NEW CATECHOLAMINE PRODRUGS FOR USE IN THE TREATMENT OF PARKINSON'S DISEASE

Abstract

This document provides compounds of formula (1), which are catecholamine prodrugs for use in the treatment of neurodegenerative diseases and disorders. This document also provides pharmaceutical compositions comprising compounds of the same and methods of treating neurodegenerative or neuropsychiatric diseases and disorders using the compounds of the same, in particular Parkinson's disease. Accordingly, this document relates to compounds of formula (2) where R 1 It's H and R 2 is selected from one of the formula substitutes (3) and (4) shown below; or R 1 is selected from one of the substituents of formula (3) and (4) listed below and R 2 is it H; or R 1 and R 2 Both are represented by the formula substituent (3) shown below; or R 1 and R 2Both are represented by the substituent of formula (4) shown below; or R 1 is a substituent of formula (3) and R 2 is a substituent of formula (4); or R 1 is a substituent of formula (4) and R 2 is a substituent of formula (3); where * indicates the attachment point; and where the carbon atom at the attachment point in the substituent of formula (3) is in the S configuration; or a pharmaceutically acceptable salt thereof.

Description

P 18 01 03436 NEW CATECHOLAMINE PRODRUGS FOR USE IN THE TREATMENT OF PARKINSON'S DISEASE FIELD OF INVENTION The present invention provides compounds that are prodrugs of the dopamine agonist (4aR,10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydro-benzo[g]quinoline-6,7-diol and their use in the treatment of Parkinson's disease and / or other conditions for which the dopamine agonist is therapeutically beneficial, such as, but not limited to, restless legs syndrome, Huntington's disease, and Alzheimer's disease, and also neuropsychiatric diseases and disorders such as, but not limited to, schizophrenia, attention deficit hyperactivity disorder, and drug addiction. The present invention also provides pharmaceutical compositions comprising compounds of the invention. BACKGROUND OF THE INVENTION Parkinson's disease (PD) is a common neurodegenerative disorder that becomes increasingly prevalent with age, affecting an estimated seven to ten million people worldwide. Parkinson's disease is a multifaceted condition characterized by both motor and non-motor symptoms. Motor symptoms include resting tremor (shakeability), bradykinesis / akinesia (slowness and poverty of movement), muscle rigidity, postural instability, and gait dysfunction; while non-motor symptoms include neuropsychiatric disorders (e.g., depression, psychotic symptoms, anxiety, apathy, mild cognitive impairment, and dementia), as well as autonomic dysfunction and sleep disturbances (Poewe et al., Nature Review, (2017) vol 3 article 17013: 1-21). 233230 2757082 of 82 P 18 01 03436 A key feature of the pathophysiology of Parkinson's disease is the loss of pigmented dopaminergic neurons in the pars compacta of the substantia nigra, which provides dopaminergic innervation to the striatum and other brain regions. Progressive neurodegeneration of this kind leads to a decrease in striatal dopamine levels, ultimately resulting in a series of changes in basal ganglia circuitry, culminating in the emergence of the four cardinal motor features of Parkinson's disease. The primary target of dopamine in the striatum consists of medium spiny GABAergic neurons (MSNs) that selectively express D1 or D2 receptors pending topographic projections.GABAergic MSNs projecting to the external globus pallidus, also called the striato-pallidal 'indirect' pathway, express D2 receptors (MSN-2); while GABAergic MSNs projecting to the pars reticulata of the substantia nigra and the internal globus pallidus, also called the striato-nigral 'direct' pathway, express D1 receptors (MSN1). Dopamine depletion due to neuronal loss results in unbalanced activity of the two pathways, leading to a marked reduction in thalamic and cortical output activities and, ultimately, motor dysfunctions (Gerfen et al., Science (1990) 250: 1429-32; DeLong, (1990) Trends in Neuroscience). 13:281-5; Alexander et Crutcher, (1990) Trends in Neuroscience 13: 266-71; and for review Poewe et al., Nature Review (2017) vol. 3 article 17013: 1-21). The most effective therapeutic strategies available for patients with Parkinson's disease, which tend to control motor symptoms, are primarily indirect and direct dopamine agonists. The classic and gold-standard treatment regimen includes the intake of 233230 2757082 of 82 P 18 01 03436 Chronic oral administration of L-3,4-dihydroxyphenylalanine (L-DOPA), which is decarboxylated in the brain to form dopamine. Other approaches involve the administration of dopamine receptor agonists such as apomorphine, which acts on both D1 and D2 receptor subtypes, or pramipexole, ropinirole, and others that are predominantly directed toward D2 receptor subtypes. Optimal motor relief is achieved with the use of both L-DOPA and apomorphine due to their activation of both D1 and D2 receptor subtypes and the holistic rebalancing of the indirect-direct pathways (i.e., whereas D2 agonists only reverse the dysfunction of the indirect pathway). L-DOPA and apomorphine with the structures represented below are currently the most effective drugs against PD in clinical use. L-DOPA apomorphine L-DOPA is a dopamine prodrug and remains the most effective drug for treating motor Parkinson's disease. However, after several years of treatment (i.e., the honeymoon period), complications arise due to disease progression (i.e., sustained loss of dopaminergic neurons) and L-DOPA's poor pharmacokinetic (PK) profile. These complications include: 1) dyskinesia, which are abnormal involuntary movements that occur during the drug's optimal effect time; and 2) off fluctuations, a period during which 233230 2757082 of 82 P 18 01 03436 the positive effect of L-DOPA wears off and symptoms re-emerge or worsen (Sprenger and Poewe, CNS Drugs (2013), 27: 259-272). Direct dopamine receptor agonists are capable of activating dopamine autoreceptors, as well as postsynaptic dopamine receptors located on the MSN1 and MSN2 medium spiny neurons. Apomorphine belongs to a class of dopamine agonists with a 1,2-dihydroxybenzene (catechol) moiety. When combined with a phenethylamine motif, catecholamines often have low or no oral bioavailability, as is the case with apomorphine. Apomorphine is used clinically in the therapy of Parkinson's disease (PD), although with non-oral administration (typically intermittent subcutaneous administration or continuous daytime parenteral infusion via a pump). The poor oral bioavailability of catecholamines has prevented their clinical use as oral drugs. For apomorphine, animal studies have shown that transdermal administration or implants may provide potential delivery routes.However, when the administration of apomorphine from implants was studied in monkeys (Bibbiani et al., Chase Experimental Neurology (2005), 192:. 73-78), it was found that in most cases the animals had to be treated with the immunosuppressant Dexamethasone to avoid local irritation and other complications after implantation surgery. Alternative administration strategies for apomorphine therapy in PD, such as inhalation and sublingual formulations, have been extensively explored (see, e.g., Grosset et al., Acta Neurol Scand. (2013), 128:166-171 and Hauser et al., Movement Disorders (2016), Vol. 32 (9): 1367-1372). However, these efforts are not yet in clinical use for the treatment of PD. 233230 2757082 of 82 P 18 01 03436 An alternative to non-oral catecholamine formulations involves the use of a prodrug that masks the free hydroxyl groups of catechol to allow oral administration. However, a known problem associated with the development of prodrugs for clinical use is the difficulty in predicting their conversion to the precursor compound in humans. Several ester prodrugs have been reported in the literature, such as enterically coated N-propylapomorphine (NPA) esters for duodenal administration (see WO 02 / 100377) and the D1-type agonist adrogolide, a diacetyl prodrug of A-86929 (Giardina and Williams; CNS Drug Reviews (2001), Vol. 7 (3): 305-316). Adrogolide undergoes extensive hepatic first-pass metabolism in humans following oral administration and, as a result, has low oral bioavailability (approximately 4%). In PD patients, intravenous (IV) adrogolide has antiparkinson efficacy comparable to that of L-DOPA (Giardina and Williams; CNS Drug Reviews (2001), Vol. 7 (3): 305-316). In addition to catecholamine ester prodrugs, an alternative prodrug approach involves masking the two hydroxyl groups of catechol as the corresponding methylenedioxyacetal (MDO), as the acetal derived from aldehydes other than formaldehyde, or as the ketal derived from various ketones. This prodrug principle has been described, for example, in Campbell et al., Neuropharmacology (1982); 21(10): 953-961 and in documents US4543256, WO 2009 / 026934 and WO 2009 / 026935. Yet another suggested approach for a catecholamine prodrug is the formation of an enone derivative as suggested, for example, in WO 2001 / 078713 and in Liu et al., Bioorganic Med. Chem. (2008), 233230 2757082 of 82 P 18 01 03436 16: 3438-3444. For additional examples of catecholamine prodrugs, see, for example, Sozio et al., Exp. Opin. Drug Disc. (2012); 7(5): 385-406. The compound (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10aoctahydro-benzo[g]quinoline-6,7-diol, represented as compound (I) below, is described in WO 2009 / 026934. The trans isomer was previously described in Liu et al., Bioorganic Med. Chem. (2008), 16: 3438-3444, including pharmacological data indicating that the compound has low bioavailability in rats. The racemate was first described in Cannon et al., J. Heterocyclic Chem. (1980); 17: 1633-1636. (YO) Compound (I) is a dopamine receptor agonist with mixed D1 and D2 activity. Three prodrug derivatives of compound (I) are known in the art. Liu et al., J. Med. Chem. (2006), 49: 1494-1498 and Liu et al., Bioorganic Med. Chem. (2008), 16: 3438-3444 describe the enone derivative of formula (Ia) represented below, which was shown to be converted into the active compound (I) in rats. 233230 2757082 of 82 P 18 01 03436 O (Ia) Documents WO 2009 / 026934 and WO 2009 / 026935 describe two types of compound prodrug derivatives (I), including an MDO derivative with the formula (Ib) shown below: (Ib) The conversion of compound (Ib) to compound (I) in rat and human hepatocytes has been demonstrated in WO 2010 / 097092. Furthermore, the in vivo pharmacology of compounds (Ia) and (Ib), as well as the precursor compound (I), has been tested in various animal models relevant to Parkinson's disease (WO 2010 / 097092). Compound (I), compounds (Ia), and (Ib) were all found to be effective, indicating that compounds (Ia) and (Ib) are converted in vivo to compound (I). All three compounds were reported to have a longer duration of action than that observed for L-dopa and apomorphine. The other prodrug compound (I) described in documents WO 2009 / 026934 and WO 2009 / 026935 is a conventional ester prodrug of formula (Ic): 233230 2757082 of 82 P 18 01 03436 Despite prolonged interest in the field, there remains a clear unmet need for the development of efficient, well-tolerated, orally active drugs for the treatment of PD. A prodrug derivative of a mixed D1 / D2 agonist that provides a stable pharmacokinetic profile and can deliver continuous dopaminergic stimulation may address this unmet need. SUMMARY OF THE INVENTION The present invention relates to novel compounds for the treatment of Parkinson's disease. More particularly, the invention relates to novel prodrug derivatives of the compound (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydro-benzo[g]quinoline-6,7-diol (compound (I)). The compounds of the invention have proven to be particularly useful for the oral administration of compound (I). Therefore, the present invention relates to compounds of formula (Id) 233230 2757082 of 82 P 18 01 03436 (Id) where R1 is H and R2 is selected from one of the substituents (i) and (ii) listed below; or R1 is selected from one of the substituents (i) and (ii) listed below and R2 is H; or R1 and R2 are both represented by the substituent (i) shown below; or R1 and R2 are both represented by the substituent (ii) shown below; or R1 is a substituent (i) and R2 is a substituent (ii); or R1 is substituent (ii) and R2 is substituent (i); (ii) where * indicates the point of attachment; and where the carbon atom at the point of attachment on the substituent (i) is in the S configuration; or a pharmaceutically acceptable salt thereof. In one embodiment, the invention relates to a pharmaceutical composition comprising a compound according to formula (Id) or a pharmaceutically acceptable salt thereof, and one or more pharmaceutically acceptable excipients. In one embodiment, the invention relates to a compound according to formula (Id) for use as a medicament. In one embodiment, the invention relates to a compound according to formula (Id) or a pharmaceutically acceptable salt thereof for use in the 233230 2757082 of 82 P 18 01 03436 treatment of a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome or Alzheimer's disease, or a neuropsychiatric disease or disorder, such as schizophrenia, attention deficit hyperactivity disorder or drug addiction. In one embodiment, the invention relates to a method for treating a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome, or Alzheimer's disease, or a neuropsychiatric disease or disorder, such as schizophrenia, attention deficit hyperactivity disorder, or drug addiction; the method comprising administering a therapeutically effective amount of a compound of formula (Id) or a pharmaceutically acceptable salt thereof to a patient in need thereof. In one embodiment, the invention relates to the use of a compound according to formula (Id) or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for the treatment of a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome or Alzheimer's disease, or for the treatment of a neuropsychiatric disease or disorder, such as schizophrenia, attention deficit hyperactivity disorder or drug addiction. In the context of the present invention, it is understood that the carbon atom at the point of attachment in the substituent (i) is in the anomeric position of (i). 