34.460 ° 34.46035 2.60051 147.7838 0.070667 36.226 ° 36.22648 2AT16TI 73.88321 0.035329 37.497 ° 37.49681 2.396604 137.836 0.06591 38.727 ° 38.72692 2.323263 90.82414 0.04343 41.126° 41.12576 2.193118 80.7093 0.038593 The DSC curve of I-7b (polymorph of pattern 1) is shown in Fig. 13 and it is evident that the salt has a high melt onset (169.99°C) and peak (172.43°C). Equally, no events were observed prior to the melt endotherm, indicating the absence of multiple physical forms in the sample, and also no conversion of physical forms prior to the melt. The thermogravimetric analysis (TGA) curve of I-7b (polymorph of pattern 1) as shown in Fig. 14 showed no significant mass lost until about 180°C at a heating rate of 10°C / min. Figs. 15A and 15B show a NMR spectrum of I-7b (polymorph of pattern 1), which indicates protonation and 1 molar equivalent of L-tartrate. In DVS experiments with polymorph of pattern 1 (Fig. 16), the first sorption cycle showed a large mass change (+4.2%, relative to 0% RH) between 80-90% RH, and a 0.7% mass increase over 0-90% RH range in the second sorption cycle. This can be seen in the DVS change in mass plot of Fig. 17. The storage stability of I-7b was also assessed by storing the solid samples for 7 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, iii) 40°C / 75% RH, and comparing to fresh sample and the sample post DVS from above by XRPD. The results are presented in Fig. 18, which showed a change in form (formation of a hydrate; pattern 3) by XRPD post storage under elevated humidity conditions and post DVS. The sample stored at 25°C in a closed vial showed no change by XRPD. The changes to I-7b (polymorph of pattern 1) pre- and post-DVS can be seen in the DSC plots of Fig. 19A and Fig. 19B, respectively, as well as the TGA plots of pre- and post-DVS material in Fig. 20A and Fig. 20B, respectively. I-7b (polymorph of pattern 1) was also subjected to maturation in 12 different solvents following the procedure detailed in Example 2. All samples were isolated as solids and retained their initial crystalline form according to XRPD analysis (Fig. 21). L-tartaric acid salt (0.5 eq). Compound 1-7 (PI-Jo, free base)(10 mM) was dissolved in 1,4-dioxane or THF and treated with a solution of L-tartaric acid (5 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-7b (L-tartrate salt of PI-Jo). As shown in Fig. 22, the X-ray powder diffraction (XRPD) pattern indicates that the obtained salts were largely amorphous, with only some weak diffraction peaks observed in the sample from THF. Example 4 Synthesis of hemi-fumarate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7c)(hemi-fumarate salt of I-7 / psilocin / psilocin-Jo / PI-Jo) Compound 1-7 (PI-do, free base)(10 mM) was dissolved in 1,4-dioxane, acetonitrile, or THF and treated with a solution of fumaric acid (0.25M solution in THF, 10 mM or 5 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-7c (as a hemi-fumarate salt of Pl-do). As shown in Fig. 23, the X-ray powder diffraction (XRPD) pattern indicates that four different crystalline polymorphs of I-7c were formed: a polymorph having pattern 1 (made from either 0.5 eq or 1 eq fumaric acid and THF), a polymorph having pattern 2 (made from 0.5 eq fumaric acid and acetonitrile), a polymorph having pattern 3 (made from either 0.5 eq or 1 eq fumaric acid in 1,4-dioxane), and a polymorph having pattern 4 (made from 1 eq fumaric acid in acetonitrile). The DSC of I-7c (polymorph of pattern 4) at 10 °C / min shows a small endothermic event at 137 °C and an endothermic event of onset at about 228 °C (Fig. 24). Additionally, TGA of I-7c (polymorph of pattern 4) at 10 °C / min shows no significant mass loss until about 220°C and 95% mass remaining at 239°C (Fig. 25). DVS experiments with polymorph of pattern 4 (Fig. 26) initially showed a decrease in mass of about 0.7% between 40-60% RH, and a 0.2% mass increase over 0-90% RH range (second sorption cycle). This can also be seen in the DVS change in mass plot of Fig. 27. The changes to I-7c (polymorph of pattern 5, obtained from scale-up using 1 eq fumaric acid in acetonitrile seeded with I-7c of pattern 4, which was a moderately crystalline form) pre-and post-DVS can be seen in the XRPD pattern of Fig. 28, in the DSC plots of pre- and post-DVS material in Fig. 29A and Fig. 29B, respectively, as well as the TGA plots of pre- and post-DVS material in Fig. 30A and Fig. 30B, respectively. The TGA plot of pre-DVS material (Fig. 30A) shoed a step mass loss of 5.9%. The XRPD peak listing for I-7c (polymorph of pattern 5) is provided in Table 14. Table 14 Caption (display) Angle d Value Net Intensity ReL Intensity 8.483 0 8.483156 10.41482 202.1152 0.424545 8.733 0 8.733033 10.11738 44.55472 0.093588 11.080° 11.08012 7.978936 307.0166 0.644891 11.351 ° 11.35111 7.789053 333.765 0.701077 11.622° 11.62241 7.607838 179.431 0.376896 12.615 ° 12.61488 7.011438 55.97579 0.117578 13.258 ° 13.25757 6.672949 73.79655 0.15501 14.977 ° 14.97686 5.910563 476.075 1 15.557° 15.55708 5.691403 143.6231 0.301682 16.089 ° 16.0892 5.504347 217.2447 0.456324 16.319° 16.31855 5.4275 276.0824 0.579914 16.606 ° 16.60595 5.334209 136.2941 0.286287 17.013 ° 17.01313 5.207448 40.47203 0.085012 18.928 ° 18.92837 4.684638 213.0289 0.447469 18.884° 18.88391 4.695568 260.5841 0.547359 19.429 ° 19.42858 4.565141 179.7858 0.377642 19.734° 19.73422 4.495121 92.05923 0.193371 20.643 ° 20.64288 4.299259 119.3917 0.250783 21.484° 21.4845 4.132707 65.13663 0.13682 22.067 ° 22.0669 4.024933 166.4906 0.349715 23.433 ° 23.43334 3.793233 203.0481 0.426504 24.466 ° 24.46598 3.635419 62.75409 0.131816 24.885 ° 24.88459 3.575203 316.7789 0.665397 26.740 ° 26.73984 3.331212 29.87601 0.062755 27.900 ° 27.89971 3.195303 75.67041 0.158946 28.557° 28.55742 3.123189 112.5171 0.236343 29.523 ° 29.52253 3.02325 32.91097 0.06913 32.888 ° 32.88833 2.721131 55.0898 0.115717 34.183 ° 34.18291 2.62098 91.18144 0.191528 36.808 ° 36.8076 2.439882 17.00791 0.035725 I-7c (polymorph of pattern 5) was also subjected to maturation in 12 different solvents following the procedure detailed in Example 2. All isolated solids showed complex polymorphism with multiple crystalline patterns obtained (polymorphs of patterns (P) 1, 6, 7, 8, 9, 10, and 11) according to XRPD analysis (Fig. 31). Example 5 Synthesis of acetate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7d)(acetate salt of I-7 / psilocin / psilocin-<^o / PI-<io) Compound 1-7 (Pl-t / o, free base)(10 mM) was dissolved in 1,4-dioxane or THF / heptane and treated with a solution of acetic acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-7d (acetate salt of Pl-do). As shown in Fig. 32, the X-ray powder diffraction (XRPD) pattern indicates that two different crystalline polymorphs of I-7d were formed: a polymorph having pattern 1 (made from 1,4-dioxane), and a polymorph having pattern 2 (made from THF / heptane). The DSC curve of I-7d (polymorph of pattern 1) is shown in Fig. 33, which indicates the salt has multiple broad unresolved endotherms, with the earliest melt onset of (71.64°C). The thermogravimetric analysis (TGA) curve of I-7d (polymorph of pattern 1) as shown in Fig. 34 showed about 6.5% mass loss between about 81 to 114°C, about 25% mass loss between about 115 to 216°C, and about 26% mass loss between about 217 to 308°C. The DSC curve of I-7d (polymorph of pattern 2) is shown in Fig. 35, which indicates the salt has a main endotherm with a melt onset of 136.15°C, higher than that of the polymorph of pattern 1. The thermogravimetric analysis (TGA) curve of I-7d (polymorph of pattern 2) as shown in Fig. 36 showed mass loss of about 20.7% between about 135 to 224°C. Example 6 Synthesis of citrate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7e)(citrate salt of I-7 / psilocin / psilocin-t / o / PI-do) Compound 1-7 (Pl-Jo, free base)(10 mM) was dissolved in 1,4-dioxane and treated with a solution of citric acid (10 mM) while being stirred at ambient temperature. Samples were then freeze dried to provide I-7e (citrate salt of Pl-Jo) as a white fluffy solid that was hygroscopic and rapidly became sticky. The obtained salt was largely amorphous, with only some weak diffraction peaks in the X-ray powder diffraction (XRPD) pattern (Fig. 37). JH NMR spectrum of I-7e (Figs. 38A and 38B) shows protonation with citric acid (1 equivalent) along with 1,4-dioxane (0.6 mole equivalent). Example 7 Synthesis of malonate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7f)(malonate salt of I-7 / psilocin / psilocin-Jo / PI-Jo) H Compound 1-7 (PI-Jb, free base)(10 mM) was dissolved in 1,4-dioxane or THF and treated with a solution of malonic acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated to produce I-7f (malonate salt of Pl-Jo). As shown in Fig. 39, the X-ray powder diffraction (XRPD) pattern indicates the salt is crystalline, with only one polymorph observed. The DSC curve at 10 °C / min shows a broad unresolved endothermic event between 98 to 132°C and an unresolved endothermic event onset of 174°C with a peak at 175°C (Fig. 40). The TGA at 10 °C / min shows 13.8% mass loss between 87 to 137°C, 16.8% between 138 to 215°C, and 22.7% between 220 to 304 °C (Fig. 41). Example 8 Synthesis of fumarate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7g)(fumarate salt of I-7 / psilocin / psilocin-Jo / PI-Jo) Compound 1-7 (PI-do, free base)(10 mM) was dissolved in 1,4-dioxane, acetonitrile, or THF and treated with a solution of fumaric acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated to produce I-7g (fumarate salt of Pl-Jo). As shown in Fig. 42, the X-ray powder diffraction (XRPD) pattern indicates that three different crystalline polymorphs of I-7g were formed: a polymorph having pattern 1 (made from THF), a polymorph having pattern 2 (made from acetonitrile), a polymorph having pattern 3 (made from 1,4-dioxane). The DSC curve of I-7g (polymorph of pattern 1) at 10 °C / min is shown in Fig. 43, which shows an endothermic event onset at 130°C (peak 136°C) and further endothermic events of onset at 223°C and 234°C. The thermogravimetric analysis (TGA) curve of I-7g (polymorph of pattern 1) at 10 °C / min is shown in Fig. 44, which shows 11% mass loss between 123 to 151°C and 29% mass loss between 228 to 311°C, corresponding to events in the DSC. The DSC curve of I-7g (polymorph of pattern 3) at 10 °C / min is shown in Fig. 45, which shows a broad endothermic event onset at 107°C, a small shallow endothermic event of onset at 174°C, and an endothermic event of onset at 237°C. The thermogravimetric analysis (TGA) curve of I-7g (polymorph of pattern 3) at 10 °C / min shows 11.7% mass loss between 104 to 134°C and 27% mass loss between 233 to 309°C (Fig. 46). Example 9 Synthesis of succinate salt of 3-(2-(dimethylamino)ethyl)-l / 7-indol-4-ol (I-7h)(succinate salt of I-7 / psilocin / psilocin-Jo / PI-Jo) Compound 1-7 (PI-Jo, free base)(10 mM) was dissolved in 1,4-dioxane or THF and treated with a solution of succinic acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated to produce I-7h (succinate salt of Pl-Jo). The X-ray powder diffraction (XRPD) pattern indicates that a single crystalline polymorph (pattern 1) was formed from either 1,4-dioxane or THF (Fig. 47). The DSC at 10°C / min shows several small events between 98 to 153 °C and an endothermic event of onset at about 185 °C (Fig. 48). TGA at 10°C / min shows about 11.1% mass loss between 109 to 165°C and about 24% mass loss between 198 to 307°C (Fig. 49). Example 10 Synthesis of oxalate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7i)(oxalate salt of I-7 / psilocin / psilocin-Jo / PI-Jo) Compound 1-7 (PI-Jo, free base)(10 mM) was dissolved in 1,4-dioxane, acetonitrile, or THF and treated with a solution of oxalic acid (10 mM or 5 mM) while being stirred at ambient temperature. Samples were refrigerated to produce I-7i (oxalate salt of PI-Jo). As shown in Fig. 50, the X-ray powder diffraction (XRPD) pattern indicates that six different crystalline polymorphs of I-7i were formed: a polymorph having pattern 1 (made from 0.5 eq oxalic acid and THF), a polymorph having pattern 2 (made from 1 eq oxalic acid and THF), a polymorph having pattern 3 (made from 0.5 eq oxalic acid and acetonitrile), a polymorph having pattern 4 (made from 1 eq oxalic acid and acetonitrile), a polymorph having pattern 5 (made from 0.5 eq oxalic acid and 1,4-dioxane), and a polymorph having pattern 6 (made from 1 eq oxalic acid and 1,4-dioxane). The DSC at 10°C / min shows that all solid crystalline material isolated from the various experiments were solvates, with several events showing in DSC (Fig. 51). Further, evidence that no anhydrous crystalline forms were isolated, the TGA shows several elements of mass loss (Fig. 52). Example 11 Synthesis of benzoate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7j)(benzoate salt of I-7 / psilocin / psilocin-do / PI-do) Compound 1-7 (PI-do, free base)(10 mM) was dissolved in 1,4-dioxane, acetonitrile, or THF and treated with a solution of benzoic acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated to produce 1-7 j (benzoate salt of Pl-do). As shown in Figs. 53A, the X-ray powder diffraction (XRPD) pattern indicates the salt is crystalline, with only one polymorph observed regardless of which solvent was employed (pattern 1). Fig. 53B shows the annotated XRPD, and Table 15 shows the XRPD peak listing for I-7j (pattern 1). Table 15 Caption (display) Angle d Value Gross Intensity Rei. Intensity 9.492 ° 9.492038 9.310002 816.1553 0.234207 11.011 0 11.01083 8.028995 225.1465 0.046314 12.391 0 12.3913 7.137437 755.566 0.210192 13.440 0 13.4398 6.58288 292.8689 0.061474 14.609 0 14.60938 6.058398 1433.992 0.417304 15.432 ° 15.43177 5.737337 182.47 0.016946 16.394 ° 16.39421 5.402621 3297.966 1 18.259 ° 18.25882 4.854886 2252.669 0.662731 18.967 ° 18.96731 4.675109 3023.974 0.904632 19.356 ° 19.35627 4.582032 977.581 0.255289 19.827° 19.82713 4.474266 1207.459 0.328425 20.843 0 20.84305 4.25842 194.7453 0.010555 21.476 ° 21.47557 4.134406 738.8857 0.187048 22.062 0 22.0625 4.025727 184.4619 0.012183 22.805 0 22.80468 3.89636 799.9279 0.203211 23.862 0 23.86174 3.726092 491.5757 0.103741 24.963 0 24.96308 3.56414 799.8894 0.201169 25.734 0 25.73424 3.459058 471.1698 0.096934 26.170 ° 26.17029 3.402404 1669.852 0.47813 26.992 ° 26.99244 3.300608 196.1326 0.015295 27.738 ° 27.73771 3.213596 498.7095 0.115793 28.593 ° 28.5934 3.119341 554.2463 0.136655 30.073 ° 30.07312 2.969141 177.3094 0.020681 30.746 ° 30.74603 2.905674 207.6318 0.030292 31.041 0 31.0409 2.878741 191.1328 0.02535 31.799 0 31.79946 2.811779 197.1789 0.02867 32.794 0 32.79412 2.728732 184.0209 0.026954 33.551 0 33.55059 2.668916 152.5839 0.019835 34.480 0 34.47956 2.599105 182.2929 0.030126 35.430 0 35.43034 2.531506 184.8386 0.031197 37.685 0 37.68499 2.385068 162.8452 0.024766 38.643 ° 38.64258 2.328139 157.4924 0.022742 The sample formed from THF was subjected to TGA analysis (Fig. 54), which indicated the crystalline form was stable until about 200°C. This mass loss in TGA associated with melt and decomposition in DSC (Fig. 55), which showed a high melt onset (226.3°C) and peak (235.2°C). Equally, no events were observed prior to the melt endotherm, indicating the absence of multiple 117 physical forms in the sample, and also no conversion of physical forms prior to the melt. XH NMR confirmed 1 equivalent of benzoic acid. The storage stability of I-7j (sample from THF) was also assessed by storing the solid samples for 22 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample by XRPD. The results are presented in Fig. 56, which showed no change in form by XRPD post storage. Further, no loss of purity was observed by 1H NMR and UPLC. I-7j (sample from THF) was also subjected to maturation in 12 different solvents following the procedure detailed in Example 2. All samples were isolated as solids and retained their initial crystalline form according to XRPD analysis (Fig. 57). DVS isotherm plot of I-7j (sample from THF) is shown in Fig. 58, which shows a 0.16% mass increase over 0-90% RH range (second sorption cycle). Fig. 59A shows the XRPD pattern of I-7j after being subjected to the DVS conditions above (post-DVS) compared to the XRPD pattern before DVS from material obtained from THF and acetonitrile (see Fig. 53 A), indicating that no changes to the crystal structure took place. There was also no loss of purity following DVS analysis according to *H NMR (Figs. 59B-59C) and UPLC. *H NMR was consistent with 1 eq of benzoic acid (0.97 eq). This data represents advantageous behavior for pharmaceutical development purposes. Example 12 Synthesis of salicylate salt of 3-(2-(dimethylamino)ethyl)-lH-indol-4-ol (I-7k)(salicylate salt of I-7 / psilocin / psilocin-t / o / PI-< / o) O OH Compound 1-7 (Pl-Jo, free base)(10 mM) was dissolved in 1,4-dioxane / heptane, acetonitrile / TBME, or THF / heptane and treated with a solution of salicylic acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated to produce I-7k (salicylate salt of Pl-Jo). As shown in Fig. 60, the X-ray powder diffraction (XRPD) pattern indicates that three different crystalline polymorphs of I-7k were formed: a polymorph having pattern 1 (made from acetonitrile / TBME), a polymorph having pattern 2 (made from THF / heptane), and a polymorph having pattern 3 (made from 1,4-dioxane / heptane). The DSC and TGA plots of these crystalline polymorphs are presented in Figs. 61 and 62, respectively. Example 13 Synthesis of benzenesulfonate salt of 3-(2-(bis(methyl-<73)amino)ethyl-l,l,2,2-<i4)-l / 7-indol-4-ol (I-3a)(benzenesulfonate salt of I-3 / psilocin-Jio / PI-t / io) Compound 1-3 (PI-t / 70, free base)(10 mM) was dissolved in acetonitrile and treated with a solution of IM benzenesulfonic acid in THF (10 mM). The resultant solution was treated with TBME and refrigerated. After several days, seeds of I-7a crystalline polymorph pattern 1 (see Example 2) were added. Crystals of I-3a (benzenesulfonate salt of PI-Jio) were slowly formed under refrigerated conditions. The X-ray powder diffraction (XRPD) pattern indicates that a single crystalline polymorph of I-3a was formed (pattern 1) (Fig, 63 A). Zoomed in and annotated versions of the XRPD pattern are presented in Figs. 63B-63C. Fig. 63D shows that the single crystalline polymorph of I-3a has the same pattern (pattern 1) as the I-7a seeds. Table 16 shows the XRPD peak listing for I-3a (pattern 1). Table 16 Name Caption (display) Angle d Value Net Intensity Rei. Intensity Peak #1 7.023 0 7.023418 12.57581 77.75247 0.000758426 Peak #2 7.767 0 7.767084 11.37332 7314.893 0.07135213 Peak #3 11.822° 11.8224 7.479583 32.03899 0.00031252 Peak #4 12.550 ° 12.54997 7.047554 78.68196 0.000767493 Peak #5 12.860° 12.85957 6.878568 21.29807 0.000207749 Peak #6 13.994° 13.99379 6.323494 1152.819 0.01124502 Peak #7 15.521 ° 15.52119 5.704481 102518.2 1 Peak #8 18.436 ° 18.43564 4.808719 365.3079 0.003563346 Peak #9 19.503 ° 19.50339 4.547799 38.2632 0.000373233 Peak #10 20.760 ° 20.7598 4.275309 47.20708 0.000460475 Peak #11 21.070° 21.06976 4.21311 278.4323 0.00271593 Peak #12 22.007 ° 22.00676 4.035797 176.9576 0.001726109 Peak #13 22.745 ° 22.74485 3.906473 76.58357 0.000747024 Peak #14 23.340° 23.34011 3.808173 16264.17 0.1586466 Peak #15 24.187° 24.18713 3.676697 57.4707 0.00056059 Peak #16 25.532 ° 25.5316 3.486051 48.40523 0.000472162 Peak #17 26.880 ° 26.87974 3.314191 24.26286 0.000236669 Peak #18 27.856 ° 27.85616 3.200199 42.07394 0.000410405 Peak #19 28.163 ° 28.16311 3.166014 143.1989 0.001396815 Peak #20 31.267° 31.26673 2.858461 12789.69 0.1247553 Peak #21 33.024° 33.02377 2.710279 28.16152 0.000274698 Peak #22 35.030 ° 35.02954 2.559547 19.00768 0.000185408 Peak #23 36.835 ° 36.83464 2.438153 42.1271 0.000410923 Peak #24 39.312° 39.31247 2.289996 2013.023 0.01963576 Peak #25 40.545 ° 40.54509 2.223177 83.841 0.000817816 Peak #26 40.988 ° 40.98812 2.200164 15.99768 0.000156047 The DSC curve of I-3a is shown in Fig. 64A, compared to that of I-7a and it is evident that the salt has a high melt onset (161.08°C) and peak (163.45°C). One small event was observed prior to the melt endotherm with an onset of 137.92°C. The thermogravimetric analysis (TGA) curve of I-3a at 10°C / min is shown in Fig. 64B, which is nearly identical to the TGA curve of I-7a. The identity of I-3a was also confirmed by !H NMR (Figs. 65A-65B). Example 14 Synthesis of tartrate salt of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-J4)-lH-indol-4-ol (I-3b)(tartrate salt of I-3 / psilocin-Jio / PI-t / io) Non-seeded. Compound 1-3 (PI-t / io, free base)(10 mM) was dissolved in THF and treated with a solution of L-tartaric acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-3b (as an L-tartrate salt of PLdio). As shown in Fig. 66, the X-ray powder diffraction (XRPD) pattern indicates that a single crystalline polymorph of I-3b was formed (pattern 1), although it was poorly crystalline compared to crystalline polymorphs of I-7b of pattern 1 (from THF) and pattern 2 (from 1,4-dioxane) (see Example 3). The DSC curve of I-3b (pattern 1) at 10°C / min is shown in Fig. 67, compared to that of the polymorph patterns 1 and 2 of I-7b, and it is again evident that polymorph of I-3b (pattern 1) was poorly crystalline. The thermogravimetric analysis (TGA) curve of I-3b (pattern 1) at 10°C / min is shown in Fig. 68. Seeded. Compound 1-3 (PLdio, free base)(10 mM) was dissolved in THF or 1,4-dioxane and treated with a solution of L-tartaric acid (10 mM) while being stirred at ambient temperature. Samples were refrigerated. After several days, seeds of I-7b crystalline polymorph pattern 1 (see Example 3) were added and crystals of I-3b were slowly formed. The X-ray powder diffraction (XRPD) pattern (Figs. 69A-69B) indicates that the seeded experiment produced a single crystalline polymorph of I-3b (pattern 2), which was substantially the same as the seeds of crystalline polymorph of I-7b of pattern 1, and having a higher crystallinity compared to the crystalline polymorph of I-3b of pattern 1 obtained from the non-seeded experiments. Table 17 shows the XRPD peak listing for I-3b (pattern 2). Table 17 Name Caption (display) Angle d Value Net Intensity Rei. Intensity Peak#l 6.732 ° 6.7315 13.1205 21.63181 0.01863163 Peak #2 12.708 ° 12.70753 6.960525 91.25528 0.0785988 Peak #3 13.470 ° 13.46988 6.568243 179.8262 0.1548855 Peak #4 14.774 0 14.77353 5.991449 265.2903 0.2284964 Peak #5 15.921 0 15.92107 5.562096 119.7453 0.1031374 Peak #6 16.268 0 16.26759 5.444388 51.88243 0.04468669 Peak #7 17.295 0 17.2945 5.123354 1161.026 1 Peak #8 18.869 ° 18.86872 4.699313 465.4803 0.4009213 Peak #9 20.079 ° 20.0787 4.418771 216.5187 0.186489 Peak #10 20.208 ° 20.20805 4.390777 379.5682 0.3269247 Peak #11 20.877 ° 20.87668 4.251637 136.9393 0.1179468 Peak #12 21.894° 21.89416 4.056297 343.8481 0.2961587 Peak #13 22.657 ° 22.65734 3.921363 598.8112 0.5157602 Peak #14 23.491 0 23.49116 3.784026 184.869 0.1592289 Peak #15 23.702 0 23.70229 3.750796 154.3493 0.1329421 Peak #16 24.636 ° 24.63617 3.610689 137.7375 0.1186342 Peak #17 24.882 ° 24.88205 3.575563 200.4769 0.1726721 Peak #18 25.569 ° 25.56915 3.481015 157.8053 0.1359188 Peak #19 26.685 ° 26.68466 3.337975 173.1976 0.1491763 Peak #20 27.060 ° 27.06003 3.292517 45.83561 0.03947853 Peak #21 27.502 ° 27.50171 3.240634 50.41544 0.04342317 Peak #22 28.179° 28.17879 3.164288 30.12094 0.02594337 Peak #23 28.597° 28.59672 3.118986 121.3689 0.1045359 Peak #24 29.035 ° 29.03487 3.072908 50.59545 0.04357821 Peak #25 29.257 ° 29.25673 3.050108 65.04179 0.05602094 Peak #26 29.527 ° 29.52666 3.022835 100.3665 0.08644637 Peak #27 31.017° 31.01673 2.880928 79.85507 0.06877972 Peak #28 31.527° 31.52703 2.835451 45.04162 0.03879466 Peak #29 32.059 ° 32.05877 2.789625 78.14873 0.06731004 Peak #30 32.307° 32.30659 2.768789 30.37478 0.02616201 Peak #31 33.012 ° 33.01181 2.711234 24.27336 0.02090681 Peak #32 34.024 ° 34.02446 2.632821 19.82419 0.01707471 Peak #33 34.388 ° 34.38762 2.605843 77.70146 0.0669248 Peak #34 34.905 ° 34.90529 2.568373 19.86779 0.01711226 Peak #35 35.361 ° 35.36144 2.53628 24.57932 0.02117033 Peak #36 36.183 ° 36.18279 2.480568 44.07069 0.03795839 Peak #37 37.372 ° 37.37207 2.404317 74.44651 0.06412129 Peak #38 37.764 ° 37.76379 2.380272 43.85532 0.03777289 Peak #39 38.657° 38.65681 2.327315 62.80877 0.05409762 Peak #40 41.049° 41.04871 2.197056 32.98244 0.028408 The DSC curve of I-3b (pattern 2) at 10°C / min is shown in Fig. 70, which shows a melt onset of 172.37°C (peak 174.49°C), similar to that of the polymorph pattern 1 of I-7b. The thermogravimetric analysis (TGA) curve of I-3b (pattern 2) at 10°C / min is shown in Fig. 71, which is also similar to that of I-7b (pattern 1). Example 15 Synthesis of hemi-fumarate salt of 3-(2-(bis(methyl-t / 3)amino)ethyl-l,l,2,2-J4)-l / / -indol-4-ol (I-3c)(hemi-fumarate salt of I-3 / psilocin-Jw / PI-t / io) Non-seeded. Compound 1-3 (PI-Jio, free base)(10 mM) was dissolved in acetonitrile or THF and treated with a solution of fumaric acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature to produce I-3c (hemi-fumarate salt of Pl-t / io). The X-ray powder diffraction (XRPD) pattern is presented in Fig. 72 comparing I-3c (pattern 1) to the crystalline polymorphs of I-7c of patterns 1 through 4 (see Example 4). The DSC curve of I-3c (pattern 1) at 10°C / min is shown in Fig. 73, compared to that of the polymorph patterns 1 through 4 of I-7c, which indicates that I-3c (pattern 1) is likely to be a mixture of polymorphs. The thermogravimetric analysis (TGA) curve of I-3c (pattern 1) at 10°C / min is shown in Fig. 74. Seeded. Compound 1-3 (PI-4 / 10, free base)(10 mM) was dissolved in acetonitrile and treated with a solution of fumaric acid (10 mM) while being stirred at ambient temperature. Samples were shaken overnight at room temperature and then seeds of I-7c crystalline polymorph pattern 4 (see Example 4) were added and crystals of I-3c were slowly formed. The X-ray powder diffraction (XRPD) pattern (Fig. 75) indicates that the seeded experiment produced a single crystalline polymorph of I-3c (pattern 2) which was different from the crystalline polymorph of I-3c of pattern 1 obtained from the non-seeded experiments. The DSC curve of I-3c (pattern 2) at 10°C / min is shown in Fig. 76, which shows a first melt onset of 229.64°C (peak 232.32°C), but the analysis was complicated by polymorphisms issues. The thermogravimetric analysis (TGA) curve of I-3c (pattern 2) at 10°C / min is shown in Fig. 77, which is similar to that of I-7c (pattern 1) obtained from the non-seeded experiment. Example 16 Synthesis of benzoate salt of 3-(2-(bis(methyl-d3)amino)ethyl-l,l,2,2-d4)-l / f-indol-4-ol (I-3j)(benzoate salt of I-3 / psilocin-Jio / PI-t / io) Compound 1-3 (PI-<7io, free base)(10 mM) was dissolved in THF and treated with a solution of benzoic acid (10 mM in THF). Samples were stirred and then seeds of I-7j crystalline polymorph pattern 1 (see Example 11) were added at room temperature to produce crystals of I-3j As shown in Figs. 78A-78B, the X-ray powder diffraction (XRPD) pattern indicates the I-3j salt is crystalline, with only one polymorph observed (pattern 1), which was the same as the pattern of the I-7j seed (Fig. 78C). Table 18 shows the XRPD peak listing for I-3j (pattern 1). Table 18 Caption (display) Angle d Value Net Intensity Rei. Intensity 9.486 ° 9.486166 9.315752 670.1039 0.22989 11.006 0 11.00646 8.032168 128.1829 0.043975 12.379 0 12.37882 7.144608 663.2478 0.227538 13.428 0 13.42827 6.588506 150.0904 0.051491 14.608 0 14.60809 6.058931 1259.188 0.431984 15.446 ° 15.44628 5.73198 71.64919 0.02458 16.389 ° 16.38903 5.404319 2914.894 1 18.247 ° 18.2471 4.857978 1790.053 0.614106 18.977 ° 18.97682 4.672788 2356.012 0.808267 19.346 ° 19.34612 4.584413 686.9104 0.235655 19.831 ° 19.83096 4.47341 856.2676 0.293756 20.868 0 20.8683 4.253326 51.75928 0.017757 21.447 ° 21.4467 4.139906 473.447 0.162423 22.860 0 22.85971 3.887104 355.8473 0.122079 23.878 0 23.87811 3.723574 292.7112 0.100419 24.944 0 24.94418 3.566798 571.3039 0.195995 25.737 0 25.73693 3.458703 237.9127 0.08162 26.144 0 26.14398 3.405768 1355.461 0.465012 26.341 ° 26.3413 3.380702 164.0407 0.056277 26.990 ° 26.98996 3.300906 45.78438 0.015707 27.708 ° 27.70765 3.217014 286.3526 0.098238 28.595 ° 28.59503 3.119166 340.7419 0.116897 30.048 ° 30.04825 2.971541 43.63537 0.01497 30.763 ° 30.76306 2.904104 92.80374 0.031838 31.127° 31.12661 2.871009 64.86243 0.022252 31.839 0 31.83931 2.80835 90.03876 0.030889 32.800 0 32.8004 2.728225 61.20367 0.020997 34.460 0 34.45993 2.600541 49.32027 0.01692 35.444 0 35.44447 2.530529 70.97894 0.02435 37.725 0 37.7249 2.382637 42.98652 0.014747 38.597 ° 38.59706 2.33078 75.10263 0.025765 JH NMR confirmed 1 equivalent of benzoic acid (Figs. 79 A and 79B). DSC of I-3j showed a high melt onset (230.57°C) and peak (239.33°C) (Fig. 80), with no events observed prior to the melt endotherm, indicating the absence of multiple physical forms in the sample, and also no conversion of physical forms prior to the melt, similar to the DSC of 1-7j. DVS isotherm plot of I-3j is shown in Fig. 81, which shows a 0.2% mass increase over 090% RH range (second sorption cycle), and thus the sample had no significant hygroscopicity, similar to I-7j which had a 0.16% mass increase over 0-90% RH range (second sorption cycle). This can be seen in the DVS change in mass plot of Fig. 82. The storage stability of I-3j was also assessed by storing the solid samples for 7 days under the following conditions: i) 25°C, closed vial, ii) 25°C / 96% RH, and iii) 40°C / 75% RH, and comparing to fresh sample and the sample post DVS from above by XRPD. The results are presented in Fig. 83, which showed no change in form by XRPD post storage or post DVS. I-3j was also subjected to maturation in 12 different solvents following the procedure detailed in Example 2. All samples were isolated as solids and retained their initial crystalline form (pattern 1) according to XRPD analysis (Fig. 84), which was similar behavior to that observed for I-7j Together, this data represents advantageous behavior for pharmaceutical development purposes. From the single crystals of 1-3j grown from THF at room temperature, a suitable crystal was selected and mounted on a glass fiber with Fomblin® oil. This was then placed on a Rigaku Oxford Diffraction SuperNova diffractometer with a dual source (Cu at zero) collection. Using Olex2 (Dolomanov, O.V., Bourhis, L.J., Gildea, R.J, Howard, J.A.K. & Puschmann, H. 2009, J. Appl. Cryst. 