233230 2757082 of 82 P 18 01 03436 DEFINITIONS Compounds of the invention The reference to compounds covered by the invention includes the free substance (hybrid ion) of compounds of the invention, pharmaceutically acceptable salts of compounds of the invention, such as salts formed by the addition of acids or salts formed by the addition of bases, and polymorphic and amorphous forms of compounds of the invention and pharmaceutically acceptable salts thereof. Furthermore, the compounds of the invention and pharmaceutically acceptable salts thereof may potentially exist in an unsolvated form, as well as in a solvated form with pharmaceutically acceptable solvents such as water, ethanol, and the like. Both the solvated and unsolvated forms are covered by the present invention. Pharmaceutically acceptable salts: Pharmaceutically acceptable salts in the present context are intended to indicate non-toxic salts, i.e., physiologically acceptable salts. The term “pharmaceutically acceptable salts” includes salts formed by the addition of pharmaceutically acceptable acids, which are salts formed with inorganic and / or organic acids at the nitrogen atom in the precursor molecule. Such acids may be selected, for example, from hydrochloric acid, hydrobromic acid, phosphoric acid, nitrous acid, sulfuric acid, benzoic acid, citric acid, gluconic acid, lactic acid, maleic acid, succinic acid, tartaric acid, acetic acid, propionic acid, oxalic acid, malonic acid, fumaric acid, glutamic acid, pyroglutamic acid, salicylic acid, gentisic acid, saccharin, and sulfonic acids, such as methanesulfonic acid, ethanesulfonic acid, toluenesulfonic acid, naphthalene-2-sulfonic acid, 2-hydroxyethanesulfonic acid, and benzenesulfonic acid. 233230 2757082 of 82 P 18 01 03436 The term pharmaceutically acceptable salts also includes salts formed by the addition of pharmaceutically acceptable bases, which are salts formed with inorganic and / or organic bases in the acidic groups of compounds of formula (Id). Such bases may be selected, for example, from zinc hydroxide, and alkali metal bases, such as sodium hydroxide, lithium hydroxide, potassium hydroxide, and alkaline earth bases, such as calcium hydroxide and magnesium hydroxide, and organic bases, such as choline, diethylamine, trimethylamine, and triethylamine. Additional examples of acids and bases useful for forming pharmaceutically acceptable salts can be found, e.g., in Stahl and Wermuth (Comps) Handbook of Pharmaceutical Salts. Properties, Selection, and Use, Wiley-VCH, 2008. Solid form In the present context, when a compound of the invention is in a solid form, this indicates that the compound is not dissolved in any liquid, such as aqueous liquids, organic liquids, and mixtures thereof. The invention encompasses solid forms of the free substance (hybrid ion) of compounds of the invention, as well as solid forms of pharmaceutically acceptable salts of compounds of the invention. The term “solid form” includes both amorphous forms of compounds of the invention and salts thereof, and crystalline forms of compounds of the invention and salts thereof. Prodrug In the present context, the term "prodrug" or "prodrug derivative" indicates a compound that, after administration to a living subject such as a mammal, preferably a human, is converted in the body into a pharmacologically active residue. The conversion 233230 2757082 of 82 P 18 01 03436 preferably takes place in a mammal such as a mouse, dog, miniature pig, rabbit, monkey, and / or human. In the present context, a prodrug of the compound (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol or a prodrug of the compound of formula (I) or a prodrug of compound (I) is understood to be a compound that, after administration, is converted within the body into the compound (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol. Such administration may be by any conventional route of administration of pharmaceutical compositions known in the art, preferably by oral administration. In the present context, the terms “precursor compound” and “precursor molecule” refer to the pharmacologically active residue obtained after the conversion of a corresponding prodrug. For example, the “precursor compound” of one of compounds (1a), (1b), (1c), or any of the compounds of the invention is understood to be the compound of formula (1). Chemical manufacturing In the present context, a compound derived by chemical fabrication” indicates that said compound has been fabricated by a chemical process such as, but not limited to, one of the processes described in the experimental section of this dissertation. Pharmacokinetic definitions and abbreviations As used herein, an “FC profile” is an abbreviation for “pharmacokinetic profile.” Pharmacokinetic profiles and pharmacokinetic parameters described herein are based on plasma concentration-time data obtained for the compound of formula (I) following oral dosing of a compound of the invention, using a non-compartmental model. The FC parameters 233230 2757082 of 82 P 18 01 03436 abbreviated are: Cmax (maximum concentration); tmax (time to Cmax); ti^ (half-life); AUC (area under the curve from dosing time to infinity). Therapeutically effective amount: In the present context, the expression “therapeutically effective amount” of a compound means a quantity sufficient to alleviate, halt, partially halt, eliminate, or delay the clinical manifestations of a given disease and its complications in a therapeutic intervention involving the administration of that compound. An amount suitable for achieving this effect is defined as a therapeutically effective amount. Effective amounts for each purpose will depend, for example, on the severity of the disease or injury, as well as the weight and general condition of the subject. It is understood that determining an appropriate dosage can be achieved through routine experimentation, constructing a matrix of values, and testing different points on the matrix—all of which is within the ordinary experience of a trained physician. In the context of the present invention, a “therapeutically effective amount” of a compound of the invention indicates an amount of said compound of the invention that is capable of providing an amount of compound (I) that is sufficient to relieve, stop, partially stop, eliminate or delay the clinical manifestations of a given disease and its complications when said compound of the invention is administered, preferably orally, preferably to a human being. Treatment and treating: In the present context, “treatment” or “to treat” is intended to indicate the attention and care of a patient in order to relieve, stop, partially stop, eliminate or delay the progression of the clinical manifestation 233230 2757082 of 82 P 18 01 03436 of the disease. The patient to be treated is preferably a mammal, in particular a human being. Conditions for treatment The compounds of the present invention are intended for the treatment of neurodegenerative diseases and disorders such as Parkinson's disease and / or conditions for which treatment with a dopamine agonist is therapeutically beneficial. Therapeutic indications include a variety of central nervous system disorders characterized by motor and / or non-motor disturbances and for which part of the underlying pathophysiology is a dysfunction of the striatum-mediated circuits. Functional disturbances of this type can be observed in neurodegenerative diseases such as, but not limited to, Parkinson's disease (PD), restless legs syndrome, Huntington's disease, and Alzheimer's disease, but also in neuropsychiatric diseases such as, but not limited to, schizophrenia, attention deficit hyperactivity disorder, and drug addiction. In addition to neurodegenerative diseases and disorders, other conditions where increased dopamine turnover may be beneficial include improved mental function, encompassing various aspects of cognition. It can also have a positive effect on patients with depression and can be used in the treatment of obesity as an anorectic agent and in the treatment of drug addiction. It may improve minimal brain dysfunction (MBD), narcolepsy, attention deficit hyperactivity disorder (ADHD), and potentially the negative, positive, and cognitive symptoms of schizophrenia. Restless legs syndrome (RLS) and the 233230 2757082 of 82 Periodic limb movement disorder (PLMD) is an alternative indication that is clinically treated with dopamine agonists. Furthermore, impotence, erectile dysfunction, SSRI-induced sexual dysfunction, ovarian hyperstimulation syndrome (OHSS), and certain pituitary tumors (prolactinoma) are also likely to be improved by treatment with dopamine agonists. Dopamine is involved in the regulation of the cardiovascular and renal systems; therefore, renal insufficiency and hypertension can be considered alternative indications for the compounds of the invention. The invention covers the use of compounds of the invention for the treatment of the diseases and disorders listed above. Combinations In one embodiment of the invention, the compounds of formula (Id) are for use as a standalone treatment as the sole active compound. In another embodiment of the invention, the compounds of formula (Id) can be used in combination with other agents useful in the treatment of a neurodegenerative disease or disorder such as Parkinson's disease. The expressions "combined use," "in combination with," and "a combination of," and the like, as used herein in the context of the method of the invention comprising the combined administration of therapeutically effective amounts of a compound of formula (Id) and another compound, which is useful in the treatment of a neurodegenerative disease or disorder, are intended to convey the simultaneous or sequential administration of a compound of formula (Id), in any order, together with said other compound. Both compounds can be administered 233230 2757082 of 82 P 18 01 03436 simultaneously or with a time interval between the administrations of the two compounds. The two compounds may be administered as part of the same formulation or pharmaceutical composition, or in separate formulations or pharmaceutical compositions. The two compounds may be administered on the same day or on different days. They may be administered by the same route, such as, for example, by oral administration, subcutaneous injection, transdermal administration, depot, intramuscular injection, or intravenous injection, or by different routes, where one compound is administered, for example, orally or by depot, and, for example, the other compound is injected.The two compounds can be administered using the same dosing regimen or interval, such as once or twice a day, weekly or monthly; or using different dosing regimens, for example, where one is administered once a day and the other is administered twice a day or weekly or monthly. In some cases, the patient may already be receiving one or more other compounds useful in the treatment of a neurodegenerative disease or disorder when treatment with a compound of formula (Id) is initiated. In other cases, the patient may already be receiving a compound of formula (Id) when treatment with one or more other compounds useful in the treatment of a neurodegenerative disease or disorder is initiated. In other cases, treatment with a compound of formula (Id) and treatment with one or more other compounds useful in the treatment of a neurodegenerative disease or disorder are initiated simultaneously. 233230 2757082 of 82 P 18 01 03436 Combination treatment compounds In the context of the invention, compounds to be used in combination with a compound of formula (Id) can be selected, for example, from L-DOPA, droxidopa, MAO-B inhibitors such as selegiline or rasagiline, COMT inhibitors such as entacapone or tolcapone, adenosine 2a antagonists such as istradephylline, antiglutamatergic agents such as amantadine or memantine, acetylcholinesterase inhibitors such as rivastigmine, donepezil or galantamine, and antipsychotic agents such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole or brexpiprazole. In addition to small molecules, combination compounds could also include emerging biological approaches in treatments for neurodegenerative diseases or disorders, such as antibodies that target alpha-synuclein, Tau, or Abeta proteins. Routes of administration Pharmaceutical compositions comprising a compound of formula (Id), either as the sole active compound or in combination with another active compound, may be specifically formulated for administration by any suitable route, such as oral, rectal, nasal, buccal, sublingual, pulmonary, transdermal, and parenteral (e.g., subcutaneous, intramuscular, and intravenous). In the context of the present invention, the oral route is the preferred route of administration. It will be understood that the route will depend on the general health status and age of the subject to be treated, the nature of the condition to be treated, and the active ingredient. 