42, 339-341), the structure was solved with the SHELXT (Sheldrick, G.M. 2015, Acta Cryst. A71, 3-8) structure solution program using Intrinsic Phasing and refined with the SHELXL (Sheldrick, G.M. 2015, Acta Cryst. C71, 3-8) refinement package using Least Squares minimization. The solid-state structure of I-3j was generated. The asymmetric unit contains a protonated 4-hydroxy-N,N-dimethyltryptamine and a benzoate counter ion as shown in Fig. 78D, with four of each in the unit cell. The structure was refined containing both hydrogen and deuterium. There is interesting whole molecule disorder related by a 180-degree rotation about an axis through C5-C8 of the benzene ring. Many of the disordered components overlap but the disorder was modelled with both components sharing the orientation of the benzene ring but with different orientations of the 5 membered ring related by the above mentioned 180 degree rotation. The NH of the indole of one orientation maps onto the OH of the other orientation and vice versa. This disorder was traced right out to the dimethylamine unit. The occupancy of the two components were linked to a free variable which refined to 70:30 and this is depicted in Fig. 78E. The minor component was refined isotropically. Several distance and thermal parameter restraints were used to give the disordered components reasonable bond lengths and thermal parameters. The NHs and OH of the main component were located in a difference map. All NHs and OHs were placed at calculated positions for the refinement. They form short contacts listed in Table 19. Table 19 D-H H...A D...A <(DHA) Bond descriptor 0.88 1.94 2.765(12) 156.2 N2Aa-H2Aa...O15 $1 0.84 1.86 2.657(4) 157.8 O7Aa-H7Aa...O16_$2 0.88 1.91 2.735(5) 154.6 N2AAb-H2AAb. ..016_$2 1.00 1.68 2.677(5) 174.6 N12Aa-H12Aa...O16 1.00 1.76 2.757(11) 174.3 N12AAb-H12AAb...O15 0.84 1.95 2.77(3) 164.2 O7AAb-H7AAb... 015_$ 1 Symmetry operators used to generate symmetry equivalent atoms in above contact were $1 -X,0.5+Y,0.5-Z, $2 1-X,1-Y,1-Z Crystal Data for C19H12D10N2O3 (AT =336.23 g / mol): monoclinic, space group P2i / c (no. 14), a = 9.6406(2) A, b = 11.5042(3) A, c = 16.6070(3) A,p= 105.895(2)°, V= 1771.42(8) A3,Z = 4, T = 200(2) K, g(CuKa) = 0.673 mm-1, Deale = 1.262 g / cm3, 20733 reflections measured (9.474° < 2® < 147.084°), 3542 unique (7?int = 0.0256, Rsigma = 0.0146) which were used in all calculations. The final Ri was 0.0931 (I > 2o(I)) and wRz was 0.2289 (all data). A complete summary of the geometry coordinates is shown in Tables 20-27. The proposed crystal structure has a very high degree of certainty and is consistent with expectation in accordance with the determined counter-ion stoichiometry. Table 20. Crystal structure and data refinement Empirical formula C19H12D10N2O3 Formula weight 336.45 Temperature / K 200(2) Crystal system monoclinic Space group P21 / c a / A 9.6406(2) b / A 11.5042(3) c / A 16.6070(3) a / ° 90 0 / ° 105.895(2) y / ° 90 Volume / A3 1771.42(8) z 4 pcalcg / cm3 1.262 p / mm-1 0.673 F(000) 696.0 Crystal size / mm3 0.2 x 0.1 x 0.08 colourless block Radiation CuKa(Z = 1.54184) 20 range for data collection / 0 9.474 to 147.084 Index ranges -11 <h< 11,-14<k< 14,-20<1 < 19 Reflections collected 20733 Independent reflections 3542 [Rint = 0.0256, Rsigma = 0.0146] Data / restraints / parameters 3542 / 42 / 252 Goodness-of-fit on F2 1.091 Final R indexes [I>=2o (I)] RI =0.0931, wR2 = 0.2265 Final R indexes [all data] RI = 0.0967, wR2 = 0.2289 Largest diff peak / hole / e A-3 0.71 / -0.49 Table 21. Fractional Atomic Coordinates (* 104) and Equivalent Isotropic Displacement Parameters (A2xl03) Atom X y z U(eq) 015 2746(2) 1021(2) 3472.8(13) 61.4(6) 016 4532(3) 1971(3) 4306.1(16) 81.6(9) N2 -870(17) 5612(16) 3089(9) 61(4) 07 3346(4) 6541(4) 5052(2) 66.5(16) C17 5015(3) 923(3) 3182.1(18) 53.1(7) C8 1183(3) 6146(2) 4057.1(16) 47.0(7) C9A 1665(6) 5056(2) 4430(4) 63(3) CIA 3032(8) 5225(5) 5015(6) 88(4) N2A 3395(5) 6420(5) 5003(4) 107(7) C7 2252(3) 6989(3) 4411(2) 60.9(8) C3 7(3) 6525(3) 3381.6(17) 51.4(7) C16 4034(3) 1329(3) 3684.5(18) 52.5(7) C18 4668(4) -43(3) 2671(2) 64.6(9) C4 -91(4) 7661(3) 3093(2) 65.6(9) C5 1004(5) 8422(3) 3490(3) 75.4(11) C22 6291(4) 1498(4) 3219(3) 75.1(10) C19 5573(6) -427(4) 2214(3) 83.2(12) N12 2647(5) 2173(4) 5220(2) 64.8(12) C6 2157(5) 8090(3) 4129(3) 72.7(10) C9 866(5) 4966(4) 4172(2) 54.4(11) C20 6821(6) 152(4) 2251(3) 92.7(15) CH 1512(7) 2982(4) 4840(3) 59.3(13) D11A 1037.97 2708.05 4265.52 71 D11B 782.26 2954.6 5159 71 C21 7177(6) 1118(4) 2748(3) 95.4(15) Cl -368(6) 4695(4) 3593(3) 58.9(12) C13 1978(9) 999(6) 5293(5) 78.4(18) D13A 1338.46 1065.96 5658.81 118 D13B 2741.76 434.52 5530.58 118 D13C 1421.26 737.61 4736.69 118 Table 21 (Continuec I) Atom X y z U(eq) CIO 1926(7) 4168(4) 4791(3) 71.8(15) D10A 2853.42 4175.66 4642.86 86 D10B 2107.74 4512.86 5356.82 86 C14 3512(7) 2589(5) 6062(3) 77.4(17) D14A 4096.13 3259.06 5992.82 116 DUB 4146.58 1962.38 6348.64 116 D14C 2860.13 2816.22 6394.9 116 N12A 1714(12) 1809(9) 4767(7) 67(3) C10A 1218(13) 3891(10) 4312(8) 60(3) D10C 320.32 3794.24 4484.27 72 D10D 997.79 3700.67 3708.36 72 C14A 158(14) 1525(13) 4485(9) 77(4) D14D 37.23 704.2 4322.84 116 D14E -311.53 2012.24 4003.48 116 D14F -282.48 1670.23 4942.03 116 C13A 2620(20) 1110(20) 5464(14) 94(7) D13D 3618.95 1391.71 5598.04 140 D13E 2587.35 293.87 5297.95 140 D13F 2257.49 1192.6 5957.61 140 CHA 2200(20) 3155(15) 4741(13) 96(4) D11C 2540.44 3439.76 5324.35 115 D11D 3038.14 3176.97 4502.73 115 07A -1010(30) 5600(30) 3127(19) 55(6) Table 22. Anisotropic displacement parameters (A2xl03) Atom Uli U22 U33 U23 U13 U12 015 48.3(12) 80.2(16) 49.9(12) -9.1(H) 3.7(9) -7.2(11) 016 62.0(15) 117(2) 65.6(15) -42.9(15) 17.6(12) -25.5(15) N2 45(4) 89(6) 38(3) 14(2) -9(3) 0(3) 07 49(2) 71(2) 61(2) -20.4(18) -15.0(15) -0.7(16) C17 56.8(17) 60.1(18) 38.9(14) 5.2(13) 7.1(12) 3.7(14) C8 46.8(15) 52.7(16) 37.7(13) -2.8(12) 5.1(11) 2.0(12) C7 57.5(18) 68(2) 55.2(17) -16.8(16) 12.6(14) -3.6(16) C3 50.2(16) 66.7(19) 36.2(13) 4.7(13) 9.9(12) 5.3(14) C16 54.1(17) 61.2(18) 37.0(14) -2.0(13) 3.4(12) -2.2(14) C18 74(2) 64(2) 50.9(17) -4.2(15) 8.9(16) 7.5(17) C4 74(2) 77(2) 45.8(16) 13.9(16) 16.7(15) 25.5(19) C5 114(3) 49.5(19) 73(2) 2.2(17) 42(2) 2(2) C22 79(3) 75(2) 79(2) -7(2) 35(2) -10(2) C19 116(4) 75(3) 62(2) -4.3(19) 29(2) 18(3) N12 85(3) 65(3) 39.1(18) 0.8(17) 8.0(19) 29(2) C6 86(3) 62(2) 75(2) -14.7(18) 29(2) -17.8(19) C9 63(3) 56(3) 32.9(19) 2.1(17) -6.4(18) 2(2) C20 127(4) 85(3) 87(3) 15(2) 66(3) 25(3) Oil 84(3) 55(3) 55(2) 12(2) 45(2) 10(2) C21 99(3) 92(3) 119(4) -1(3) 70(3) -7(3) Cl 73(3) 55(3) 43(2) 2.7(19) 7(2) -13(2) C13 97(6) 76(4) 68(4) 11(3) 33(4) 2(4) CIO 91(4) 57(3) 48(2) 2(2) -14(3) H(3) C14 92(4) 91(4) 36(2) 1(2) -4(2) 34(3) Table 23. Bond lengths Atom Atom Length / A Atom Atom Length / A 015 C16 1.246(4) C3 O7A 1.43(3) 016 C16 1.253(4) C18 C19 1.377(6) N2 C3 1.352(17) C4 C5 1.392(6) N2 Cl 1.352(17) C5 C6 1.365(6) 07 C7 1.377(5) C22 C21 1.378(6) C17 C16 1.497(5) C19 C20 1.362(7) C17 C18 1.383(5) N12 Cll 1.443(6) C17 C22 1.383(5) N12 C13 1.516(9) C8 C9A 1.4200 N12 C14 1.496(6) C8 C7 1.4200 C9 Cl 1.345(6) C8 C3 1.427(4) C9 CIO 1.539(6) C8 C9 1.416(5) C20 C21 1.370(7) C9A CIA 1.4200 Cll CIO 1.431(8) C9A C10A 1.405(12) N12A C14A 1.481(17) CIA N2A 1.4200 N12A C13A 1.48(2) N2A C7 1.4200 N12A CHA 1.62(2) C7 C6 1.344(5) C10A CHA 1.33(2) C3 C4 1.386(5) Table 24. Bond angles Atom Atom Atom Angle / 0 Atom Atom Atom Angle / 0 C3 N2 Cl 107.5(8) 015 C16 C17 119.1(3) C18 C17 C16 120.6(3) 016 C16 C17 119.1(3) C18 C17 C22 118.3(3) C19 C18 C17 120.9(4) C22 C17 C16 121.0(3) C3 C4 C5 117.3(3) C9A C8 C3 135.0(3) C6 C5 C4 122.8(3) C7 C8 C9A 108.0 C21 C22 C17 120.3(4) C7 C8 C3 116.6(3) C20 C19 C18 120.2(4) C9 C8 C7 139.3(3) CH N12 C13 108.7(5) C9 C8 C3 104.1(2) CH N12 C14 111.4(4) C8 C9A CIA 108.0 C14 N12 C13 110.5(5) C10A C9A C8 136.9(6) C7 C6 C5 119.9(4) C10A C9A CIA 114.7(6) C8 C9 CIO 122.2(4) N2A CIA C9A 108.0 Cl C9 C8 107.9(4) CIA N2A C7 108.0 Cl C9 CIO 129.4(4) 07 C7 C8 112.3(3) C19 C20 C21 119.8(4) C8 C7 N2A 108.0 CIO Cll N12 116.7(5) C6 C7 07 125.9(3) C20 C21 C22 120.5(4) C6 C7 C8 121.8(3) C9 Cl N2 111.0(8) C6 C7 N2A 129.9(3) Cll CIO C9 117.5(5) N2 C3 C8 109.3(6) C14A N12A CHA 118.6(11) N2 C3 C4 129.1(6) C13A N12A C14A 117.3(12) C8 C3 07A 109.7(12) C13A N12A CHA 115.1(14) C4 C3 C8 121.6(3) CHA C10A C9A 112.8(13) C4 C3 07A 128.6(12) C10A CHA N12A 117.0(15) 0 15 C16 016 121.8(3) Table 25. Hydrogen bonds D H A d(D-H) / A d(H-A) / A d(D-A) / A D-H-A / ° N2 H2 0151 0.88 1.94 2.765(12) 156,2 07 H7 0162 0.84 1.86 2.657(4) 157.8 N2A H2A 0162 0.88 1.91 2.735(5) 154.6 N12 H12 016 1.00 1.68 2.677(5) 174.6 N12A H12A 015 1.00 1.76 2.757(11) 174.3 O7A H7A 0151 0.84 1.95 2.77(3) 164.2 ^X, Vz+Y,1 / 2-Z; 21-X, 1-Y, 1-Z Table 26. Hydrogen Atom Coordinates (Ax 104) and Isotropic Displacement Parameters (A2xl03) Atom X y z U(eq) H2 -1628.75 5615.1 2649.87 74 H7 3853.1 7086.72 5313.46 100 H1A 3604.02 4641.02 5354.36 105 H2A 4188.78 6749.65 5308.8 128 H18 3794.52 -447.67 2635.49 78 H4 -875.14 7909.18 2642.63 79 H5 947.53 9208.16 3307.27 90 H22 6557.96 2158.3 3571.61 90 H19 5326.1 -1097.93 1870.56 100 H12 3301.85 2092.76 4848.79 97 H6 2891.82 8634.68 4374.4 87 H20 7442.52 -111.75 1933.85 111 H21 8041.09 1528.28 2768.33 115 Hl -825.73 3956.74 3545.65 71 H12A 2037.03 1487.8 4289 140(70) H7A -1412.87 5655.14 2612.09 82 Table 27. Atomic occupancy Atom Occupancy Atom Occupancy Atom Occupancy N2 0.702(4) H2 0.702(4) 07 0.702(4) H7 0.702(4) C9A 0.298(4) CIA 0.298(4) H1A 0.298(4) N2A 0.298(4) H2A 0.298(4) N12 0.702(4) H12 0.702(4) C9 0.702(4) Cll 0.702(4) D11A 0.702(4) D11B 0.702(4) Cl 0.702(4) Hl 0.702(4) C13 0.702(4) D13A 0.702(4) D13B 0.702(4) D13C 0.702(4) CIO 0.702(4) D10A 0.702(4) D10B 0.702(4) C14 0.702(4) DMA 0.702(4) D14B 0.702(4) D14C 0.702(4) N12A 0.298(4) H12A 0.298(4) C10A 0.298(4) D10C 0.298(4) D10D 0.298(4) C14A 0.298(4) D14D 0.298(4) D14E 0.298(4) D14F 0.298(4) C13A 0.298(4) D13D 0.298(4) D13E 0.298(4) D13F 0.298(4) CHA 0.298(4) D11C 0.298(4) D11D 0.298(4) O7A 0.298(4) H7A 0.298(4) III. Free base compound forms As described in Example 1, 1-3 (PI-<7io, free base) was only isolated as a crystalline solid having an XRPD diffraction pattern 1 (see Figs. 2A-2C). Attempts were made to prepare an amorphous form of 1-3 (PI-Jio, free base) using a variety of techniques using the crystalline form (pattern 1) as input. The following techniques were tried but were not successful in the preparation of amorphous material: i) Crash cooling / freeze drying. Crash cooling and freeze-drying solutions of 1-3 (PI-dio, free base) in 1,4-dioxane, t-BuOH, 1,4-dioxane / water, MeCN / water all gave material that still showed XRPD diffraction peaks of Pattern 1 (Fig. 85). ii) Fast evaporation. Fast evaporation of a solution of 1-3 (Pl-t / io, free base) in dichloromethane (DCM) gave a crystalline material that still showed diffraction peaks of pattern 