233230 2757082 of 82 P 18 01 03436 Pharmaceutical formulations and excipients In what follows, the term excipient or the expression pharmaceutically acceptable excipient refers to pharmaceutical excipients that include, but are not limited to, carriers, fillers, diluents, anti-adherents, binders, coatings, colors, disintegrants, flavorings, glidants, lubricants, preservatives, sorbents, sweeteners, solvents, vehicles, and adjuvants. The present invention also provides a pharmaceutical composition comprising a compound of formula (Id), such as one of the compounds described in the Experimental Section of this specification. The present invention further provides a process for producing a pharmaceutical composition comprising a compound of formula (Id). Pharmaceutical compositions according to the invention can be formulated with pharmaceutically acceptable excipients using conventional techniques such as those described in Remington, The Science and Practice of Pharmacy, 22nd edition (2012), edited by Allen, Lloyd V., Jr. The pharmaceutical composition comprising a compound of the present invention is preferably a pharmaceutical composition for oral administration. Pharmaceutical compositions for oral administration include solid oral dosage forms such as tablets, capsules, powders, and granules; and liquid oral dosage forms such as solutions, emulsions, suspensions, and syrups, as well as powders and granules to be dissolved or suspended in a suitable liquid. Solid oral dosage forms may be presented as discrete units (e.g., hard or soft tablets or capsules), each containing a predetermined amount of the active ingredient, and preferably one or more suitable excipients. In cases where 233230 2757082 of 82 P 18 01 03436 Where appropriate, solid dosage forms may be prepared with coatings such as enteric coatings, or may be formulated to provide modified release of the active ingredient, such as delayed or prolonged release, according to methods well known in the art. Where appropriate, the solid dosage form may be a dosage form that disintegrates in saliva, such as, for example, an orodispersible tablet. Examples of suitable excipients for solid oral formulations include, but are not limited to, microcrystalline cellulose, maize starch, lactose, mannitol, povidone, croscarmellose sodium, sucrose, cyclodextrin, talc, gelatin, pectin, magnesium stearate, stearic acid, and lower alkyl cellulose ethers. Similarly, the solid formulation may include excipients for delayed-release or prolonged-release formulations known in the art, such as glyceryl monostearate or hypromellose. If solid material is used for oral administration, the formulation may be prepared, for example, by mixing the active ingredient with solid excipients and then compressing the mixture in a conventional tablet-forming machine; or the formulation may be placed, for example, in a hard capsule, e.g., in powder, granule, or mini-tablet form.The amount of solid excipient will vary widely, but will typically range from approximately 25 mg to approximately 1 g per dosage unit. Liquid oral dosage forms may be presented, for example, as elixirs, syrups, oral drops, or a liquid-filled capsule. Liquid oral dosage forms may also be presented as powders for dissolution or suspension in an aqueous or non-aqueous liquid. Examples of suitable excipients for 233230 2757082 of 82 P 18 01 03436 Liquid oral formulations include, but are not limited to, ethanol, propylene glycol, glycerol, polyethylene glycols, poloxamers, sorbitol, polysorbate, mono- and diglycerides, cyclodextrins, coconut oil, palm oil, and water. Liquid oral dosage forms may be prepared, for example, by dissolving or suspending the active ingredient in an aqueous or non-aqueous liquid, or by incorporating the active ingredient into an oil-in-water or water-in-oil emulsion. Additional excipients such as colorants, flavorings, and preservatives, etc., may be used in solid and liquid oral formulations. Pharmaceutical compositions for parenteral administration include sterile aqueous and non-aqueous solutions, dispersions, suspensions, or emulsions for injection or infusion, concentrates for injection or infusion, and sterile powders to be reconstituted into sterile solutions or dispersions for injection or infusion prior to use. Examples of suitable excipients for parenteral formulation include, but are not limited to, water, coconut oil, palm oil, and cyclodextrin solutions. Aqueous formulations should be adequately buffered, if necessary, and made isotonic with sufficient saline or glucose solution. Other types of pharmaceutical compositions include suppositories, inhalants, creams, gels, dermal patches, implants, and formulations for oral or sublingual administration. It is a requirement that the excipients used for any pharmaceutical formulation comply with the intended route of administration and are compatible with the active ingredients. Dose: In one embodiment, the compound of the present 233230 2757082 of 82 The invention P 18 01 03436 is administered in an amount of approximately 0.0001 mg / kg of body weight to approximately 5 mg / kg of body weight per day. In particular, daily dosages may be in the range of approximately 0.001 mg / kg of body weight to approximately 1 mg / kg of body weight per day. The exact dosages will depend on the frequency and method of administration, the sex, age, weight, and general condition of the subject being treated, the nature and severity of the condition being treated, any concomitant diseases being treated, the desired effect of the treatment, and other factors known to those skilled in the art. A typical oral dosage for adults will be in the range of 0.01-100 mg / day of a compound of the present invention, such as 0.05-50 mg / day, 0.1-10 mg / day, or 0.1-5 mg / day. Conveniently, the compounds of the invention are administered in a unit-dose form containing said compounds in an amount of approximately 0.01 to 50 mg, such as 0.05 mg, 0.1 mg, 0.2 mg, 0.5 mg, 1 mg, 5 mg, 10 mg, 15 mg, 20 mg, or up to 50 mg of a compound of the present invention. BRIEF DESCRIPTION OF THE FIGURES Figure 1: Graphical illustration of the conjugation and deconjugation equilibrium in the body between compound (I) and compounds (Id-ia), (Id-ib), (Id-iia) and (Id-iib). Figure 2: PK profiles in Wistar rats obtained after oral dosing according to Example 4. The profiles are based on mean plasma concentrations from 3 subjects for each of the compounds. X-axis: time (hours); Y-axis: plasma concentration of Compound (I) (pg / mL) obtained after dosing the following compounds: ·: compound (la) ▲: compound (Ib); ♦: compound (Id-ia); X: compound (Id-ib); ▲: 233230 2757082 of 82 P 18 01 03436 compound (Id-iia); +: compound (Id-iib), X : compound (Id-iab) and ♦: compound (Id-iiab). Figures 3 and 4: Time course of locomotor activity (Figure 3) and total distance traveled (Figure 4) after treatment with vehicle H2O, po), or compound (Id-ia) (10, 30, 100, or 300 pg / kg, po) and compared with standard care (SoC) treatments: apomorphine (APO, 3 mg / kg, sc), pramipexole (PPX, 0.3 mg / kg, sc). Animals were dosed at t=60 minutes after a 60-minute habituation period in test chambers, and activity was monitored 350 minutes thereafter. Data were assessed using a Kruskal-Wallis test with Dunn's multiple comparisons test, resulting in an overall P-value of <0.0001. Figure 3: X-axis: time (min); Y-axis: Distance traveled (cm) ± SEM / 5-minute-containers Figure 4: Y-axis: Total distance traveled (cm) ± SEM. Significance levels for post-hoc comparisons (with respect to the vehicle group) are indicated: *<0.05, **<0.01, ***<0.001, ****<0.0001. Figures 5 and 6: Relationships between plasma concentrations of compound (Id-ia) and compound (I) and compound (Id-ia) induced hyperactivity (100 pg / kg, po) (Figure 5) and the corresponding relationship between plasma apomorphine concentrations and apomorphine induced hyperactivity (3 mg / kg, sc) (Figure 6). X-axis: time (min); left Y-axis: Distance traveled (cm) ± SEM / 5-minute-containers; right Y-axis (Figure 5): plasma concentration of compound (I) (pg / mL); right Y-axis (Figure 6): plasma concentration of apomorphine (ng / mL). □: Distance traveled (cm) · plasma concentration. 233230 2757082 of 82 P 18 01 03436 Figure 7; conversion of compounds (Id-ia), (Id-ib), (Idiia), (Id-iib) and (Id-iab) into compound (I) in rat (7a) and human (7b) hepatocytes. X-axis: time (min); Y-axis: compound concentration (I) (pg / mL). ♦: compound (Id-ia); X: compound (Id-ib); ▲: compound (Id-iia); + : compound (Id-iib); ·: compound (Id-iab). Figure 8: Conversion of compounds (Id-ia), (Id-ib), (Idiia), (Id-iib) and (Id-iab) into compound (I) in rat (8a) and human (8b) whole blood. X-axis: time (min); Y-axis: compound concentration (I) (pg / mL). ♦: compound (Id-ia); X: compound (Id-ib); ▲: compound (Id-iia); I : compound (Id-iib). DETAILED DESCRIPTION OF THE INVENTION The inventors have identified novel compounds that are prodrugs of (4aR,lOaR)-1-n-propyl1,2,3,4,4a,5,10,1Oa-octahydro-benzo[g]quinoline-6,7-diol [compound (I)] which is a dual D1 / D2 agonist with in vitro data listed in Table 2. The inventors have observed that compound (I) is conjugated in rat and human hepatocytes to the glucuronide derivatives (Id-ia) and (Id-ib), and to the sulfate derivatives (Id-iia) and (Id-iib). The conjugates have been shown to be converted back into compound (I) by conjugation and deconjugation in the body, as illustrated in Figure 1. Glucuronide and sulfate derivatives are generally known to be unstable in the intestine. These derivatives are formed as highly polar and soluble metabolites to facilitate the elimination of compounds from the body and are therefore readily excreted. For example, in rats with bile duct cannulation, glucuronide and sulfate conjugates are often found in the 233230 2757082 of 82 P 18 01 03436 is found in bile, while its deconjugate (i.e., the precursor compound) is found in feces. The reverse conversion of glucuronide and sulfate conjugates in the intestine to the precursor compound, which is then sometimes subsequently reabsorbed, is known as part of the enterohepatic recirculation process. As mentioned earlier, oral dosing of phenethylcatecholamines, such as apomorphine, has generally proven unsuccessful due to low bioavailability. Similarly, compound (I) suffers from low oral bioavailability (Liu et al., Bioorganic Med. Chem. (2008), 16: 3438-3444). With this in mind, and considering the instability of glucuronide and sulfate conjugates in the gastrointestinal tract, it was not expected that oral dosing of glucuronide and sulfate conjugates of compound (I) could be used to achieve sufficient plasma exposure of the compound. The principle of using glucuronide derivatives as prodrugs for oral administration has been explored for retinoic acid (Goswami et al., J. Nutritional Biochem. (2003) 14: 703-709) and for morphine (Stain-Texier et al., Drug Metab. and Disposition (1998) 26 (5): 383-387). Both studies showed very low levels of exposure to the precursor compounds after oral dosing of the derivatives. Another study suggests the use of budesonide-BD-glucuronide as a prodrug for the local administration of budesonide to the large intestine for the treatment of ulcerative colitis, based on poor absorption of the prodrug itself from the intestinal system (Nolen et al., J. Pharm Sci. (1995), 84 (6): 677-681). However, surprisingly, the authors of the present invention found that the oral dosage of the glucuronide conjugates (Id-ia), (Id-ib) and the conjugates 233230 2757082 of 82 P 18 01 03436 of sulfate (Id-iia) and (Id-iib), which have all been identified as metabolites of compound (I) in rats and miniature pigs, provides systemic exposure of compound (I) in plasma, suggesting the utility of the glucuronide and sulfate derivatives of compound (I) as orally active prodrugs of compound (I). The inventors further explored compounds (Id-iab) and (Id-iiab), each of which is substituted with glucuronide or sulfate on both hydroxyl groups of catechol, and found that these two compounds also exhibit prodrug activity. The plasma profiles of compound (I) resulting from the oral dosing of compounds (Ia) and (Ib) and of each of the compounds (Id-ia) and (Id-ib), (Id-iia), (Id-iib), (Id-iab), and (Id-iiab) to Wistar rats according to Example 4 are shown in Figure 2. For all compounds, the doses were corrected for molecular weight to equate a dose of 300 µg / kg of compound (Ib) to 287 µg / kg of compound (I). The inventors have found that the oral dosing of compounds (Id-ia) and (Id-ib) to Wistar rats results in early and elevated peak concentrations of compound (I). Such elevated peak concentrations are likely associated in humans with dopaminergic side effects, such as nausea, vomiting, and dizziness.In contrast, the dosage of compounds (Id-ia), (Id-ib), (Id-iia), (Id-iib), (Id-iab), and (Id-iiab) results in a slower absorption rate, avoiding rapid peak concentrations associated with sustained plasma exposure of compound (I). Additionally, plasma exposure to compound (I) in Wistar rats is maintained over 24 hours, although the AUC obtained for compound (I) is generally lower than the AUC obtained after [the following]. 233230 2757082 of 82 P 18 01 03436 dosage of compound (Ib). However, since the peak concentrations of compound (I), which are expected to drive side effects, are lower, higher doses of compounds (Id-ia), (Id-ib), (Id-iia), (Id-iib), (Id-iab), and (Id-iiab) could be administered to potentially achieve higher overall plasma concentrations of compound (I) compared to what can be achieved with the dosage of compounds (Ia) and (Ib). When investigating the PK properties of compound (Ic), the inventors found that the plasma concentrations of compound (I) were extremely low, rendering compound (Ic) unsuitable as a prodrug of compound (I) for oral administration and confirming that the oral bioavailability of the compounds of the invention is highly unpredictable. Table 3 lists the PK parameters for PK studies in Wistar rats. PK experiments were also performed with oral dosing of compounds (Id-ia), (Id-ib), (Id-iia), and (Id-iib) to miniature pigs according to Example 5. The study demonstrated that all four compounds are converted to compound (I) in miniature pigs and provided plasma exposure to compound (I) following oral dosing. Table 4 lists the PK parameters for this study. The bioconversion of compounds (Id-ia), (Id-ib), (Id-ia), (Id-iib) and (Id-iab) in humans is supported by the Experiments in Example 1, demonstrating the conversion of the compounds into the compound of formula (I) in rat and human hepatocytes and to (Id-ia), (Id-ib), (Id-iia), (Id-iib) in rat and human blood (Figures 7 and 8). Therefore, in conclusion, the compounds of the invention are useful as orally active prodrugs of compound (I) and have been observed in rats to provide a 233230 2757082 of 82 P 18 01 03436 PK profile that avoids the peak Cmax observed for known prodrugs (Ia) and (Ib) and provides a significantly higher AUC of compound (I) than of compound (Ic). Preferred compounds of the invention are the glucuronide conjugates (Id-ia), (Id-ib) and (Id-iab). As a comparative example, a glucuronide conjugate and two apomorphine sulfate conjugates ((2S,3S,4S,5R,6S)-6-[[(6aR)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10-yl]oxy]-3,4,5-trihydroxy-tetrahydropyran-2-carboxylic acid; [(6aR)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro4H-dibenzo[de,g]quinolin-10-yl] hydrogen sulfate and [(6aR)-10-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4Hdibenzo[de,g]quinolin-11-yl] hydrogen sulfate) were dosed to Wistar rats. Dosing apomorphine conjugates orally to Wistar rats at doses as high as 4977 pg / kg did not result in measurable plasma apomorphine exposure (lower limit of quantification 500 pg / ml), except for 916 pg / ml at one time point (4 h) of dosing the glucuronide conjugate, indicating low / no oral bioavailability of the apomorphine conjugates.In comparison, oral administration of 3000 pg / kg of apomorphine resulted in a plasma AUC > 100 times lower than that observed after subcutaneous administration of 3000 pg / kg of apomorphine, confirming the poor oral bioavailability of apomorphine. This further supports the notion that the oral bioavailability of the compounds of the invention is highly unexpected (for the experimental part, see Example 4). The compound (Id-ia) has been further explored in the locomotor activity assay in rats according to Example 6. This assay demonstrated a dopaminergic effect obtained after oral administration of compound (Id-ia), 233230 2757082 of 82 P 18 01 03436 see figures 3, 4 and 