1. Ui) Anti-solvent precipitation. The addition of concentrated solutions of 1-3 (PI-dio, free base) in either dimethylformamide (DMF) or dimethylsulfoxide (DMSO) to water did not result in precipitation. Instead, solutions were formed which became dark within 4 hours, signifying degradation Next, a melt / crash cooling technique was investigated. An initial cyclic DSC experiment was conducted in which a portion of the crystalline input of 1-3 (PI-Jio, free base) was heated to 185°C (beyond the melting point with endothermic event onset at 178°C) and then rapidly cooled to -60°C. The sample was then heated to 300°C at 10°C / min. As can be seen in the DSC plot (Fig. 86), 1-3 (PI-Jio, free base) showed a glass transition onset at about 27°C and 2 exothermic events (onset at 70°C and 122°C) prior to the endothermic event onset at 177°C. A melt / crash cooling experiment (>185°C / 30°C) was then conducted by heating 1-3 (PI-<7io, free base) in DSC beyond the melting point (to 185°C) and then rapidly cooled to 30°C. The resulting sample was then analyzed by XRPD, which indicated an amorphous form of 1-3 (Pl-dw, free base) was successfully prepared (Fig. 87). The amorphous material was not stable for prolonged periods, and crystallized overnight to crystal polymorph pattern 2, which was different from the crystalline polymorph pattern 1 used as input in the experiment (Fig. 87). In summary, attempts to prepare amorphous psilocin-Jio (1-3) by crash cooling / freeze drying or fast evaporation gave only crystalline material. Attempts to prepare amorphous psilocin-<7io(I-3) by anti-solvent precipitation by addition to water did not yield solid material. Amorphous psilocin-Jio (1-3) was successfully prepared by DSC melt / crash cooling (>185°C / 30°C). The amorphous form was unstable upon standing and reverted to a new crystalline form (pattern 2). The amorphous material shows a low glass transition temperature (27 °C ). Preparation of 1-3 crystalline pattern 2 by DSC. Eleven portions of 1-3 (pattern 1) (each ca. 40 mg) were weighed into 100 pL aluminum DSC pans and the following DSC experiment was performed on each one. (The sample was heated from 30 to 185 °C at 10 °C / min, held at 185 °C for 5 minutes, rapidly cooled at -100 °C / min to 0 °C, heated to 90 °C at 10 °C / min and then cooled at 10 °C / min to 30 °C.) After the experiments the DSC pans were opened and the contents scraped out. A portion of each was analyzed by XRPD to check that Pattern 2 had formed. The eleven samples were then combined to give Psilocin-dio free base crystals of Pattern 2 as a white solid (356 mg). Fig. 88 shows the X-ray powder diffraction (XRPD) pattern of 1-3 (pattern 2) from the DSC scale-up experiment, with Fig. 89 showing the annotated XRPD version. Table 28 shows the XRPD peak listing for 1-3 (pattern 2). Table 28 Name Caption (display) Angle d Value Net Intensity Rei. Intensity Peak #1 8.124 ° 8.123984 10.87445 1288.204 0.5911127 Peak #2 8.357 ° 8.357478 10.57115 409.2122 0.1877734 Peak #3 10.059 0 10.05879 8.78668 89.95876 0.04127898 Peak #4 12.630 0 12.63015 7.002995 40.84302 0.01874146 Peak #5 13.420 0 13.41959 6.592748 323.3918 0.1483934 Peak #6 13.743 0 13.74308 6.438281 159.5939 0.07323217 Peak #7 14.053 ° 14.05272 6.297107 739.7607 0.3394507 Peak #8 15.220 ° 15.22 5.816685 167.2829 0.07676034 Peak #9 16.272 ° 16.27205 5.442906 523.0821 0.2400244 Peak #10 16.763 ° 16.76291 5.284614 195.402 0.08966326 Peak #11 16.954 ° 16.95446 5.225336 235.4412 0.1080359 Peak #12 17.328 ° 17.32756 5.113654 48.59261 0.02229748 Peak #13 17.662 0 17.66165 5.017669 71.53699 0.03282586 Peak #14 18.062 ° 18.06191 4.907367 97.47566 0.04472823 Peak #15 18.742 0 18.74222 4.730745 32.0491 0.01470623 Peak #16 19.413 0 19.41254 4.568877 745.5985 0.3421295 Peak #17 19.658 0 19.65764 4.512459 521.7926 0.2394327 Peak #18 20.172 0 20.17238 4.398462 2179.287 1 Peak #19 20.836 0 20.8364 4.259765 152.215 0.06984623 Peak #20 21.267° 21.26686 4.174506 317.3733 0.1456317 Peak #21 21.833 ° 21.83276 4.067565 271.5293 0.1245954 Peak #22 22.213 ° 22.21281 3.998823 157.6812 0.07235449 Peak #23 22.504 ° 22.50401 3.947733 245.7072 0.1127466 Peak #24 23.334 ° 23.3343 3.809107 73.21411 0.03359544 Peak #25 23.701 ° 23.70123 3.750961 125.4296 0.05755533 Peak #26 24.385 ° 24.3849 3.647322 65.75739 0.0301738 Peak #27 25.431 ° 25.43138 3.49956 94.61557 0.04341583 Peak #28 25.721 ° 25.72122 3.46078 232.2516 0.1065723 Peak #29 26.049 ° 26.04914 3.417951 68.57748 0.03146784 Peak #30 27.291 ° 27.29145 3.265122 29.86893 0.01370582 Peak #31 28.368 ° 28.36801 3.14361 86.29607 0.0395983 Peak #32 30.349 ° 30.3493 2.942747 108.3302 0.04970898 Peak #33 30.656 ° 30.65631 2.913972 42.82265 0.01964984 Peak #34 31.337 ° 31.33691 2.85222 18.87493 0.008661055 Peak #35 31.538 ° 31.53802 2.834489 34.52836 0.01584388 Peak #36 32.091 ° 32.09148 2.786855 70.13274 0.0321815 Peak #37 35.870 ° 35.86994 2.501483 26.79949 0.01229736 Peak #38 38.514 ° 38.51409 2.33561 153.147 0.07027388 Peak #39 41.361 ° 41.36089 2.181192 26.51964 0.01216895 IV. Fatty acid salt forms Materials. Super Refined® oleic acid commercially available from Croda. Caprylic (octanoic) acid, stearic acid, capric (decanoic) acid, myristic acid, lauric acid, and sodium stearate commercially available from Sigma-Aldrich. Linoleic acid and sodium oleate commercially available from Sigma. Example 17 Synthesis of laurate salt of 3-(2-(bis(methyl-J3)amino)ethyl-l,l, 2,2-^)- l / / -indol-4-ol (I-3m) (laurate salt of I-3 / psilocin-Jio / PWio) Compound 1-3 (PI<Zio, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM lauric acid in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3m were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 90, the X-ray powder diffraction (XRPD) pattern indicates the I-3m salt is crystalline, with only one polymorph observed (pattern 1), which was different from the diffraction patterns 1 and 2 of the free base 1-3. Example 18 Synthesis of linoleate salt of 3-(2-(bis(methyl-J3)amino)ethyl-l,l,2,2-J4)-17 / -indol-4-ol (I-3n) (linoleate salt of I-3 / psilocin-Jio / PI-t / io) Compound 1-3 (PI-4 / 10, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM linoleic acid (commercially available from Aldrich) in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3n were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 91, the X-ray powder diffraction (XRPD) pattern indicates the I-3n salt is crystalline, with only one polymorph observed (pattern 1), which was different from the diffraction patterns 1 and 2 of the free base 1-3. Example 19 Synthesis of myristate salt of 3-(2-(bis(methyl-4 / 3)amino)ethyl-l,l,2,2-J4)-lH-indol-4-ol (I-3o) (myristate salt of I-3 / psilocin-Jio / PI-t / io) Compound 1-3 (PI-4 / 10, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM myristic acid in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3o were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 92, the X-ray powder diffraction (XRPD) pattern indicates the I-3o salt is poorly crystalline, with only one polymorph observed (pattern 1), which was different from the diffraction patterns 1 and 2 of the free base 1-3. Example 20 Synthesis of caprate salt of 3-(2-(bis(methyl-< / 3)amino)ethyl-l,l,2,2-d4)-l / / -indol-4-ol (I-3p) (caprate salt of I-3 / psilocin-dio / PI-dio) Compound 1-3 (Pl-i / w, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM capric acid in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3p were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 93, the X-ray powder diffraction (XRPD) pattern indicates the I-3p salt is crystalline, with only one polymorph observed (pattern 1), which was different from the diffraction patterns 1 and 2 of the free base 1-3. Example 21 Synthesis of stearate salt of 3-(2-(bis(methyl-t / 3)amino)ethyl-l,l,2,2-J4)-l / f-indol-4-ol (I-3q) (stearate salt of I-3 / psilocin-dio / PI-dio) Compound 1-3 (Pl-t / w, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of 0.5 M stearic acid (commercially available stearic acid or stearic acid obtained by desalting sodium stearate with IM HC1) in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3q were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 94, the X-ray powder diffraction (XRPD) pattern indicates that two different polymorphs were formed: pattern 1 obtained from commercially available stearic acid, and pattern 2 obtained from desalting sodium stearate. Both polymorphs of I-3q were poorly crystalline and different from the diffraction patterns 1 and 2 of the free base 1-3. Example 22 Synthesis of oleate salt of 3-(2-(bis(methyl-<73)amino)ethyl-1,1,2,2-^)- 12 / -indol-4-ol (I-3r) (oleate salt of I-3 / psilocm-dio / PI-dio) Compound 1-3 (Pl-t / w, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM oleic acid (commercially available Super Refined® oleic acid or oleic acid obtained by desalting sodium oleate with IM HC1) in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3r were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 95, the X-ray powder diffraction (XRPD) pattern indicates that two different polymorphs were formed: pattern 1 obtained from desalting sodium oleate, and pattern 2 obtained from commercially available oleic acid. Polymorph of pattern 1 of I-3r was poorly crystalline. Polymorph of pattern 2 of I-3r was crystalline. Both polymorphs of I-3r were different from the diffraction patterns 1 and 2 of the free base 1-3. Example 23 Synthesis of caprylate salt of 3-(2-(bis(methyl-4 / 3)amino)ethyl-l,l,2,2-d4)-l#-indol-4-ol (I-3s) (caprylate salt of I-3 / psilocin-dio / PI-dio) Compound 1-3 (PI-t / w, free base)(ca. 50 mg) was dissolved in chloroform (ca. 25 mg / mL) in a glass vial. 1 molar equivalent of IM caprylic acid in chloroform was added to the free base solution and the sample was stirred at room temperature overnight. The solvent was then removed using a Biotage® V-10 evaporator. The resulting material was scraped and stored at -20°C to induce crystallization. Crystals of I-3s were produced, which were then stored at 5°C prior to analysis. As shown in Fig. 96, the X-ray powder diffraction (XRPD) pattern indicates the I-3s salt is crystalline, with only one polymorph observed (pattern 1), which was different from the diffraction patterns 1 and 2 of the free base 1-3. Lipid solubility assessment. Approximately 2-5 mg of test item was added to 0.5 mL of