5. The fact that the compounds of the invention, including (Id-ia), do not possess dopaminergic activity in vitro, see example2 and table 1, further indicates that the effect of compound (Id-ia) in the locomotor activity assay in rats is obtained by conversion of compound (Id-ia) into compound (I). Finally, an important aspect associated with compound (Ib) of the prior art is that this compound is a 5-HT2B receptor agonist. Since 5-HT2B receptor agonists have been linked to the pathogenesis of valvular heart disease (VHD) following long-term exposure, such compounds are not suitable for use in the treatment of chronic diseases (Rothman et al., Circulation (2000), 102: 2836-2841; and Cavero and Guillon, J. Pharmacol. Toxicol. Methods (2014), 69: 150-161). Therefore, an additional advantage of the compounds of the invention is that they are not 5-HT2B receptor agonists, see Example 3 and Table 1. The compounds of the invention are useful for the treatment of neurodegenerative diseases and disorders such as Parkinson's disease and / or other conditions for which treatment with a dopamine agonist is therapeutically beneficial. Being suitable for oral administration, the compounds have the potential to provide a new treatment paradigm for Parkinson's disease. In one embodiment of the invention, the compounds are for use as a stand-alone treatment for a neurodegenerative disease or disorder. In another embodiment of the invention, the compounds are to be used in combination with other agents for the treatment of PD, such as a compound selected from the group consisting of L-DOPA, an MAO-B inhibitor, such as selegiline or rasagiline, a COMT inhibitor, such as entacapone or tolcapone, a 233230 2757082 of 82 P 18 01 03436 an adenosine 2a antagonist, such as istradephylline, an antiglutamatergic agent, such as amantadine or memantine, an acetylcholinesterase inhibitor, such as rivastigmine, donepezil, or galantamine, an antipsychotic agent, such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole, or brexpiprazole; or a combination with an antibody that targets alpha-synuclein, TAU protein, or A-beta. EMBODIMENTS OF THE INVENTION Embodiments of the invention are disclosed below. The first embodiment is designated E1, the second embodiment is designated E2, and so on. E1 A compound according to the formula (Id) (Id) where R1 is H and R2 is selected from one of the substituents (i) and (ii) listed below; or R1 is selected from one of the substituents (i) and (ii) listed below and R2 is H; or R1 and R2 are both represented by the substituent (i) shown below; or R1 and R2 are both represented by the substituent (ii) shown below; or R1 is a substituent (i) and R2 is a substituent (ii); or R1 is substituent (ii) and R2 is substituent (i); 233230 2757082 of 82 P 18 01 03436 where * indicates the point of attachment; and where the carbon atom at the point of attachment on the substituent (i) is in the S configuration; or a pharmaceutically acceptable salt thereof. E2 The pharmaceutically acceptable compound or salt thereof according to embodiment 1, wherein R1 is H and R2 is selected from one of the substituents (i) and (ii); or R1 is selected from one of the substituents (i) and (ii) and R2 is H; or R1 and R2 are both represented by the substituent (i); or R1 and R2 are both represented by the substituent (ii). E3 The pharmaceutically acceptable compound or salt thereof according to embodiment 1, wherein R1 is H and R2 is substituent (i); or R1 is substituent (i) and R2 is H; or R1 and R2 are both represented by the substituent (i). E4 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-ia) shown below 233230 2757082 of 82 P 18 01 03436 (Id-ia) or a pharmaceutically acceptable salt thereof. E5 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-ib) shown below or a pharmaceutically acceptable salt thereof. E6 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-iab) shown below or a pharmaceutically acceptable salt thereof. E7 The pharmaceutically acceptable compound or salt thereof according to embodiment 1, wherein R1 is H and R2 is a substituent (ii); or R1 is a substituent (ii) and R2 is H; or R1 and R2 are both represented by the substituent (ii). E8 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-iia) shown below 233230 2757082 of 82 P 18 01 03436 (Id-iia) or a pharmaceutically acceptable salt thereof. E9 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-iib) shown below OH (Id-iib) or a pharmaceutically acceptable salt thereof. E10 The compound according to embodiment 1, wherein said compound is the compound represented by the formula (Id-iiab) shown below / HO (Id-iiab) or a pharmaceutically acceptable salt thereof. E11 The compound according to embodiment 1, wherein the compound is selected from the group consisting of: (Id-ia): acid (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6(((4aR,10aR)-7-hydroxy-1-propyl-1,2,3,4,4a,5,10,10a 233230 2757082 of 82 P 18 01 03436 octahydrobenzo[g]quinolin-6-yl)oxy)tetrahydro-2H-pyran-2carboxylic; (Id-ib): (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6(((4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl)oxy)tetrahydro-2H-pyran-2carboxylic acid; (Id-iia): (4aR,10aR)-7-hydroxy-1propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6-yl hydrogen sulfate; (Id-iib): (4aR,10aR)-6-hydroxy-1propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7yl hydrogen sulfate); (Id-iab): acid (2S,2'S,3S,3'S,4S,4'S,5R,5'R,6S,6'S)-6,6'(((4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10aoctahydr obenzo[g]quinoline-6,7-diyl)bis(oxy))bis(3,4,5trihydroxytetrahydro-2H-pyran-2-carboxylic); (Id-iiab): bis(hydrogen sulfate of (4aR,10aR)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diyl; or a pharmaceutically acceptable salt of any of these compounds. E12 The compound or pharmaceutically acceptable salt thereof according to any embodiment 1-11, wherein said compound is derived from outside the body of a mammal. E13 The pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-12, wherein said compound is derived by chemical manufacturing. E14 The pharmaceutically acceptable compound or salt thereof according to any embodiment 1-13, wherein said compound is in an isolated form. E15 The compound or pharmaceutically acceptable salt thereof according to any embodiment 1-14, wherein said compound is in a substantially compound-free form within which it is naturally in equilibrium. 233230 2757082 of 82 P 18 01 03436 E16 The pharmaceutically acceptable compound or salt thereof according to any embodiment 1-15, wherein said compound is in an isolated form, substantially free from the compound of formula (I). E17 A compound that is a prodrug of the compound (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol (compound (I)), wherein said prodrug provides a PK profile, wherein the Cmax of (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol is between 500 and 2500 pg / mL, such as between 750 and 2500 pg / mL, such as between 1000 and 2500 pg / mL, such as between 1000 and 2000 pg / mL when said prodrug is administered orally to a Wistar rat at a dose corresponding to 287 μg / kg of (4aR,10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydro-benzo[g]quinoline-6,7-diol; or a pharmaceutically acceptable salt of said compound.E18 The pharmaceutically acceptable compound or salt thereof according to embodiment 17, which is a prodrug of the compound (4aR,10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol (compound (I)), wherein said prodrug provides a PK profile, wherein the AUC0 of (4aR,10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol is more than 7000 pg*h / mL, such as more than 8000, such as more than 9000, such as more than 10000, such as more than 11000, such as more than 12000, such as more than 13000, such as more than 14000, such as more than 15000, such as more than 16000 pg*h / mL when said prodrug is administered orally to a Wistar rat at a dose corresponding to 287 mg / kg of (4aR,10aR)-1-n-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol. E19 The pharmaceutically acceptable compound or salt thereof according to any of embodiments 17-18, wherein said PK profile has been obtained by a 233230 2757082 of 82 P 18 01 03436 experiment PK as described in Example 4 in this memoir. E20 The pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-19, wherein said pharmaceutically acceptable compound or salt is in a solid form. E21 A pharmaceutically acceptable salt of a compound according to any of embodiments 1-20. E22 The pharmaceutically acceptable salt according to embodiment 21, wherein said salt is an acid addition salt of a compound according to any of embodiments 1-20. E23 The pharmaceutically acceptable salt according to embodiment 21, wherein said salt is a base addition salt of a compound according to any of embodiments 1-20. E24 The pharmaceutically acceptable compound or salt thereof in accordance with any of embodiments 1-23, for use in therapy. E25 A pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-23, for use as a medicament. E26 A pharmaceutically acceptable compound or salt for use as a medicament according to embodiment 25, wherein said medicament is an oral medicament such as a tablet or capsule for oral administration. E27 A pharmaceutical composition comprising a therapeutically effective amount of the compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23, and one or more pharmaceutically acceptable excipients. E28 The pharmaceutical composition according to embodiment 27, wherein said pharmaceutical composition is for oral administration. 233230 2757082 of 82 P 18 01 03436 E29 The pharmaceutical composition according to any of embodiments 27-28, wherein said pharmaceutical composition is an oral pharmaceutical composition. E30 The pharmaceutical composition according to any of embodiments 27-29, wherein said pharmaceutical composition is a solid oral dosage form. E31 The pharmaceutical composition according to any of embodiments 27-30, wherein said pharmaceutical composition is a tablet or capsule for oral administration. E32 The pharmaceutical composition according to any of embodiments 27-31, wherein said pharmaceutical composition further comprises another agent that is useful in the treatment of a neurodegenerative disease or disorder such as Parkinson's disease. E33 The pharmaceutical composition according to any of embodiments 27-31, wherein said pharmaceutical composition further comprises a compound selected from the group consisting of L-DOPA, an MAO-B inhibitor such as selegiline or rasagiline, a COMT inhibitor such as entacapone or tolcapone, an adenosine 2a antagonist such as istradephylline, an antiglutamatergic agent such as amantadine or memantine, an acetylcholinesterase inhibitor such as rivastigmine, donepezil or galantamine, an antipsychotic agent such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole or brexpiprazole; or an antibody targeting alpha-synuclein, TAU protein or Abeta protein. E34 A pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-23, for use in the treatment of a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome 233230 2757082 of 82 P 18 01 03436 or Alzheimer's disease, or a neuropsychiatric illness or disorder, such as schizophrenia, attention deficit hyperactivity disorder, or drug addiction. E35 A pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-23, for use in the treatment according to embodiment 34, wherein said neurodegenerative disease or disorder is Parkinson's disease. E36 A pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-23, for use in the treatment according to any of embodiments 34-35, wherein said compound is to be used in combination with another agent that is useful in the treatment of a neurodegenerative disease or disorder such as Parkinson's disease. E37 The compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23, for use in the treatment according to any of embodiments 34-35, wherein said compound is to be used in combination with a compound selected from the group consisting of L-DOPA, an MAO-B inhibitor such as selegiline or rasagiline, a COMT inhibitor such as entacapone or tolcapone, an adenosine 2a antagonist such as istradephylline, an antiglutamatergic agent such as amantadine or memantine, an acetylcholinesterase inhibitor such as rivastigmine, donepezil or galantamine, an antipsychotic agent such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole or brexpiprazole; or in combination with an antibody that targets alpha-synuclein, TAU protein or A-beta. E38 The pharmaceutically acceptable compound or salt thereof according to any of embodiments 1-23, 233230 2757082 of 82 P 18 01 03436 for use in the treatment according to any of embodiments 34-37, wherein said treatment is carried out by oral administration of said compound. E39 The compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23, for use in the treatment according to any of embodiments 34-38, wherein said compound is comprised in an oral pharmaceutical composition, such as a tablet or capsule for oral administration. E40 A method for treating a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome, or Alzheimer's disease, or a neuropsychiatric disease or disorder, such as schizophrenia, attention deficit hyperactivity disorder, or drug addiction; the method comprising administering a therapeutically effective amount of a compound or pharmaceutically acceptable salt thereof, in accordance with any embodiment 1-23, to a patient in need thereof. E41 The method according to realization 40, wherein said neurodegenerative disease or disorder is Parkinson's disease, E42 The method according to any of embodiments 40-41, wherein said compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23 is used in combination with another agent that is useful in the treatment of a neurodegenerative disease or disorder such as Parkinson's disease. E43. The method according to any of embodiments 40-41, wherein said compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23, is used in 233230 2757082 of 82 P 18 01 03436 combination with a compound selected from the group consisting of L-DOPA, an MAO-B inhibitor such as selegiline or rasagiline, a COMT inhibitor such as entacapone or tolcapone, an adenosine 2a antagonist such as istradephylline, an antiglutamatergic agent such as amantadine or memantine, an acetylcholinesterase inhibitor such as rivastigmine, donepezil or galantamine, an antipsychotic agent such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole or brexpiprazole; or in combination with an antibody that targets alpha-synuclein, TAU protein or A-beta. E44 The method in accordance with any of embodiments 40-43, wherein said administration is carried out orally. E45 The method according to any of embodiments 40-44, wherein said compound or pharmaceutically acceptable salt thereof according to any of embodiments 1-23 is comprised in an oral pharmaceutical composition, such as a tablet or capsule for oral administration. E46 Use of a compound or pharmaceutically acceptable salt thereof in accordance with any of embodiments 123, in the manufacture of a medicament for the treatment of a neurodegenerative disease or disorder, such as Parkinson's disease, Huntington's disease, restless legs syndrome or Alzheimer's disease, or a neuropsychiatric disease or disorder, such as schizophrenia, attention deficit hyperactivity disorder or drug addiction. E47 Use in accordance with realization 46, where said neurodegenerative disease or disorder is Parkinson's disease. E48 Use in accordance with any of the realizations 233230 2757082 of 82 P 18 01 03436 46-47, where said drug is used in combination with another agent that is useful in the treatment of a neurodegenerative disease or disorder such as Parkinson's disease. E49 Use in accordance with any of embodiments 46-47, wherein said medicinal product is used in combination with a compound selected from the group consisting of LDOPA, an MAO-B inhibitor such as selegiline or rasagiline, a COMT inhibitor such as entacapone or tolcapone, an adenosine 2a antagonist such as istradephylline, an antiglutamatergic agent such as amantadine or memantine, an acetylcholinesterase inhibitor such as rivastigmine, donepezil or galantamine, an antipsychotic agent such as quetiapine, clozapine, risperidone, pimavanserin, olanzapine, haloperidol, aripiprazole or brexpiprazole; or in combination with an antibody that targets alpha-synuclein, TAU protein or A-beta. E50 Use in accordance with any of embodiments 46-49, wherein said medicinal product is an oral medicinal product such as a tablet or capsule for oral administration. In the context of the present invention, it is understood that the carbon atom at the point of attachment in the substituent (i) (represented in embodiment 1) is in the anomeric position of (i). All references, including publications, patent applications and patents, cited in this report are incorporated in full by reference and to the same extent as if each reference were individually and specifically indicated to be incorporated by reference and set out in full (to the fullest extent permitted by law). 233230 2757082 of 82 P 18 01 03436 The titles and subtitles used in this document are for convenience only and should not be interpreted as limiting the invention in any way. The description in this specification of any aspect or feature of the invention using expressions such as “comprising”, “having”, “including”, or “containing” with reference to an element or elements is intended to provide support for a similar aspect or feature of the invention that “consists of”, “consists essentially of”, or “substantially comprises” that particular element or those elements, unless otherwise stated or clearly contradicted by the context (e.g., a composition described in this specification that comprises a particular element should also be understood as describing a composition that consists of that element, unless otherwise stated or clearly contradicted by the context). The use of any and all examples or exemplary vocabulary (including for example, e.g. and such as) in this description is merely intended to further illuminate the invention and does not constitute a limitation on the scope of the invention unless otherwise stated. It should be understood that the different aspects, realizations, implementations and features of the invention mentioned herein may be claimed separately or in any combination. The present invention includes all modifications and equivalents of the content mentioned in the appended claims, to the extent permitted by applicable law. COMPOUNDS OF THE INVENTION Table 1: Illustrated compounds of the invention 233230 2757082 of 82 P 18 01 03436 Example Compound (Id-ia) acid (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6- (((4aR,10aR)-7-hydroxy-1-propyl-1,2,3,4,4a,5,10,10a- . octahydrobenzo[g]quinolin-6-yl)oxy)tetrahydro-2Hpyran-2-carboxylic (Id-ib) acid (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6- (((4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl)oxy)tetrahydro-2Hpyran-2-carboxylic (Idiia) . (4aR,10aR)-7-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl hydrogen sulfate (Idiib) . (4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl hydrogen sulfate (Idiab) acid (2S,2'S,3S,3'S,4S,4'S,5R,5'R,6S,6'S)-6,6'- (((4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10a- octahydrobenzo[g]quinoline-6,7- diyl)bis(oxy))bis(3,4,5-trihydroxytetrahydro-2Hpyran-2-carboxylic) (Idiiab) bis(hydrogen sulfate of (4aR,10aR)-1-propyl- 1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7- diol EXPERIMENTAL SECTION Preparation of the compounds of the invention Compounds of formula (Id) can be prepared by methods described below, along with known synthetic methods in the art of organic chemistry, or modifications familiar to those with ordinary experience in the art. The starting materials used in this dissertation are commercially available or can be prepared by routine methods known in the art, such as those described in standard reference books such as Compendium of Organic Synthetic Methods, Vol. I-XII (published by Wiley Interscience). Preferred methods include, but are not limited to, those described below. The schemes are representative of useful methods in synthesizing the compounds of the present invention. 233230 2757082 of 82 P 18 01 03436 do not intend to limit the scope of the invention in any way. LC-MS methods The LC-MS analytical data were obtained using the methods identified below. Method 550: The LC-MS were performed on Waters Aquity UPLCMS consisting of Waters Aquity, including column delivery, binary solvent delivery, sample organizer, PDA detector (operating at 254 nM), ELS detector and TQ-MS equipped with APPI source operating in positive ion mode. LC conditions: The column was Acquity UPLC BEH C18 1.7pm; 2.1 x 50 mm operating at 60°C with 1.2 ml / min of a binary gradient consisting of water + 0.05% trifluoroacetic acid (A) and acetonitrile / water (95:5) + 0.05% trifluoroacetic acid. Gradient: 0.00 min 10% of B 1.00 min 100% B 1.01 min 10% of B 1.15 min 10% of B Total operating time: 1.15 min Method 551: The LC-MS were performed on Waters Aquity UPLCMS consisting of Waters Aquity, including column delivery, binary solvent delivery, sample organizer, PDA detector (operating at 254 nM), ELS detector and TQ-MS equipped with APPI source operating in positive ion mode. LC conditions: The column was an Acquity UPLC HSS T3 1.8 pm; 2.1 x 50 mm operating at 60°C with 1.2 ml / min of a binary gradient consisting of water + 0.05% trifluoroacetic acid (A) and acetonitrile / water (95:5) + 0.05% trifluoroacetic acid. 233230 2757082 of 82 P 18 01 03436 Gradient: 0.00 min 2% of B 1.00 min 100% B 1.15 min 2% B Total run time: 1.15 min Method 555: LC-MS were performed on Waters Aquity UPLCMS consisting of Waters Aquity, including column delivery, binary solvent delivery, sample organizer, PDA detector (operating at 254 nM), ELS detector and TQ-MS equipped with APPI source operating in positive ion mode. LC conditions: The column was an Acquity UPLC BEH C18 1.7 pm; 2.1 x 150 mm operating at 60°C with 0.6 ml / min of a binary gradient consisting of water + 0.05% trifluoroacetic acid (A) and acetonitrile / water (95:5) + 0.05% trifluoroacetic acid. Gradient: 0.00 min 10% of B 3.00 min 100% B 3.60 min 10% B Total operating time: 3.6 min Method 111: The LC-MS were performed on a Shimadzu LCMS2020 consisting of a PDA detector operating at 190-800 nM and an MS equipped with an ESI source operating in positive mode. LC conditions: The column was a Phenomenex Kinetex EVOC18 2.6 pm; 2.1x100 mm operating at 25°C with 0.5 ml / min of a gradient consisting of water + 0.1% formic acid (A) and acetonitrile + 0.1% formic acid (B). Gradient: 0.00 min 2% B 1.00 min 2% B 10.00 min 90% B 13.00 min 90%B 13.10 min 2% B 233230 2757082 of 82 P 18 01 03436 18.00 min 2% B Total operating time: 18 min Method 222: The LC-MS were performed on a Shimadzu LCMS2020 consisting of a PDA detector operating at 190-800 nM and an MS equipped with an ESI source operating in positive mode. LC conditions: The column was a Phenomenex Kinetex EVOC18 2.6 pm; 2.1 x 100 mm operating at 25°C with a 0.5 ml / min gradient consisting of water + 0.1% formic acid (A) and acetonitrile (B). Gradient: 0.00 min 2% B 1.00 min 2% B 10.00 min 90% B 13.00 min 90%B 13.10 min 2% B 18.00 min 2 %B Total operating time: 18 min Preparative LCMS was performed using the method identified below. Waters AutoPurification System using combined mass / UV detection. Column: Sunfire 30x100 mm, 5 µm particles. Operation at 40°C with 90 ml / min of a binary gradient consisting of water + 0.05% trifluoroacetic acid (A) and acetonitrile / water (3:5) + 0.05% trifluoroacetic acid. Gradient: 0.00 min 98%A 5.00 min 50%A 5.50 min 98%A 6.00 min 98%A MS HighRes was performed on a Bruker Compact qTOF scanner equipped with electroprojection operating in positive or negative mode. Direct infusion was used, and calibration was performed with sodium formate. 233230 2757082 of 82 P 18 01 03436 Preparation of compounds of the invention - general methods Compound (I), which can be prepared, for example, as described in document WO 2009 / 026934, was used as an intermediate compound in the synthesis of compounds of the invention. In summary, compounds (Id-ia) and (Id-ib) of the invention can be prepared from (I) by reacting (I) with triisopropylsilyl chloride in the presence of DIPEA (N,N-diisopropylethylamine) in dichloromethane, yielding a mixture of monosilylated intermediate compounds (4aR,10aR)-1-propyl-7-((triisopropylsilyl)oxy)1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6-ol and (4aR,10aR)-1-propyl-6-((triisopropylsilyl)oxy)1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7-ol, which were subsequently subjected to protection with a tert-butyloxycarbonyl protecting group (Boc protection), yielding intermediate compounds tert-butyl carbonate [A] and tert-butyl carbonate [B].Subsequent separation of the silyl group, using TEA-3HF (triethylamine trihydrofluoride), and re-protection using acetyl anhydride can be performed to provide a mixture of silyl acetate. (4aR,10aR)-6-((tert-butoxycarbonyl)oxy)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7-yl acetate (4aR,10aR)-7-((tert-butoxycarbonyl)oxy)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6-yl. A coupling can then be performed with glucuronides, using the coupling donor tetra-acetate ((2S,3R,4S,5S,6S)-6-(methoxycarbonyl)tetrahydro-2H-pyran2,3,4,5-tetrayl tetraacetate) in the presence of boron trifluoride and. 233230 2757082 of 82 P 18 01 03436 diethyl etherate (BF3-OEt2) as an acid catalyst Lewis, to provide a mixture of the desired triacetate coupling adducts (2S,3R,4S,5S,6S)-2(((4aR,10aR)-7-acetoxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl)oxy)-6(methoxycarbonyl)tetrahydro-2H-pyran-3,4,5-triyl and triacetate (2S,3R,4S,5S,6S)-2-(((4aR,10aR)-6-acetoxy-1propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7yl)oxy)-6-(methoxycarbonyl)tetrahydro-2H-pyran-3,4,5-triyl. The crude mixture can then be subjected to hydrolysis using KCN in wet methanol to provide (Id-ia) and (Id-ib), which can be separated by column chromatography. In summary, compounds (Id-iia) and (Id-iib) of the invention can be prepared from (I) by reacting (I) with pyridine complex and sulfur trioxide in pyridine, providing a mixture of mono-sulfates (Id-iia) and (Id-iib) that can be separated by column chromatography. Exemplified compounds of the invention (Id-iia): (4aR,10aR)-7-hydroxy-1-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6yl hydrogen sulfate, (Id-iib): (4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-7yl hydrogen sulfate. (Id-iia) (4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinoline-6,7-diol, hydrochloride (1.51 g) 233230 2757082 of 82 P 18 01 03436 was suspended in pyridine (25 ml) under a nitrogen atmosphere at room temperature, pyridine and sulfur trioxide complex (2.31 g) was added and the suspension was stirred at room temperature. After 15 h and 23 h, additional pyridine and sulfur trioxide complex (2 x 2.1 g, 13.1 mmol) was added and the mixture was stirred at room temperature overnight. After stirring for a total of two days, the crude mixture was diluted with MeOH / dichloromethane and evaporated directly into the filtration aid. Purification by column chromatography (eluent: ethyl acetate / triethylamine / MeOH, 95:5:0–70:5:25) yielded an approximate 3:1 ratio of the two sulfates. The mixture was resuspended in 10 mL of MeOH, 50 mL of water were slowly added, and the resulting suspension was stirred at room temperature. After 7 h, the suspension was filtered, and the precipitate was washed with 2 x 10 mL of water and dried overnight in a vacuum oven at 40°C to give a crude yield of 1.26 g as a solid. The sulfate mixture was separated using preparative LC-MS and both (Id-iib) and (Id-iia) were purified via trituration by refluxing in 50 mL of MeOH and stirred at room temperature for 32 h.The suspension was filtered and the precipitate was washed with 2 x 5 mL of MeOH and dried in a vacuum oven at 40°C overnight, then resuspended in 50 mL of acetonitrile and shaken at room temperature for 19 h. The precipitate was washed with 2 x 10 mL of acetonitrile and dried in a vacuum oven at 40°C to give (Id-iib) hydrogen sulfate of (4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinoline-7-yl (0.52 g, 1.5 mmol, 30% yield) as a solid and (Id-iia) hydrogen sulfate of (4aR,10aR)-7-hydroxy-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6-yl (0.15. 233230 2757082 of 82 P 18 01 03436 g, 0.45 mmol, 9% yield) in the form of a solid. (Id-iib) LCMS (method 555) 1.29 min. 1H NMR (600 MHz, DMSO-d e) δ 9.06 (s, 1H), 8.89 (s,1H), 6.89 (d, J = 8.2 Hz, 1H), 6.58 (d, J = 8.3 Hz, 1H),3.52 (d, J = 12.1 Hz, 1H), 3.35-3.32 (m, 1H), 3.31-3.22 (m,2H), 3.10-3.01 (m, 2H), 2.97 (dd, J = 17.4, 5.1 Hz, 1H),2.74 (dd, J = 15.6, 11.1 Hz, 1H), 2.18 (dd, J = 17.4, 11.6 Hz, 1H), 1.97 - 1.69 (m, 5H), 1.68-1.56 (m, 1H), 1.35 (cd, J = 13.0, 3.8 Hz, 1H), 0.96 (t, J = 7.3 Hz, 3H). (Id-iia) LCMS (método 555) 1.37 min. 1H RMN (600 MHz, DMSO-d6) δ 9.07 (s, 1H), 8.84 (s,1H), 6.82 (d, J = 8.3 Hz, 1H), 6.70 (d, J = 8.3 Hz, 1H),3.51 (d, J = 12.0 Hz, 1H), 3.34 - 3.30 (m, 1H), 3.26 (s a, 2H), 3.17 - 2.94 (m, 3H), 2.75 - 2.67 (m, 1H), 2.35 (dd, J = 17.6, 11.9 Hz, 1H), 1.90 (t, J = 13.8 Hz, 2H), 1.85 -1.69 (m, 3H), 1.67-1.57 (m, 1H), 1.40-1.31 (m, 1H), 0.95 (t, J = 7.3 Hz, 3H). (Id-iiab) :bis(hidrógeno sulfato) de (4aR,10aR)-1-propil1,2,3,4,4a,5,10,10a-octahidrobenzo[g]quinolina-6,7-diilo (sal trietilamina) HO (Id-iiab) (4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinoline-6,7-diol hydrochloride (0.500 g, 1.68 mmol) and pyridine and sulfur trioxide complex (5.34 g, 33.6 mmol) were suspended in acetonitrile (10 ml) and triethylamine (7.02 ml, 50.4 mmol) was added at room temperature. 