each excipient. The excipients used were corn oil (mixture of unsaturated triglycerides, from Mazola), Crodamol® GTCC (medium chain glyceride, from Croda), and Maisine® CC (mixture of unsaturated mono-, di-, and triglycerides, from Gattefosse). Samples were shaken at room temperature overnight (ca. 18 hours) on an orbital shaker. Where significant solid was present, samples were centrifugated (12500 rpm, 3 min) prior to sampling. A 100 pL aliquot of sample was spiked with 100 pL of internal standard (2 mg / mL benzophenone in 1:1 2-propanol / acetonitrile). The resulting sample was diluted with diluent (resultant ten-fold dilution). For com oil the diluent was 3:1 2-propanol / acetonitrile. For Crodamol® GTCC andMaisine® CC, the diluent was 1:12-propanol / acetonitrile. The samples were analysed by UPLC. Table 29 presents the lipid solubility data. Table 29 Chain length of fatty acid Test item Salt Concentration (mg / mL) Com oil GTCC Mai sine CC N / A 1-3 0.40 1.93 1.08 C8 I-3s >1.16 >0.90 >2.67 CIO I-3p 0.40 1.33 2.17 C12 1-3 m 0.83 2.19 >1.04 C14 I-3o 0.87 2.12 3.59 C18 I-3q (pattern 2) 0.65 1.08 3.05 I-3q (pattern 1) 0.64 1.17 2.48 C18, (18:1) I-3r (pattern 1) 0.71 3.03 >4.02 I-3r (pattern 2) 1.01 >0.57 >1.91 C18, (18:2) I-3n 1.29 3.10 >2.37 V. Psilocin Solution Stability Studies Materials and methods. Psilocin (I-7 / PFpsilocm-Jo / PI-6 / o) (free base) (1 mg / ml in acetonitrile:water 1:1, nonschedule) was purchased from Cayman Chemicals. Ascorbic acid (AsA), acetic acid (AcA), tartaric acid (TA), fumaric acid (FA), citric acid (CA), malic acid (MA), benzenesulfonic acid (BSA), stearic acid (SA), sodium citrate dihydrate, monosodium phosphate hydrate, disodium phosphate were purchased from Sigma Aldrich. Aluminum (EQ) chloride (AlCh) and iron (III) chloride (FeCh) were purchased from Sigma Aldrich. Antioxidants, i.e., ethylenediaminetetraacetic acid (EDTA), ascorbic acid (AsA), L-cysteine (Cys), sodium metabisulfite (NamBiSOs) and propyl gallate (PG) were purchased from Sigma Aldrich. Hydroxypropyl-P-cyclodextnn (CAVASOL® W7 HP, CAVfTRON® W7 HP7) and methyLp-cyclodextrin (CAVASOL® W7 M) were provided by DuPont. The following chromatographic conditions were used: Column Stationary Phase Material / Dimensions Mobile Phase A Mobile Phase B ZorbaxSB 18 3.5 mm Stainless steel, 4.6 x 150 mm Water:TFA (100:0.1 v / v) ACN:TFA (100:0.1 v / v) Gradient Time Time (Min) %A     %B 0.0           95        5 1.0            95         5 21           60       40 27           5         95 31            5         95 34           95        5 36           95        5 Flow rate          0.8 mL / min Column Temp           30 °C Injection Vol        10 pL Needle wash       Diluent Detection wavelength      269 nm Run Time         36 min Diluent. The diluent used in the below studies was prepared as follows: 100 mL of acetonitrile (ACN) was mixed with 800 mL of water and 100 mL of 1.0 M citric acid and mixed well to prepare 1 L of diluent. Stability studies in acid solutions (PI salt solutions) The stability of psilocin in 0.1 M solutions of various acids was tested. Furthermore, psilocin stability was explored in the presence of metal ions (Fe3+ and Al3+), both with and without the presence of the acids. Test solutions: To prepare the test solutions, 0.1 M solutions of AsA, AcA, TA, FA, CA, MA, BSA, and SA were prepared in DI water. 10 pM solutions of AlCh and FeCh were prepared in the above solutions. Typically, the psilocin solution was mixed with the 0.1 M acid solution, with or without metal ions, and incubated at 40°C for designated timepoints (0, 2, 4, 6, 8,18, 24H). The samples were diluted (1:1) with the diluent before submitting to chromatography to determine the % psilocin remaining. Results: As can be seen from the results presented in Figs. 97-104, the solution stability of psilocin (free base) without acid was poor, with nearly all psilocin being degraded within 24 hours. The presence of Fe3+ and Al3+ metal ions in the solutions without acid also resulted in significant psilocin degradation. To the contrary, all tested acid solutions of psilocin (solution-phase salts of psilocin) provided excellent stability for up to 24, the highest time point tested, at 40°C. The stabilizing effect of the various acids was seen in both the acid solutions and those doped with the metal salts. Stability studies in citric acid solution The stability of psilocin in the presence of citric acid was tested at 4°C, 23°C, and 40°C. Furthermore, psilocin stability was explored in the presence of metal ions (Fe3+ and Al3+), both with and without the presence of citric acid. Stock solutions: A 0.2 mg / ml stock solution of citric acid was prepared in DI water with a pH of 3.2. 20 pM stock solutions of AlCh and FeCh were freshly prepared in the above prepared 0.2 mg / ml citric acid solution. Test solutions: To prepare the test solutions, psilocin solution (1 mg / ml) was mixed with (i) 0.2 mg / ml citric acid solution (1:1 v / v), (ii) 20 pM FeCh, and (iii) 20 pM AlCh in 1:1 v / v ratio. The samples were incubated at 4°C, 23°C, and 40°C for designated timepoints (0, 2, 4, 6, 8, 18, 24H). The samples were diluted (1:1) with the diluent before submitting to chromatography to determine the % psilocin remaining. Results: As can be seen from the results presented in Figs. 105-107, the solution stability of psilocin (free base) in solutions without citric acid was poor, with nearly all psilocin being degraded by the 18 horn time point at all temperatures tested. The presence of Fe3+ and Al3+ metal ions in these solutions without citric acid also resulted in significant psilocin degradation. However, even the addition of small quantities of citric acid (10 pg), forming solution-phase citrate 145 salts of psilocin with a pH of 3.2, greatly enhanced the stability of psilocin at 4°C and room temperature (23°C). Psilocin stabilization at 40°C with small quantities of citric acid was not efficient at the 24 hour time point (30%, Fig. 107), but provided increased protection compared to solutions without citric acid. A similar behavior was observed in the presence of trace metals. Stability studies in sodium citrate buffer The stability of psilocin in the presence of 0.1 M sodium citrate buffer was tested at 4°C, 23°C, and 40°C. Furthermore, psilocin stability was explored in the presence of metal ions (Fe3+ and Al3+), both with and without the presence of sodium citrate buffer. Preparation of 0.1 M sodium citrate buffer (pH 6.01): 2.427 g of sodium citrate dihydrate and 0.336 g of citric acid were dissolved in 80 ml of DI water. The pH was adjusted to 6.0 using a 1 M NaOH solution. The final volume was adjusted to 100 ml. Test solutions: 20 pM stock solutions of AlCh and FeCh were freshly prepared in above prepared 0.1 M sodium citrate buffer. Psilocin (1 mg / ml) was mixed with (i) 0.1 M sodium citrate buffer (1:1 v / v), (ii) 10 pM FeCh, and (iii) 10 pM AlCh in 1:1 v / v ratio. The samples were incubated at 4°C, room temperature (RT, 23°C), and 40°C for designated timepoints (0, 2, 4, 6, 8, 18, 24H). The samples were diluted (1:1) with the diluent before submitting to chromatography to determine the % psilocin remaining. Results: As seen from Figs. 108A-108C, the solution stability of psilocin (free base) without sodium citrate buffer was poor, with nearly all psilocin being degraded by the 18 hour time point at all temperatures tested. The presence of Fe3+ and Al3+ metal ions in these non-citrate buffered solutions also resulted in significant psilocin degradation. Conversely, 0.1 M sodium citrate buffer greatly stabilized psilocin at 4°C and room temperature. Furthermore, no detrimental effects on psilocin were observed due to metal salts (Fe3+ and Al3+) in the citrate buffer. A minimal degradation (10-15%) of psilocin was observed at the higher temperature (40°C) condition. Stability comparison between sodium citrate and phosphate buffer The effect of buffer type and pH on the stability of psilocin was assessed. Preparation of 0.1 M sodium citrate buffer (pH 6.01): 2.427 g of sodium citrate dihydrate and 0.336 g of citric acid were dissolved in 80 ml of DI water. The pH was adjusted to 6.0 using a 1 M NaOH solution. The final volume was adjusted to 100 ml. Preparation of 0.1 M phosphate buffer (pH 6.0 and pH 7.5): Monosodium phosphate (0.339 g, 0.002 moles) and disodium phosphate (2.021 g, 0.014 moles) were dissolved in 80 ml water and the pH was adjusted as necessary using sodium hydroxide or phosphoric acid. The volume was adjusted to 100 ml using water. Test solutions: Psilocin (1 mg / ml) was mixed with (i) 0.1 M sodium citrate buffer (pH 6.01), (ii) 0.1 M phosphate buffer (pH 6.0), and (iii) 0.1 M phosphate buffer (pH 7.5) in a 1:1 v / v ratio. The samples were incubated at 40°C for designated timepoints (0, 2, 4, 6, 8, 18, 24H) and diluted (1:1) with the diluent before submitting to chromatography to determine the % psilocin remaining. Results: The role of the different buffer solutions and pH on psilocin stability can be seen in Fig. 109. Overall, both phosphate and citrate buffers (pH 6.01 and pH 7.5) provided better stability to psilocin than water at 40°C after 24 hours. Phosphate buffer at pH 6.0 provided better stability than at pH 7.5. Comparing the two different buffers with the same pH value, citrate buffer (95% efficiency) outperformed phosphate buffer (50%) in stabilizing psilocin at 40°C. Long term stability studies with citric acid and sodium citrate buffer The long-term stability (up to 25 days) of psilocin in a citric acid solution (0.1 M, pH 1.60) and a sodium citrate buffer (0.1 M, pH 6.01) at 4°C and 23°C was assessed. Preparation of 0.1 M sodium citrate buffer (pH 6.01): 2.427 g of sodium citrate dihydrate and 0.336 g of citric acid were dissolved in 80 ml of DI water. The pH was adjusted to 6.0 using a 1 M NaOH solution. The final volume was adjusted to 100 ml. Preparation of 0.1 M citric acid solution (pH 1.60): 0.1 M solution of citric acid was prepared in DI water without any pH adjustment. Test solutions: Psilocin (1 mg / ml) was mixed with (i) sodium citrate buffer (0.1 M, pH 6.01) and (ii) citric acid solution (0.1 M, pH 1.60) in 1:1 v / v. The samples were stored at 4°C and 23°C, and aliquots were sampled at designated timepoints (days 0, 7, 17, and 25). The samples were diluted (1:1) with the ...