233230 2757082 of 82 P 18 01 03436 The suspension was heated to 80°C and stirred under a nitrogen atmosphere for 16.5 h. The mixture was allowed to cool to room temperature and evaporated over a filtration aid (10 g). Purification by column chromatography (eluent: ethyl acetate / triethylamine / MeOH, 75:5:20–45:5:50) yielded an oil (1.51 g). The oil was diluted with MeOH (10 mL + 3 drops of DMSO) and tert-butyl methyl ether (MTBE) (2 x 10 mL) was added using a syringe. An oily solid immediately precipitated. The suspension was concentrated, and the resulting residue was collected in MeOH (20 mL) and triethylamine (5 mL) and filtered. MTBE (40 mL) was added to the filtrate over two minutes, and a solid gradually precipitated. The precipitate was filtered and dried in a vacuum oven at 35°C for 15 minutes to provide bis(hydrogen sulfate) of (4aR,10aR)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diyl in the form of a solid and in the form of a 1:1 complex.3 with triethylamine by 1H NMR analysis (0.531 g, 0.957 mmol, yield of 57%). LCMS (method 555) rt=1.00 min. Due to the instability of disulfate under acidic conditions, LCMS does not give a good indication of purity. 1H NMR (600 MHz, DMSO-de) δ8.93 (s, 1H), 8.80 (s, 1H), 7.40 (d, J = 8.5 Hz, 1H), 6.77 (d, J = 8.6 Hz, 1H), 3.48 (d, J = 11.7 Hz, 1H), 3.37 - 3.19 (m, 5H),3.10 (c, J = 7.3 Hz, 7.8H, triethylamine), 3.02 (s, 1H), 2.76 - 2.67 (m, 1H), 2.46 (dd, J = 17.7, 12.2 Hz, 1H), 1.85 (d, J = 11.3 Hz, 2H), 1.81 - 1.56 (m, 4H), 1.37 - 1.26 (m, 1H), 1.17 (t, J = 7.3 Hz, 11.7H, triethylamine), 0.95 (t, J = 7.3 Hz, 3H). HRMS (ESI): calcd. m / z for C16H21NO8S22- [M - 2H+] 209.5360, found 209.5360 Intermediate compounds for the preparation of (Id-ia), (Id 233230 2757082 of 82 P 18 01 03436 ib) and (Id-iab). Intermediate compounds: (4aR,10aR)-1-propyl-7((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-ol and (4aR,10aR)-1-propyl-6((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-ol. (4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol, hydrochloride (2.21 g, 7.43 mmol) was suspended in dichloromethane (80 ml) under a nitrogen atmosphere at room temperature, N,Ndiisopropylethylamine (4.44 g, 6.0 ml, 34.4 mmol) was added, followed by triisopropylsilyl chloride (2.73 g, 3.0 ml, 14.16 mmol) and the mixture was stirred at room temperature for 92 h. 10 mL of MeOH were added, and the crude mixture was evaporated, co-evaporated twice with dichloromethane / heptane, redissolved in dichloromethane and evaporated directly in the filtration aid and purified by column chromatography (eluent: n-heptane / ethyl acetate / triethylamine, 100:0:0 - 35:60:5), providing 3.14 g in the form of a mixture of (4aR,10aR)-1-propyl-7((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-ol (3.14 g) and (4aR,10aR)-1propyl-6-((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-ol in the form of an oil.NMR (CDCl3) showed a mixture >30:1 of silylated isomers. Intermediate compounds:((4aR,10aR)-1-propyl-7((triisopropylsilyl)oxi)-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-6-yl) carbonate de tert-butyl [A] y ((4aR,10aR)-1-propyl-6-((triisopropylsilyl)oxi)233230 2757082 of 82 P 18 01 03436 1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7-yl) tert-butyl carbonate [B]. ,.„,930 ..jpo OBoc OTIPS The previous step mixture (4aR,10aR)-1-propyl-7((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-ol and (4aR,10aR)-1-propyl-6((triisopropylsilyl)oxy)-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-ol (2.94 g, 7.04 mmol) was dissolved in dichloromethane (30 ml) under a nitrogen atmosphere and cooled to 0°C. Pyridine (6.00 ml) was added, followed by di-tert-butyl dicarbonate (6.30 g), and the reaction mixture was allowed to warm to room temperature for 3-4 hours and then stirred at room temperature overnight. 10 mL of MeOH was added and the reaction mixture was evaporated, co-evaporated with dichloromethane / n-heptane twice, dissolved in dichloromethane and evaporated in the filtration aid. La purificación por cromografía en columna (eluyente: nheptano / acetato de ethylo / trietilamina, 100:0:0 - 75:20:5) dio una mezcla de ((4aR,10aR)-1-propil-7((triisopropilsilyl)oxi)-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-6-il) carbonato de ter-butilo [A] y ((4aR,10aR)-1-propil-6-((triisopropilsilyl)oxi)1,2,3,4,4a,5,10,10a-octahidrobenzo[g]quinolin-7-il) carbonato de ter-butilo [B] (3.6 g) en forma de un aceite. The MRI (CDCl3) showed, after drying, a mixture of regioisomers. Intermediate compounds: Acetate of (4aR,10aR)-6-((terbutoxycarbonyl)oxi)-1-propyl-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-7-ilo and acetate of (4aR,10aR)-7233230 2757082 of 82 P 18 01 03436 ((tert-butoxycarbonyl)oxi)-1-propyl-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-6-yl. OBoc Ó Ac ((4aR,10aR)-1-propyl-7-((triisopropylsilyl)oxy)1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6-yl) ter-butyl carbonate (3,600 g, 6,95 mmol) (mixture demol) [A]:[B] from the previous step) was dissolved in THF (150 ml) under a nitrogen atmosphere at 0°C, triethylamine trihydrofluoride (2.97 g, 3.00 ml, 18.42 mmol) was added and the mixture was stirred at 0°C. After 3 h at 0°C, pyridine (10.0 ml, 124 mmol) and acetic anhydride (4.33 g, 4.00 ml, 42.4 mmol) were added directly to the reaction mixture at 0°C and the reaction mixture was allowed to warm to room temperature. After 16 h, 20 mL of MeOH were added, and the reaction mixture was evaporated, redissolved in dichloromethane / heptane and evaporated in the filtration aid, followed by purification by dry vacuum column chromatography, providing (4aR,10aR)-6-((tert-butoxycarbonyl)oxy)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl acetate and (4aR,10aR)-7((tert-butoxycarbonyl)oxy)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl acetate in the form of an oil / foam. LCMS (method 550) ta=0.56 min, [M+H]+ =404 e / z. Intermediate compounds: Triacetate of (2S,3R,4S,5S,6S)-2(((4aR,10aR)-7-acetoxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl)oxy)-6(methoxycarbonyl)tetrahydro-2-H-3,4-tripyl (2S,3R,4S,5S,6S)-2-(((4aR,10aR)-6-acetoxy-1 233230 2757082 of 82 P 18 01 03436 propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-7yl)oxy)-6-(methoxycarbonyl)tetrahydro-2H-pyran-3,4,5-triyl. (4aR,10aR)-6-((tert-butoxycarbonyl)oxy)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-7-yl acetate (2.489 g, 6.17 mmol) (assumed mixture of (4aR,10aR)-6-((tertbutoxycarbonyl)oxy)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl acetate (4aR,10aR)-7((tert-butoxycarbonyl)oxy)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl) was dissolved in dichloromethane (60 ml) under a nitrogen atmosphere at room temperature, added (2S,3R,4S,5S,6S)-6-(methoxycarbonyl)tetrahydro-2H-pyran2,3,4,5-tetrayl tetraacetate (7.529 g, 20.01 mmol), followed by the addition of diethyl boron trifluoride etherate (6.72 g, 6.0 mL, 47.3 mmol) and the mixture was stirred at room temperature for 5 days. The mixture was diluted with dichloromethane and MeOH and evaporated in the filtration aid.Purification by dry vacuum column chromatography to give a triacetate mixture of (2S,3R,4S,5S,6S)-2-(((4aR,10aR)-7-acetoxy-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6-yl)oxy)-6(methoxycarbonyl)tetrahydro-H-H-3,4a triaceto-3,4 of (2S,3R,4S,5S,6S)-2-(((4aR,10aR)-6-acetoxy-1propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-7yl)oxy)-6-(methoxycarbonyl)tetrahydro-pyran-H-3,4,5,3. g) in the form of a foam / solid. LC-MS (method 555) rt=1.94 min, [M+H]+ =620e / z. 233230 2757082 of 82 P 18 01 03436 Intermediate compound: (2S,3S,4S,5R,6S)-6-[[(4aR,10aR)-1propyl-6-[(2S,3R,4S,5S,6S)-3,4,5-triacethoxy-6methoxycarbonyl-tetrahydropyran- 2-yl]oxy-3,4,4a,5,10,10ahexahydro-2H-benzo[g]quinoline-7-yl]oxy]-3,4,5-triacetoxytetrahydropyran-2-carboxylate of methyl (2S,3S,4S,5R,6R)-2-(methoxycarbonyl)-6-(2,2,2-trichloro-1-iminoethoxy)tetrahydro-2H-pyran-3,4,5-triyl triacetate (1.286 g, 2.69 mmol) and (4aR,10aR)-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7-diol hydrochloride (0.4 g, 1.343 mmol) were dissolved in dichloromethane (5.28 g, 4.00 ml, 62.2 mmol), then boron trifluoride diethyl etherate (0.381 g, 0.340 ml, 2.69 mmol) was added under a nitrogen atmosphere and the mixture was stirred for 3 d under nitrogen in an 8 mL vial. Additional (2S,3S,4S,5R,6R)-2(methoxycarbonyl)-6-(2,2,2-trichloro-1-iminoethoxy)tetrahydro2H-pyran-3,4,5-triyl triacetate (1.286 g, 2.69 mmol) and diethyl borofluoride etherate (0.381 g, 0.340 mL, 2.69 mmol) were added and the mixture was stirred for 4 h, then the mixture was poured into saturated aqueous NaHCO3 (30 mL), then extracted with dichloromethane (2 x 20 mL) and the collected organic phases were dried (Na2SO4), filtered and evaporated to dryness under vacuum.The crude foam was suspended in heptane / ethyl acetate (1:1) and stirred overnight. Subsequently, HCl in ether (0.672 ml, 1.343 mmol, 2 molar) was added, the mixture was stirred for 1 hour, evaporated to dryness under vacuum, and added. 233230 2757082 of 82 P 18 01 03436 MTBE (40 mL) and the mixture was heated under reflux and allowed to cool to room temperature, then the mixture was filtered and the solid was dried in a vacuum oven for 1 day at 40°C, yielding (2S,3S,4S,5R,6S)-6-[[(4aR,10aR)-1propyl-6-[(2S,3R,4S,5S,6S)-3,4,5-triacetoxy-6-methoxycarbonyl-tetrahydropyran-2-yl]oxy-3,4,4a,5,10,10ahexahydro-2H-benzo[g]quinolin-7-yl]oxy]-3,4,5-triacetoxytetrahydropyran-2-carboxylate methyl hydrochloride (1.0854 g, 1.167 mmol, 87% yield). LC-MS method 550 rt=0.63min, [M+H]+ =895.7e / z. y (Id-ia): ácido (2S,3S,4S,5R,6S)-3,4,5-trihidroxy-6((4aR,10aR)-7-hidroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-6-il)oxi)hydroxid-2H-piran-2carboxilo. A mixture of triacetato de (2S,3R,4S,5S,6S)-2 (((4aR,10aR)-7-acetoxy-1-propyl-1,2,3,4,4a,5,10,10aoctahidrobenzo[g]quinolin-6-yl)oxi)-6-(metoxicarbonyl) tetrahydro-2H-piran-3,4,5-triilo y triacetato de (2S,3R,4S,5S,6S)-2-(((4aR,10aR)-6-acetoxy-1-propyl1,2,3,4,4a,5,10,10a-octahidrobenzo[g]quinolin-7-yl)oxi)-6(metoxicarbonyl)tetrahydro-2H-piran-3,4,5-triilo (3.82 g, 6.17 mmol) was dissolved in MeOH (100 ml) and water (20 ml), cooled to 0°C, and potassium cyanide (7.295 g, 112 233230 2757082 of 82 P 18 01 03436 mmol) and the mixture was allowed to warm slowly to room temperature for 17.5 h. The crude mixture was evaporated in the filtration aid and dried. The crude mixture was purified by silica gel column chromatography (eluent ethyl acetate / MeOH / water 100:0:0 0:50:50), providing a 5-6:1 ratio of (Id-ib) and (Id-ia). The mixture was separated by preparative LCMS. The collected Pico 1 fractions containing (Id-ib) were pooled, evaporated, and combined with another batch of 186 mg of (Id-ib)-TFA that had been prepared in a similar manner, using evaporated MeOH and dried to give a solid. (Id-ib) was re-suspended in 10 mL of EtOH, and 100 mL of MTBE was added, and the resulting suspension was stirred at room temperature for 8 h, the suspension was filtered and the precipitate was washed with 2 x 10 mL of MTBE and dried in a vacuum oven overnight to provide (Id-ib) 1.601 g, in the form of a solid, corresponding to (2S,3S,4S,5R,6S)-3,4,5-trihydroxy6-(((4aR,10aR)-6-hydroxy-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl)oxy)tetrahydro-2H-pyran-2-carboxylic acid. The collected Pico 2 fractions containing (Id-ia) were pooled, evaporated, transferred to a smaller flask with MeOH, evaporated, redissolved in approximately 12 mL of MeOH, and re-purified by preparative LC-MS and evaporated to give a froth / solid. Appropriate fractions were pooled, evaporated, transferred with MeOH to a smaller flask, evaporated, and combined with another batch of 40.7 mg (Id-ia), which had been prepared in a similar manner. The combined batch was dissolved in 2.5 mL of EtOH, 25 mL of MTBE was added, and the suspension was stirred at room temperature. After 8 hours, the suspension was filtered, and the precipitate was washed with two 2.5 mL volumes of MTBE and dried overnight. 233230 2757082 of 82 P 18 01 03436 the vacuum oven to give 362.2 mg of (Id-ia) in the form of a solid. (Id-ia) was re-suspended in approx. 10 mL of EtOH, and 50 mL of MTBE were added, and the resulting suspension was stirred at room temperature and filtered after 19 h. The precipitate was washed with 2 x 10 mL of MTBE and dried in a vacuum oven at 40°C to give 0.279 g of (2S,3S,4S,5R,6S)3,4,5-trihydroxy-6-(((4aR,10aR)-7-hydroxy-1-propyl1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinolin-6yl)oxy)tetrahydro-2H-pyran-2-carboxylic acid (Id-ia) in the form of a solid. (Id-ib) LCMS (method 551) rt=0.37 min. 1H NMR (600 MHz, Methanol-d 4) δ 7.02 (d, J = 8.4 Hz, 1H), 6.65 (d, J = 8.4 Hz, 1H), 4.73 (d, J = 7.7 Hz, 1H),3.89 (d, J = 9.7 Hz, 1H), 3.68 - 3.58 (m, 2H), 3.54 (dd, J = 9.3, 7.7 Hz, 1H), 3.49 (t, J = 9.1 Hz, 1H), 3.47 - 3.36(m, 2H), 3.30 (dt, J = 11.2, 5.6 Hz, 1H), 3.21 - 3.11 (m,3H), 2.85 (dd, J = 15.4, 11.3 Hz, 1H), 2.35 (dd, J = 17.6,11.5 Hz, 1H), 2.12 - 2.02 (m, 2H), 2.02 - 1.84 (m, 3H), 1.811.71 (m, 1H), 1.49 (cd, J = 13.0, 3.7 Hz, 1H), 1.09 (t, J = 7.3 Hz, 3H). (Id-ia) LCMS (método 551) rt=0.39 min. 1H RMN (600 MHz, Metanol-d4) δ 6.87 (d, J = 8.3 Hz, 1H), 6.74 (d, J = 8.4 Hz, 1H), 4.62 (d, J = 7.9 Hz, 1H),3.75 (dd, J = 17.7, 4.9 Hz, 1H), 3.66-3.62 (m, 2H), 3.61 -3.51 (m, 2H), 3.50 - 3.35 (m, 3H), 3.31 - 3.22 (m, 1H),3.14 (cd, J = 12.7, 4.0 Hz, 2H), 2.83 (dd, J = 15.2, 11.3 Hz, 1H), 2.37 (dd, J = 17.7, 11.7 Hz, 1H), 2.12 (d, J =13.4 Hz, 1H), 2.08 - 2.00 (m, 1H), 1.98 - 1.83 (m, 3H), 1.811.71 (m, 1H), 1.44 (cd, J = 13.2, 3.9 Hz, 1H), 1.09 (t, J = 7.3 Hz, 3H). (Id-iab):ácido (2S,2'S,3S,3'S,4S,4'S,5R,5'R,6S,6'S)-6,6'(((4aR,10aR)-1-propil-1,2,3,4,4a,5,10,10a233230 2757082 de 82 P 18 01 03436 octahydrobenzo[g]quinoline-6,7-diyl)bis(oxy))bis(3,4,5 trihydroxytetrahydro-2H-pyran-2-carboxylic acid) (Id-iab) Synthesis A (1S,4aR,10aR)-1-propyl-6,7-bis(((2S,3R,4S,5S,6S)-3,4,5triacetoxy-6-(methoxycarbonyl)tetrahydro-2H-pyran-2-yl)oxy)1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline (0.25g, 0.269 mmol) was dissolved in water (1.209 g, 1.209 ml, 67.1 mmol) and MeOH (3.83 g, 4.84 ml, 120 mmol) and KOH (0.393 g, 0.270 ml, 3.22 mmol, 46%) were added and shaken overnight at room temperature in a sealed vial. Overnight a precipitate had formed, which was isolated by filtration. The solid was washed with MeOH (1.5mL), yielding (2S,2'S,3S,3'S,4S,4'S,5R,5'R,6S,6'S)-6,6'-(((4aR,10aR)-1propyl-1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline-6,7diyl)bis(oxy))bis(3,4,5-trihydroxytetrahydro-2H-pyran-2carboxylic) 2Potassium (0.096 g, 0.139 mmol, yield of 51.6%) LC-MS method 551 rt 0.31min, [M+H]+=614.2e / z. Synthesis B (1S,4aR,10aR)-1-propyl-6,7-bis(((2S,3R,4S,5S,6S)-3,4,5triacetoxy-6-(methoxycarbonyl)tetrahydro-2H-pyran-2-yl)oxy)1,2,3,4,4a,5,10,10a-octahydrobenzo[g]quinoline (0.2585 g, 0.278 mmol) was dissolved in WATER (1.250 g, 1.25 mL, 69.4 mmol) and MeOH (3.96 g, 5 mL, 124 mmol) and KCN (0.344 g, 5.28 mmol) were added and stirred overnight at 233230 60 2757082 of 82 P 18 01 03436 at room temperature in a sealed vial. Overnight a precipitate had formed, which was isolated by filtration. The solid was washed with MeOH (1.5 mL), yielding (2S,2'S,3S,3'S,4S,4'S,5R,5'R,6S,6'S)6,6'-(((4aR,10aR)-1-propyl-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinoline-6,7-diyl)bis(oxy))bis(3,4,5trihydroxytetrahydro-2H-pyran-2-carboxylic) 2Potassium (0.0963 g, 0.139 mmol, 50.1% yield) LC-MS method 551 rt=0.34min, [M+H]+=614.6e / z. 1H NMR (600 MHz, DMSO-d6) δ 7.09 (d, J = 8.5 Hz, 1H),6.84 (d, J = 8.5 Hz, 1H), 4.91 - 4.79 (m, 1H), 4.78 - 4.66(m, 1H), 3.93 (sa, 22H (OH / water)), 3.42 (d, J = 9.8 Hz, 1H), 3.37 - 3.21 (m, 7H), 3.19 (s, 1H), 3.11 (dd, J = 16.2,4.9 Hz, 1H), 2.90 (d, J = 11.0 Hz, 1H), 2.67 (ddd, J =12.9, 10.7, 5.6 Hz, 1H), 2.49 (dd, J = 15.9, 10.9 Hz, 1H), 2.39 2.27 (m, 1H), 2.15 (dt, J = 17.5, 11.5 Hz, 2H), 2.05 (td, J = 10.4, 4.9 Hz, 1H), 1.86 (d, J = 11.7 Hz, 1H), 1.67 -1.38 (m, 5H), 1.03 (cd, J = 12.3, 5.1 Hz, 1H), 0.85 (t, J =7.3 Hz, 3H). Additional items added for the purpose of invention The following two compounds are also covered by the scope of the invention: (Id-iaiib): (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6(((4aR,10aR)-1-propyl-7-sulfo-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-6-yl)oxy)tetrahydro-2H-pyran-2carboxylic acid, and (Id-iiaib): (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6(((4aR,10aR)-1-propyl-6-sulfo-1,2,3,4,4a,5,10,10aoctahydrobenzo[g]quinolin-7-yl)oxy)tetrahydro-2H-pyran-2carboxylic acid. 233230 2757082 of 82 P 18 01 03436 (R)-11-hydroxy-6-methyl-5,6,6a,7tetrahydro-4H-dibenzo[de,g]quinolin-10-yl hydrogen sulfate 1.0 g (3.19 mmol, 1.0 eq) of apomorphine hydrochloride hemihydrate was suspended in 3.3 mL of pyridine under an argon atmosphere at room temperature. 1.7 g (10.68 mmol, 3.34 eq) of sulfur trioxide-pyridine complex was added to the suspension and stirred at 40°C for 17 hours and purified by preparative HPLC. The main isomer hydrogen sulfate of (R)-11hydroxy-6-methyl-5,6,6a,7-tetrahydro-4Hdibenzo[de,g]quinolin-10-yl (78 mg), 98.8% UV purity, was isolated. LC-MS method 111 rt=5.18min, [M+H]+ =348.1e / z. 1H NMR (500 MHz, DMSO-d6) δ 9.91 (a, 1H), 9.30 (s, 1H), 8.27 (d, J = 5.0 Hz, 1H), 7.39 (m, 1H), 7.20 (d, J =5.0 Hz, 1H), 7.10 (d, J = 5.0Hz, 1H), 6.84 (d, J = 5.0 Hz, 1H), 4.42 (sa, 1H), 3.77 (sa, 1H), 3.45 (d, J = 10.0 Hz, 2H), 3.25 - 3.21 (m, 1h), 3.20 - 3.10 (m, 4h), 2.71 (t, J = 10.0 Hz, 1H). 233230 2757082 of 82 P 18 01 03436 (R)-10-hydroxy-6-methyl-5,6,6a,7tetrahydro-4H-dibenzo[de,g]quinolin-11-yl hydrogen sulfate: The same method was used as for (R)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10-yl hydrogen sulfate, with only slight modifications to obtain the secondary component: the reaction time was reduced to 3 hours and pyridine sulfur trioxide was added in three portions (three batches were carried out starting from 850 mg and two from 500 mg). The reaction mixtures were pooled and purified by preparative HPLC, yielding 50 mg of the secondary isomer (R)-10-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-11-yl hydrogen sulfate. LC-MS method 222 rt=4.99min, [M+H]+ =348.1e / z. 1H NMR (500 MHz, DMSO-d6) δ 10.00 (a, 1H), 9.30 (s,1H), 8.26 (sa, 1H), 7.23 (sa, 1H), 7.11 (sa, 1H), 7.01(d, J = 10.0 Hz, 1H), 6.78 (d, J = 10.0 Hz, 1H), 3.50 - 2.20(m, 7h). Compuesto intermedio: Triacetato de (2S,3R,4S,5S,6S)-2((R)-11-hidroxi-6-methyl-5,6,6a,7-tetrahydro-4Hdibenzo[de,g]quinolin-10-il)oxi)-6(metoxicarbonyl)hydroxi-2H-piran-3,4,5-triilo 233230 2757082 of 82 P 18 01 03436 480 mg (1.796 mmol) of apomorphine (free base) and 4.72 g (12.54 mmol, 7.0 eq.) of 1,2,3,4-tetra-o-acetyl-6-D-glucopyranuronate were dissolved in 40 mL of dichloromethane under an argon atmosphere at room temperature. The starting materials dissolved in 10 minutes, giving a blue solution. To this solution, 3.0 mL (3.45 g, 13.5 eq.) of diethyl boron trifluoride etherate was added under an argon atmosphere, and the mixture was stirred at room temperature for 2 hours. The reaction was poured into 80 mL of saturated sodium bicarbonate solution, stirred for 10 minutes, and then separated. The aqueous phase was extracted with CH₂Cl₂ (3 x 40 mL). The collected organic phases were washed with saturated sodium bicarbonate solution (1 x 40 mL) and brine (1 x 40 mL), dried over sodium sulfate, filtered and evaporated, yielding 4.5 g of solid (theoretical yield ~1.0 g). The crude product was purified by flash resolution chromatography, using CH2Cl2:MeOH = 96:4. After purification, 190 mg of (2S,3R,4S,5S,6S)-2-(((R)-11-hydroxy-6-methyl5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10-yl)oxy)-6(methoxycarbonyl)tetrahydro-2H-pyran-3,4,5-triyl triacetate were obtained. (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6-(((R)-11-hydroxy6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10yl)oxy)tetrahydro-2H-pyran-2-carboxylic acid 250 mg (0.432 mmol) of (2S,3R,4S,5S,6S)-2(((R)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4Hdibenzo[de,g]quinolin-10-yl)oxy)-6(methoxycarbonyl)tetrahydro-2H-pyran-3,4,5-triyl triacetate 233230 2757082 of 82 P 18 01 03436 were dissolved in a mixture of 6.1 mL of MeOH and 1.2 mL of water and cooled to 0°C. At that temperature, they were added 526 mg (8.07 mmol 18.7 eq) of KCN. The reaction mixture was stirred and allowed to cool to room temperature, then stirred for an additional 2 hours. The reaction mixture was filtered and purified directly on preparative HPLC in a 0.1% water-acetonitrile-TFA eluent. From the collected fractions, the acetonitrile was evaporated at room temperature under vacuum, and the aqueous residue was lyophilized, yielding 133 mg of the TFA salt of (2S,3S,4S,5R,6S)-3,4,5-trihydroxy-6-(((R)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10yl)oxy)tetrahydro-2H-pyran-2-carboxylic acid in powder form. Its structure was verified using LCMS and NMR. LC-MS method 111 rt=4.30min, [M+H]+=444.2e / z. 1H NMR (500 MHz, DMSO-d6) δ 12.84 (a, 1H), 10.00 (sa, 1H), 8.87 (s, 1H), 8.29 (d, J = 10.0 Hz, 1H), 7.40 (m, 1H), 7.21 (d, J =5.0 Hz, 1H), 7.02 (d, J = 10.0Hz, 1H), 6.83 (d, J = 5.0 Hz, 1H), 5.77 (s, 1H), 5.45-5.20 (m, 2H), 4.84(d, J =5.0 Hz, 1H), 4.34 (sa, 1H), 3.92 (d, J = 10.0 Hz, 1H), 3.76 (sa, 1h), 3.55 - 3.00 (m, 11H, OH / water), 2.75 -3.30 (m,4H). In vitro and in vivo characterization of compounds of the invention. Example 1a: Conversion of the compounds of the invention in rat and human hepatocytes The compounds (Id-ia), (Id-ib), (Id-iia), (Id-iib), (Idiab), and (Id-iiab) were incubated separately at a concentration of 1 gg / mL with human or rat hepatocytes suspended in DMEM (Dulbecco's Modified Eagle Medium) using HEPES (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid) at pH 7.4. The cell concentration in the incubation was 1 x 10⁶ viable cells / mL. Incubations were performed in glass tubes at 37°C with a total incubation volume of 3.5 mL. 233230 2757082 of 82 P 18 01 03436 mL and with duplicate incubations for each of the test products. The 3.5 mL of hepatocyte suspension were equilibrated for 10 minutes in a water bath set at 37°C, after which the incubations were initiated by adding 3.5 pL of a stock solution of the test product in DMSO (dimethyl sulfoxide), and the tubes were gently inverted. The final solvent concentration in the incubations was 0.1% DMSO. 600 pL samples were removed from the incubations at predetermined times of 0.25, 5, 15, 30, and 60 minutes after ensuring the homogeneity of the hepatocyte suspensions. The withdrawn volume was added to 1 mL Nunc cryotubes on wet ice containing 60 pL of ice-cooled ascorbic acid (100 mg / mL) and 30 pL of ice-cooled 100 mM saccharic acid 1,4-lactone in 0.5 M citric acid. The tubes were mixed and 35 pL of an ice-cooled 20% formic acid solution was added.The tubes were thoroughly mixed and stored at -80°C pending analysis. The analytical method and instrumentation used for the analysis of (I) from the dosage of (Id-ia), (Id-ib), (Id-iia) and (Id-iib) was as described in Examples 4 and 5 below in the section Instrumentation used for the analysis of compound (I) from the dosage of compounds (Ic), (Id-ia), (Id-ib), (Id-üa), (Id-iií), (Id-iab) and (Id-iab). The analytical method and instrumentation used for the analysis of (I) from the dosage of (Id-iab) and (Id-iiab) consisted of mixing equal aliquots of the samples and precipitation solution (10% acetonitrile (MeCN) with methanol (MeOH) and 1% formic acid), followed by centrifugation at 4°C at 16,000 g for 10 minutes. The supernatants were collected and analyzed by LC-MS / MS. Mass spectrometer: 233230 2757082 of 82 P 18 01 03436 Waters Acquity - Waters Xevo TQ-MS. Analytical column: Acquity UPLC HSS T3, 100 x 2.1 mm, 1.8 μm Mobile phase A: 0.2% formic acid in water. Mobile phase B: 0.2% formic acid in acetonitrile. The gradient ran from 95 / 5% to 60 / 40 in 5 min. Flow rate 0.3 mL / min. MRM monitoring of (I) in the study samples and in the analytical standards. Figure 7 shows a time-dependent conversion to compound (I) from (Id-ia), (Id-ib), (Id-iia), (Id-iib), and (Id-iab) in both rat and human hepatocytes. For (Id-iiab), the formation of compound (I) could not be detected under the assay conditions. Example 1b: Conversion of the compounds of the invention into fresh rat and human blood The conversion of (Id-ia), (Id-ib), (Id-iia) and (Id-iib) in human blood (mean of 3 donors) and rat blood (mean of 45 donors) to (I) was demonstrated in fresh blood at 37°C enriched with 1 μg / mL of (Id-ia), (Id-ib), (Id-iia) and (Id-iib) separately, (I) was measured at 0, 5, 15, 30 and 60 minutes in isolated plasma. The method of analysis and instrumentation, as described in Examples 4 and 5 below in the section Instrumentation used for the analysis of compound (I) from the dosage of compounds (Ic), (Idia), (Id-ib), (Id-iia), (Id-üb), (Id-iab) and (Id-iiab). Figure 8 shows a time-dependent conversion to compound (I) from (Id-ia), (Id-ib), (Id-iia) and (Id-iib) in both rat and human blood. Example 2: Dopamine agonist activity Dopamine D1 receptor agonism Dopamine D1 receptor agonism was measured using a CisBio HTRF cAMP with the protocol developed by HD Biosciences (China). In summary, the assay is a resonant energy transfer assay. 233230 2757082 of 82 P 18 01 03436 time-resolved fluorescence (HTRF) measuring cAMP production by cells in a competitive immunoassay between cell-produced native cAMP and XL-665-labeled cAMP. A cryptate-labeled anti-cAMP antibody visualizes the tracer. The assay was performed according to the manufacturer's instructions. The assay compounds were added to microplate wells (384 format). HEK-293 cells expressing the human D1 receptor were spread at a rate of 1000 cells / well and incubated for 30 min at room temperature. cAMP d2 tracer was added to the wells, followed by the addition of anti-cAMP antibody cryptate preparation, and incubated for 1 h at room temperature in the dark. HTRF cAMP was measured by laser excitation of the donor at 337 nm (the “TRF light unit”) and subsequent measurement (100 µs delay time) of cryptate and d2 emission at 615 nm and 665 nm over a 200 µs time window with a 2000 µs time window between repeats / 100 flashes. HTRF measurements were performed on an Envision microplate reader (PerkinElmer). The HTRF signal was calculated as the ratio of emission at 665 nm to 615 nm.The HTRF ratio reading for the test compounds was normalized to 0% and 100% stimulation using control wells with DMSO solvent or 30 uM dopamine. The potency of the test compound (CE50) was estimated by nonlinear regression using sigmoidal dose-response (variable slope) using Xlfit 4 (IDBS, Guildford, Surrey, UK, model 205). y = (A+((BA) / (1+((C / x)AD)))) where y is the normalized measurement of the HTRF ratio for a given concentration of test compound, x is the concentration of test compound, A is the efficiency 233230 2757082 of 82 P 18 01 03436 is estimated at an infinite dilution of the compound, and B is the maximum efficacy. C is the EC50 value, and D is the Hill slope coefficient. The EC50 estimates were obtained from an independent experiment and the logarithmic mean was calculated. Dopamine D2 receptor agonism Dopamine D2 receptor agonism was measured using a mobilization assay protocol developed by HD Biosciences (China). Briefly, human D2 receptor-expressing HEK293 / G15 cells were spread to a density of 15,000 cells / well in 384-well, transparent-bottom plates coated with Matrigel and cultured for 24 h at 37°C in the presence of 5% CO2. The cells were incubated with the calcium-sensitive fluorescent dye Fluo8 for 60–90 minutes at 37°C in the dark. Assay compounds were prepared as a 3-fold concentrated solution in IxHBSS buffer containing Ca2+ and Mg2+. The calcium flow signal was recorded immediately after adding the compounds from the compound plate to the cell plate using FLIPR (Molecular Devices). Fluorescence data were normalized to provide responses for no stimulation (buffer) and full stimulation (1 μM dopamine) of 0% and 100% stimulation, respectively.The potency of the test compound (CE50) was estimated by nonlinear regression using sigmoidal dose-response (variable slope) using Xlfit 4 (IDBS, Guildford, Surrey, UK, model 205). y = (A+((BA) / (1+((C / x)AD)))) where y is the normalized measurement of the ratio for a given concentration of test compound, x is the concentration of test compound, A is the estimated efficacy at an infinite dilution of compound, and B is the maximum efficacy. C is the EC50 value and D is the 233230 2757082 of 82 P 18 01 03436 Hill slope coefficient. CE50 estimates were obtained from an independent experiment and the logarithmic mean was calculated. Example 3: 5-HT2B agonist activity and binding assay 5-HT2B agonist activity assay The agonist activity of compounds (I), (Ia), and (Ib) on the human 5-HT2B receptor was evaluated by Eurofins / Cerep (France) by measuring the effects on the production of the inositol monophosphate compound (IP1) using the HTRF detection method. In summary, the human 5-HT2B receptor was expressed in transfected CHO cells. The cells were suspended in a buffer containing 10 mM Hepes / NaOH (pH 7.4), 4.2 mM KCl, 146 mM NaCl, 1 mM CaCl2, 0.5 mM MgCl2, 5.5 mM glucose, and 50 mM LiCl, then distributed into microplates at a density of 4100 cells / well and incubated for 30 min at 37°C in the presence of buffer (basal control), assay compound, or reference agonist. For the stimulated control measurement, separate assay wells contained 1 μM of 5-HT. After incubation, the cells were lysed and the fluorescence acceptor (fluorophene D2-labeled IP1) and fluorescence donor (europium cryptate-labeled anti-IP1 antibody) were added.After 60 min at room temperature, fluorescence transfer was measured at λ(Ex) 337 nm and λ(Em) 620 and 665 nm using a microplate reader (Rubystar, BMG). The IP1 concentration was determined by dividing the signal measured at 665 nm by the signal measured at 620 nm (ratio). Results were expressed as a percentage of the control response to 1 μM 5-HT. The standard reference agonist was 5-HT, which was assayed in each experiment at various concentrations to generate a concentration-response curve. The EC50 value was calculated as described above for each assay. 