Claims

1. A pharmaceutically acceptable salt of a compound of Formula (I), or a polymorph, stereoisomer, or solvate thereof,r8OHr5r9r2N H(I)wherein:R2, R5, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium,Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, andXi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium.

2. The pharmaceutically acceptable salt of claim 1, wherein R2, R5, Re, and R7 are hydrogen.

3. The pharmaceutically acceptable salt of claim 1, wherein at least one of R2, R5, Re, and R7 is deuterium.

4. The pharmaceutically acceptable salt of claim 1, wherein Rs and R9 are -CH3.

5. The pharmaceutically acceptable salt of claim 1, wherein Rs and R9 are -CD3.

6. The pharmaceutically acceptable salt of claim 1, wherein Xi, X2, Yi, and Y2 aredeuterium.

7. The pharmaceutically acceptable salt of claim 1, wherein Xi and Xzare deuterium.

8. The pharmaceutically acceptable salt of claim 1, wherein Yi and Yiare deuterium.

9. The pharmaceutically acceptable salt of claim 1, wherein Yi and Y2 are hydrogen.

10. The pharmaceutically acceptable salt of claim 1, wherein the compound of Formula(I) is selected from the group consisting of:(1-8),11. The pharmaceutically acceptable salt of claim 1, wherein the compound of Formula(I) is12. The pharmaceutically acceptable salt of claim 1, wherein the compound of Formula (I) is13. The pharmaceutically acceptable salt of claim 1, wherein the compound of Formula (I) is an agonist of a serotonin 5-HT2 receptor.

14. The pharmaceutically acceptable salt of claim 1, wherein the compound of Formula (I) is an agonist of a serotonin 5-HT2A receptor.

15. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, a salicylate salt, an ascorbate salt, a hydrochloride salt, a maleate salt, a malate salt, a methanesulfonate salt, a toluenesulfonate salt, a glucuronate salt, or a glutarate salt of the compound of Formula (I).

16. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt, a tartrate salt, a hemi-fumarate salt, an acetate salt, a citrate salt, a malonate salt, a fumarate salt, a succinate salt, an oxalate salt, a benzoate salt, or a salicylate salt of the compound of Formula (I).

17. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt or a benzoate salt of the compound of Formula (I).

18. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt of the compound of Formula (I).

19. The pharmaceutically acceptable salt of claim 1, which is a benzoate salt of the compound of Formula (I).

20. The pharmaceutically acceptable salt of claim 1, which is a citrate salt of the compound of Formula (I).

21. The pharmaceutically acceptable salt of claim 1, which is a tartrate salt of the compound of Formula (I).

22. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt of 3-(2-(bis(methyl-6 / 3)amino)ethyl-l,l,2,2-6?4)-l / / -indol-4-ol (I-3a).

23. The pharmaceutically acceptable salt of claim 22, wherein the benzenesulfonate salt of 3-(2-(bis(methyl-6 / 3)amino)ethyl-l,l,2,2-^4)-1 A / -indol-4-ol (I-3a) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.023°, 7.767°, 11.822°, 12.550°, 12.860°, 13.994°, 15.521°, 18.436°, 19.503°, 20.760°, 21.070°, 22.007°, 22.745°, 23.340°, 24.187°, 25.532°, 26.880°, 27.856°, 28.163°, 31.267°, 33.024°, 35.030°, 36.835°, 39.312°, 40.545°, and 40.988°.

24. The pharmaceutically acceptable salt of claim 1, which is a benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-17 / -indol-4-ol (I-7a).

25. The pharmaceutically acceptable salt of claim 24, wherein the benzenesulfonate salt of 3-(2-(dimethylamino)ethyl)-17f-indol-4-ol (I-7a) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.002°, 7.733°, 11.768°, 12.516°, 12.882°, 13.546°, 13.968°, 14.788°, 15.225°, 15.474°, 18.370°, 19.737°, 20.703°, 21.050°, 21.873°, 21.982°, 22.315°, 22.639°, 23.282°, 23.775°, 24.125°, 25.193°, 25.475°, 25.931°, 26.813°, 27.778°, 28.127°, 30.866°, 31.207°, 32.941°, 33.222°, 33.698°, 36.803°, 38.668°, and 39.289°.

26. The pharmaceutically acceptable salt of claim 1, which is a benzoate salt of 3-(2-(bis(methyl-t / 3)amino)ethyl-1,1,2,2-^)-l / f-indol-4-ol (1-3j).

27. The pharmaceutically acceptable salt of claim 26, wherein the benzoate salt of 3-(2-(bis(methyl-<73)arnino)ethyl-l, 1,2,2-^)-l / / -indol-4-ol (I-3j) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 9.486°, 11.006°, 12.379°, 13.428°, 14.608°, 15.446°, 16.389°, 18.247°, 18.977°, 19.346°, 19.831°, 20.868°, 21.447°, 22.860°, 23.878°, 24.944°, 25.737°, 26.144°, 26.341°, 26.990°, 27.708°, 28.595°, 30.048°, 30.763°, 31.127°, 31.839°, 32.800°, 34.460°, 35.444°, 37.725°, and 38.597°.

28. The pharmaceutically acceptable salt of claim 1, which is a benzoate salt of 3-(2-(dimethylamino)ethyl)- l / / -indol-4-ol (I-7j).

29. The pharmaceutically acceptable salt of claim 28, wherein benzoate salt of 3-(2-(dimethylamino)ethyl)-l / / -indol-4-ol (I-7j) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°)selected from the group consisting of 9.492°, 11.011°, 12.391°, 13.440°, 14.609°, 15.432°,16.394°, 18.259°, 18.967°, 19.356°, 19.827°, 20.843°, 21.476°, 22.062°, 22.805°, 23.862°,24.963°, 25.734°, 26.170°, 26.992°, 27.738°, 28.593°, 30.073°, 30.746°, 31.041°, 31.799°,32.794°, 33.551°, 34.480°, 35.430°, 37.685°, and 38.643°.

30. The pharmaceutically acceptable salt of claim 1, which is a citrate salt of 3-(2-(bi s(methyl -^ami no)ethyl -1,1,2,2-<4)-177-i ndol -4 -ol (1-3 e).

31. The pharmaceutically acceptable salt of claim 30, wherein the citrate salt of 3-(2-(bis(methyl-<73)amino)ethyl-l,l,2,2-6 / 4)-l#-indol-4-ol (I-3e) is amorphous by X-ray powder diffraction.

32. The pharmaceutically acceptable salt of claim 1, which is a citrate salt of 3-(2-(dimethylamino)ethyl)- l / / -indol-4-ol (I-7e).

33. The pharmaceutically acceptable salt of claim 32, wherein citrate salt of 3-(2-(dimethylamino)ethyl)- l / / -indol-4-ol (I-7e) is amorphous by X-ray powder diffraction.

34. The pharmaceutically acceptable salt of claim 1, which is a tartrate salt of 3-(2-(bi s(methyl-<73)ami no)ethyl -1,1,2,2-^)-1 H-indol-4-ol (1-3b).

35. The pharmaceutically acceptable salt of claim 34, wherein the tartrate salt of 3-(2-(bis(methyl-d3)amino)ethyl-1,1,2,2-^)-l / / -indol-4-ol (I-3b) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 6.732°, 12.708°, 13.470°, 14.774°,15.921°, 16.268°, 17.295°, 18.869°, 20.079°, 20.208°, 20.877°, 21.894°, 22.657°, 23.491°,23.702°, 24.636°, 24.882°, 25.569°, 26.685°, 27.060°, 27.502°, 28.179°, 28.597°, 29.035°,29.257°, 29.527°, 31.017°, 31.527°, 32.059°, 32.307°, 33.012°, 34.024°, 34.388°, 34.905°,35.361°, 36.183°, 37.372°, 37.764°, 38.657°, 41.049°.

36. The pharmaceutically acceptable salt of claim 1, which is a tartrate salt of 3-(2-(dimethylamino)ethyl)-l / / -indol-4-ol (I-7b).

37. The pharmaceutically acceptable salt of claim 36, wherein the tartrate salt of 3-(2-(dimethylamino)ethyl)-17 / -indol-4-ol (I-7b) is crystalline and characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 6.798°, 11.360°, 12.764°, 13.535°, 14.837°, 15.973°, 16.351°, 17.367°, 18.937°, 20.168°, 20.929°, 21.946°, 22.719°, 23.604°, 23.814°, 24.874°, 25.609°, 26.745°, 27.111°, 27.558°, 28.653°, 29.630°, 31.129°, 31.567°, 32.180°, 33.073°, 34.096°, 34.460°, 36.226°, 37.497°, 38.727°.

38. The pharmaceutically acceptable salt of claim 1, wherein the pharmaceutically acceptable salt of the compound of Formula (I) has a water solubility from about 1 mg / mL to about 400 mg / mL.

39. The pharmaceutically acceptable salt of claim 1, which is a fatty acid salt of the compound of Formula (I).

40. The pharmaceutically acceptable salt of claim 39, which is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, a caprylate salt, a palmitate salt, a sebacate salt, an undecylenate salt, or a caproate salt of the compound of Formula (I).

41. The pharmaceutically acceptable salt of claim 39, which is an adipate salt, a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, or a caprylate salt of the compound of Formula (I).

42. The pharmaceutically acceptable salt of claim 39, which is a laurate salt, a linoleate salt, a myristate salt, a caprate salt, a stearate salt, an oleate salt, or a caprylate salt of the compound of Formula (I).

43. The pharmaceutically acceptable salt of claim 39, which is a laurate salt, a linoleate salt, a caprate salt, or a caprylate salt of the compound of Formula (I).

44. A pharmaceutical composition comprising the pharmaceutically acceptable salt of claim 1, and a pharmaceutically acceptable vehicle.

45. The pharmaceutical composition of claim 44, which is adapted for intraoral administration.

46. The pharmaceutical composition of claim 45, wherein the pharmaceutical composition is in an orodispersible dosage form.

47. The pharmaceutical composition of claim 45, wherein the pharmaceutical composition is in a form of an orally disintegrating tablet (ODT).

48. The pharmaceutical composition of claim 47, wherein the pharmaceutically acceptable vehicle comprises a water-soluble polymer and a matrix material, filler, or diluent.

49. The pharmaceutical composition of claim 48, wherein the water-soluble polymer is gelatin, and the matrix material, filler, or diluent is mannitol.

50. The pharmaceutical composition of claim 48, wherein the pharmaceutically acceptable vehicle further comprises an acid.

51. The pharmaceutical composition of claim 50, wherein the acid is citric acid and / or tartaric acid.

52. The pharmaceutical composition of claim 45, wherein the pharmaceutical composition is in a form of an orodispersible film (ODF).

53. The pharmaceutical composition of claim 44, wherein the pharmaceutical composition is in an immediate release (IR) dosage form.

54. The pharmaceutical composition of claim 53, wherein the immediate release (IR) dosage form is an immediate release (IR) tablet.

55. The pharmaceutical composition of claim 54, wherein the immediate release (IR) tablet comprises microcrystalline cellulose, sodium carboxymethylcellulose, and magnesium stearate.

56. The pharmaceutical composition of claim 53, wherein the immediate release (IR) tablet comprises mannitol, crospovidone, and sodium stearyl fumarate.

57. A method of treating a subject with a disease or disorder, comprising:administering to the subject a therapeutically effective amount of the pharmaceutically acceptable salt of claim 1.

58. A method of treating a subject with a disease or disorder associated with a serotonin 5-HTi receptor, comprising:administering to the subject a therapeutically effective amount of the pharmaceutically acceptable salt of claim 1.

59. The method of claim 58, wherein the disease or disorder is a neuropsychiatric disease or disorder or an inflammatory disease or disorder.

60. The method of claim 58, wherein the disease or disorder is a central nervous system (CNS) disorder.

61. The method of claim 60, wherein the central nervous system (CNS) disorder is at least one selected from the group consisting of major depressive disorder (MDD), treatmentresistant depression (TRD), post-traumatic stress disorder (PTSD), bipolar and related disorders, obsessive-compulsive disorder (OCD), generalized anxiety disorder (GAD), social anxiety disorder, a substance use disorder, an eating disorder, Alzheimer’s disease, cluster headache and migraine, attention deficit hyperactivity disorder (ADHD), pain and neuropathic pain, aphantasia, childhood-onset fluency disorder, major neurocognitive disorder, mild neurocognitive disorder, sexual dysfunction, suicidal ideation, suicidal behavior, major depressive disorder with suicidal ideation or suicidal behavior, melancholic depression, atypical depression, dysthymia, non-suicidal self-injury disorder (NSSID), chronic fatigue syndrome, Lyme’s disease, gambling disorder, a paraphilic disorder, sexual dysfunction, peripheral neuropathy, and obesity.

62. The method of claim 60, wherein the central nervous system (CNS) disorder is major depressive disorder (MDD).

63. The method of claim 60, wherein the central nervous system (CNS) disorder is treatment-resistant depression (TRD).

64. The method of claim 60, wherein the central nervous system (CNS) disorder is generalized anxiety disorder (GAD).

65. The method of claim 60, wherein the central nervous system (CNS) disorder is social anxiety disorder.

66. The method of claim 60, wherein the central nervous system (CNS) disorder is obsessive-compulsive disorder (OCD).

67. The method of claim 60, wherein the central nervous system (CNS) disorder is a substance use disorder.

68. The method of claim 67, wherein the central nervous system (CNS) disorder is alcohol use disorder.

69. The method of claim 58, wherein the disease or disorder is an autonomic nervous system (ANS) condition.

70. The method of claim 58, wherein the disease or disorder is a pulmonary disorder.

71. The method of claim 58, wherein the disease or disorder is a cardiovascular disorder.

72. The method of claim 58, wherein the pharmaceutically acceptable salt is administered orally to the subject.

73. The method of claim 72, wherein the pharmaceutically acceptable salt is administered intraorally to the subject.

74. The method of claim 58, wherein the pharmaceutically acceptable salt is administered transdermally to the subject.

75. The method of claim 58, wherein the pharmaceutically acceptable salt is administered subcutaneously to the subject.

76. The method of claim 58, wherein the pharmaceutically acceptable salt is administered at a psychedelic dose of about 0.083 mg / kg to about 1 mg / kg.

77. The method of claim 76, wherein the pharmaceutically acceptable salt isadministered at the psychedelic dose once per week or less over a treatment course.

78. The method of claim 58, wherein the pharmaceutically acceptable salt isadministered at a sub-psychedelic dose of about 0.00001 mg / kg to less than about 0.083 mg / kg.

79. The method of claim 78, wherein the pharmaceutically acceptable salt isadministered at the sub-psychedelic dose once per day or more over a treatment course.

80. A method for stabilizing the compound of Formula (I) comprising preparing the pharmaceutically acceptable salt of the compound of Formula (I) of claim 1.

81. A method for decreasing time of therapeutic onset relative to a psilocybin-based drug, comprising:administering a therapeutically effective amount of the pharmaceutically acceptable salt of the compound of Formula (I) of claim 1 to a subject in need thereof.

82. A method of reducing psychedelic side effects relative to a psilocybin-based drug, comprising:administering a therapeutically effective amount of the pharmaceutically acceptable salt of the compound of Formula (I) of claim 1 to a subject in need thereof.

83. A method of decreasing duration of therapeutic effect relative to a psilocybin-based drug, comprising:administering a therapeutically effective amount of the pharmaceutically acceptable saltof the compound of Formula (I) of claim 1 to a subject in need thereof.

84. A solution-phase composition, comprising:the pharmaceutically acceptable salt of the compound of Formula (I) of claim 1, in solvated form.

85. The solution-phase composition of claim 84, which is an aqueous solution-phase composition comprising the pharmaceutically acceptable salt of the compound of Formula (I), in solvated form.

86. A crystalline polymorph of a compound of Formula (I), or a stereoisomer or a solvate thereof,R7wherein:R2, Rs, R6, and R7 are independently selected from the group consisting of hydrogen or deuterium,Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, andXi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium.

87. The crystalline polymorph of claim 86, which is a crystalline form of 3-(2-(bis(methyl-6?3)amino)ethyl-l,l,2,2-J4)-l^-indol-4-ol (1-3) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0.2°)selected from the group consisting of 7.582°, 8.395°, 9.647°, 10.444°, 11.319°, 12.614°,13.372°, 14.222°, 15.157°, 16.524°, 16.787°, 17.693°, 19.468°, 19.699°, 20.901°, 21.132°,21.859°, 22.547°, 23.699°, 24.630°, 25.034°, 25.264°, 26.867°, 27.399°, 27.929°, 28.219°,28.871°, 29.430°, 30.120°, 30.675°, 31.373°, 32.365°, 33.880°, 34.418°, 34.792°, 35.884°,36.254°, 37.156°, 38.200°, and 38.417°.

88. The crystalline polymorph of claim 86, which is a crystalline form of 3-(2-(bis(methyl-d3)amino)ethyl-1,1,2,2-^)-l / 7-indol-4-ol (1-3) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (29 ± 0.2°)selected from the group consisting of 8.124°, 8.357°, 10.059°, 12.630°, 13.420°, 13.743°,14.053°, 15.220°, 16.272°, 16.763°, 16.954°, 17.328°, 17.662°, 18.062°, 18.742°, 19.413°,19.658°, 20.172°, 20.836°, 21.267°, 21.833°, 22.213°, 22.504°, 23.334°, 23.701°, 24.385°,25.431°, 25.721°, 26.049°, 27.291°, 28.368°, 30.349°, 30.656°, 31.337°, 31.538°, 32.091°,35.870°, 38.514°, and 41.361°.

89. The crystalline polymorph of claim 86, which is a crystalline form of 3-(2-(dimethylamino)ethyl)-l / / -indol-4-ol (1-7) characterized by an X-ray powder diffraction pattern containing at least three characteristic peaks at diffraction angles (20 ± 0.2°) selected from the group consisting of 7.563°, 8.375°, 12.626°, 13.383°, 15.211°, 16.753°, 17.671°, 19.668°, 21.112°, 21.863°, 22.201°, 22.560°, 23.711°, 24.592°, 25.415°, 26.820°, 27.357°, 27.921°, 28.228°, 29.253°, 30.653°, 31.364°, 32.401°, 33.797°, 34.445°, 39.867°90. A pharmaceutical composition comprising the crystalline polymorph of claim 86, and a pharmaceutically acceptable vehicle.

91. The pharmaceutical composition of claim 90, wherein the pharmaceutically acceptable vehicle comprises an acid.

92. The pharmaceutical composition of claim 91, wherein the acid is citric acid and / or tartaric acid.

93. A method of treating a subject with a disease or disorder associated with a serotonin 5-HTi receptor, comprising:administering to the subject a therapeutically effective amount of the crystalline polymorph of claim 86.

94. An amorphous compound of Formula (I), or a stereoisomer or a solvate thereof,(I)wherein:R2, R5, Re, and R7 are independently selected from the group consisting of hydrogen or deuterium,Rs and R9 are independently selected from the group consisting of -CH3 and -CD3, andXi, X2, Yi, and Y2 are independently selected from the group consisting of hydrogen or deuterium.

95. The amorphous compound of claim 94, which is an amorphous form of 3-(2-(bis(methyl-d3)amino)ethyl-l,l,2,2-d4)-l / / -indol-4-ol (1-3), as determined by X-ray powder diffraction.

96. The amorphous compound of claim 94, which is an amorphous form of 3-(2-(dimethylamino)ethyl)-l / / -indol-4-ol (1-7), as determined by X-ray powder diffraction.

97. The amorphous compound of claim 94, which has a glass transition temperature of about 26°C to about 30°C as determined by differential scanning calorimetry (DSC).

98. The amorphous compound of claim 94, which is prepared by melting a crystalline form of the compound of Formula (I) to beyond a melting point of the crystalline form, and then rapidly cooling to a glass transition temperature.

99. A pharmaceutical composition comprising the amorphous compound of claim 94, and a pharmaceutically acceptable vehicle.

100. A method of treating a subject with a disease or disorder associated with a serotonin 5-HTi receptor, comprising:administering to the subject a therapeutically effective amount of the amorphous compound of claim 94.

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