233230 2757082 of 82 P 18 01 03436 functional dopamine. 5-HT2B bonding test The affinity of compounds (Id-ia), (Idib), (Id-iia), (Id-iib) and (Id-iab) for the human 5-HT2B receptor was assessed in a radioligand binding assay in Eurofins / Cerep (France). Membrane homogenates, prepared from CHO cells expressing the receptor Human 5-HT2B cells were incubated for 60 min at room temperature with 0.2 nM [125I](±)DOI (1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine) in the absence or presence of the test compound in a buffer containing 50 mM Tris-HCl (pH 7.4), 5 mM MgCl₂, 10 µM pargyline, and 0.1% ascorbic acid. Non-specific binding was determined in the presence of 1 µM (±)DOI. After incubation, samples were rapidly vacuum-filtered through glass fiber filters (GF / B, Packard) pre-soaked with 0.3% polyethyleneimine (PEI) and rinsed several times with ice-cooled 50 mM Tris-HCl using a 96-sample cell collector (Unifilter, Packard). The filters were dried and radioactivity was counted using a scintillation counter (Topcount, Packard) with a scintillation cocktail (Microscint 0, Packard). The results are expressed as a percentage of inhibition of specific binding to the control radioligand.The standard reference compound was (±)DOI, which was tested in each of the experiments at various concentrations to obtain a competitive curve from which the IC50 was calculated. Table 2 In vitro activities for the compounds of the invention obtained according to Examples 2 and 3. Compound D1 CE50 (nM) / Emax D2 CE50 (nM) / Emax 5-HT2B CE50 (nM) / Emax Precursor compound (I) 3.3 / 99% 1.3 / 91% 2900nM / 50% Prodrugs of the technique (Ia) >1000 >1000 >6000nM,58% @30uM (Ib) >1000 46nM / 100% 3.8nM / 79% 233230 2757082 of 82 P 18 01 03436 previous (Ic) nd nd -5%@10μΜ Compounds of the invention (Id-ia) 2700 / 98% 1100 / 92% -25%@10μΜ* (Id-ib) 1800 / 94% 1300 / 100% -39%@10μΜ* (Id-iia) >30000 / 49% >30000 / 48% 6%@10μΜ* (Id-iib) >30000 / 42% >30000 / 54% 25%@10μΜ* (Id-iab) nd nd 17%@10μΜ (Id-iiab) nd nd nd * indicates binding affinity (% control inhibition, specific binding at the indicated concentration) nd: not determined Example 4: PK experiments in rats For all experiments, approximately 0.68 mL blood samples were taken from the tail or sublingual vein and placed into pre-cooled K3EDTA tubes prepared with a stabilizing solution consisting of 80 µL of ascorbic acid and 40 µL of 100 mM D-saccharic acid, 1,4-lactone in water. The tubes were gently inverted 6–8 times to ensure thorough mixing and then placed on moist ice. The collection tube was placed on moist ice for up to 30 minutes prior to centrifugation. Once removed from the moist ice, centrifugation was started immediately. Immediately after centrifugation was complete, the samples were returned to the moist ice. Three 130 μL subsamples of plasma were transferred to each of the three appropriately labeled cryotubes containing 6.5 μL of pre-cooled (20%) formic acid (tubes were pre-enriched and stored refrigerated prior to use).The tube stopper was immediately replaced, and the plasma solution was thoroughly mixed by gently inverting it 6–8 times. Samples were stored frozen at nominal -70°C within 60 minutes of collection. Centrifugation was performed at 3000 G for 10 minutes at 4°C. The plasma was placed in ice water after collection. Final storage was at approximately 70°C. 233230 2757082 of 82 P 18 01 03436 Plasma samples were analyzed by solid-phase extraction or direct protein precipitation, followed by UPLC-MS / MS. Detection was performed by MS using electroprojection in positive ion mode with monitoring of specific mass-to-charge transitions for compound (I), using internal standards to correct the response. Concentration-time data were analyzed using standard software, employing appropriate non-compartmental techniques to obtain estimates of the derived PK parameters. Instrumentation used for compound analysis (I) from dosing compound (a) Waters Acquity-Sciex API 5000 LC-MS / MS mass spectrometer. Waters BEH UPLC Phenyl analytical column, 100 x 2.1 mm, particle size 1.7 µm. Mobile phase A: 20 mM ammonium formate (aq) + 0.5% formic acid. Mobile phase B: Acetonitrile. The gradient ran from 95 / 5% to 2 / 98% in 6.1 min. Flow rate 0.5 mL / min. Multiple reaction monitoring (MRM) of the test product and added analytical standards. Dosage and Blood Sampling: Han Wistar rats were supplied by Charles River Laboratories, Sulzfeld, Germany. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. The rats were fed a standard Brogaarden laboratory diet (Altromin 1324 granules). The rats had unrestricted access to the diet. During the study (a 4-week toxicity study), the rats received once-daily doses of (Ia) orally via gavage. Blood samples were collected from 3 male satellite animals of the rats given 300 pg / kg of (la) on Day 29 at the following times: 0.5, 1, 2, 4, 6, 8, 12, and 24 hours post-dosing. 233230 2757082 of 82 P 18 01 03436 Instrumentation used for the analysis of compound (I) from dosed compound (Ib): Mass Spectrometer (LC-MS / MS) Waters Acquity -Sciex API 5000. Analytical column Waters BEH UPLC Phenyl 100 x 2.1 mm, particle size 1.7 pm. Mobile phase A: ammonium formate (aq.) 20 mM + 0.5% formic acid. Mobile phase B: Acetonitrile. The gradient ran from 95 / 5% to 2 / 98% in 6.1 min. Flow rate 0.5 mL / min. MRM monitoring of the test product and added analytical standards. Dosage and blood sampling: Han rats Wistar rats were supplied by Charles River Laboratories, UK. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. Rats were fed a standard laboratory diet (Teklad Diet 2014C). Rats had unrestricted access to the diet. During the study (a 26-week toxicity study), rats received once-daily doses of (Ib) orally via gavage. Blood samples were collected from three male satellite animals of the rats given 300 pg / kg of (Ib) on day 182 at the following time points: 0.5, 1, 2, 4, 8, and 24 hours post-dosing. Instrumentation used for the analysis of compound (I) from the dosage of compounds (Ic), (Id-ia), (Idib), (Id-iia), (Id-iib), (Id-iab) and (Id-iiab). Waters Acquity Xevo TQ-S LC-MS / MS mass spectrometer. Analytical column: Acquity BEH C18 100 x 2.1 mm, 1.7 pm. Mobile phase A: 20 mM NH4 formate + 0.2% formic acid. Mobile phase B: Acetonitrile + 0.2% formic acid. The gradient ran from 95 / 5% to 5 / 95% in 11.0 min. Flow rate: 0.3 mL / min. MRM monitoring of the test product and added analytical standards. Dosage and blood sampling for compounds (Id-ia), (Id-ib), (Id-iia) and (Id-iib): Han Wistar rats were supplied by Charles River Laboratories, 233230 2757082 of 82 P 18 01 03436 Wiga GmbH, Germany. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. Rats were fed a standard Brogaarden laboratory diet (Altromin 1324 granules). Rats had unrestricted access to the diet. Male Han Wistar rats were dosed orally via a single oral tube with (Id-ia), (Id-ib), (Id-iia), and (Id-iib), respectively. Blood samples were collected from 3 male rats on Day 1 at the following time points: 1, 2, 4, 6, 8, and 24 hours post-dosing. Dosage and blood sampling for compounds (Ic), (Id-iab), and (Id-iiab): Han Wistar rats were supplied by Envigo, UK. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. Rats were fed a Teklad 2014C laboratory diet. Rats had unrestricted access to the diet. Male Han Wistar rats were dosed orally via a single oral tube with (Ic), (Id-iab), and (Id-iiab), respectively. Rats received 793 μg / kg of (Idiab), 703 μg / kg of (Id-iiab), and 494 pg / kg of (Ic). Blood samples from 3 male animals were collected on Day 1 at the following time points: 1, 2, 4, 6, 8, and 24 hours post-dosing. Instrumentation used for the analysis of apomorphine from the apomorphine dosage and the corresponding glucuronide conjugate: (((2S,3S,4S,5R,6S)-6[[(6aR)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10-yl]oxy]-3,4,5-trihydroxytetrahydropyran-2-carboxylic acid and sulfate conjugates: [(6aR)-11-hydroxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinolin-10-yl] hydrogen sulfate 233230 2757082 of 82 P 18 01 03436 [(6aR)-10-hydroxy-6-methyl-5,6,6a,7-tetrahydro4H-dibenzo[de,g]quinolin-11-yl] sulfate): Mass spectrometer (UPCLC-MS / MS) Waters Acquity IClass-Waters Xevo TQ-S. Analytical column: Acquity HSS T3 C18 50 x 2.1 mm, 1.8 pm. Mobile phase A: 10 mM NH4 formate, 0.2% formic acid:acetonitrile (95:5). Mobile phase B: 10 mM NH4 formate, 0.2% formic acid:acetonitrile (5:95). The gradient ran from 95 / 5% to 5 / 95% in 2.40 min. Flow rate 0.3 mL / min. MRM detection of the test product and added analytical standards. Dosage and blood sampling: Han Wistar rats were supplied by Charles River Laboratories, Wiga GmbH, Germany. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. Rats were fed a standard Brogaarden laboratory diet (Altromin 1324 pellets). Rats had unrestricted access to the diet. Han Wistar rats were administered a single dose of apomorphine subcutaneously or orally via gavage, or a single dose of apomorphine conjugates orally via gavage. Blood samples were collected from 3 male rats on Day 1 at the following times: 0.25, 0.5, 1, 2, 4 and 8 hours SC administration and 0.5, 1, 2, 4, 8 and 24 hours administration of rats administered 3000 μg / kg (apormophine) or 3899 μg / kg (sulfate conjugate) or 4977 pg / kg (glucuronide conjugates). PO after dosing. 233230 2757082 of 82 P 18 01 03436 Table 3 PK parameters for (4aR, 10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydro-benzo[g]quinoline-6,7-diol (compound (I)) after oral dosing of 0.300 mg / kg of (la), 0.300 mg / kg of (Ib), 0.633 mg / kg (Id-ai), 0.633 mg / kg of (Id-ib), 0.392 mg / kg of (Id-iia), 0.392 mg / kg of (Id-iib), 793 pg / kg of (Id-iab), 703 pg / kg of (Idiiab) and 494 pg / kg of (Ic) to Wistar rats according to the Example 4. Compound Tmax (h) Cmax (pg / mL) AUCo-2 4 (pg*h / mL) t1 / 2 (h) 2 4 h of exposure (pg / mL) Prodrugs of the prior art (Ia) 1.0 3160 13600 4.0 9 48 ± 26 (Ib) 0.5 4990 31000 N / A 147 ± 28 (Ic) 1.0 14 104 N / A N / A Compounds of the invention (Id-ia) 4.0 1350 15500 6.8 208 ± 89 (Id-ib) 4.0 2150 21100 7.1 270 ± 112 (Id-iia) 6.0 945 11300 7.7 192 ± 14 (Id-iib) 8.0 665 7800 8.0 166 ± 94 (Id-iab) 4.0 964 18900 N / A 800 ± 244 (Id-iiab) 24 68 1040 N / A 68 ± 38 Example 5: PK experiments in dwarf pigs Blood samples of approximately 0.5 mL were drawn from the jugular vein using a syringe and placed in pre-cooled EDTA tubes containing a stabilizing solution, as described for rats in Example 4. Compound concentrations were measured in plasma. Plasma samples were analyzed by solid-phase extraction or direct protein precipitation, followed by UPLC-MS / MS. Detection was performed by MS using electroprojection in positive-ion mode, monitoring specific mass-to-charge transitions for the compound of interest using internal standards to correct the response. Concentration-time data were analyzed using standard software and appropriate non-compartmental techniques to obtain estimates of derived PK parameters. 233230 2757082 of 82 P 18 01 03436 Instrumentation used for compound analysis (I) from compound dosage (Id-ia), (Id-ib), (Id-Ha) and (Id-üb). Waters Acquity Xevo TQ-S LC-MS / MS mass spectrometer. Analytical column: Acquity BEH C18 100 x 2.1 mm, 1.7 pm. Mobile phase A: 20 mM NH4 formate + 0.2% formic acid. Mobile phase B: Acetonitrile + 0.2% formic acid. The gradient ran from 95 / 5% to 95 / 5% in 11.0 min. Flow rate: 0.3 mL / min. MRM monitoring of the test product and added analytical standards. Dosage and blood sampling for a single-dose pharmacokinetic study in female Ellegaard Göttingen miniature pigs supplied by Ellegaard, Denmark. A 12-hour, automatically controlled, artificial light-dark cycle was maintained. The miniature pigs were fed a standard Brogaarden laboratory diet (Altromin pellets). The miniature pigs had unrestricted access to the diet. The compounds (Id-ia), (Id-ib), (Id-iia), and (Id-iib), respectively, were administered orally via feeding tube. Blood samples were collected from 3 female animals on Day 1 at the following times: 1, 2, 4, 6, 8, 12 and 24 hours after dosing. From dwarf pigs given 160 μg / kg of compounds (Id-ia) and (Id-Ib), respectively, or 80 pg / kg of compounds (Id-iia) and (Id-iib)), respectively. 233230 2757082 of 82 P 18 01 03436 Table 4 PK parameters for (4aR, 10aR)-1-n-propyl1,2,3,4,4a,5,10,10a-octahydro-benzo[g]quinoline-6,7-diol (compound (I)) after oral dosing of 0.160 mg / kg of (Id-ia), 0.160 mg / kg of (Id-ib), 0.050 mg / kg of (Id-üa), 0.050 mg / kg of (Id-iib) to dwarf pigs according to Example 5. compound Tmax (h) Cmax (pg / mL) AUC0-24 (pg*h / mL) (Id-ia) 8.0 1120 13000 (Id-ib) 5.3 1300 14300 (Id-iia) 7.3 501 6280 (Id-iib) 12 328 4160 Example 6: PK / PD of compound (Id-ia) / compound (I) in the rat hyperactivity assay Animals A total of 206 male CD rats (Charles River, Germany) weighing 200–250 grams (165–190 grams at arrival) were used in the study. The animals were housed at a standard temperature (22 ± 1°C) and in a light-controlled environment (lights from 7 am to 8 pm) with ad libitum access to food and water. The experiment described below was conducted in accordance with the standard operating procedures of Charles River Discovery Research Services Finland Ltd. and in accordance with the Finnish National Animal Experimentation Council (Elainkoelautakunta, ELLA), the authority on animal testing. Locomotor activity test, open field The test device is a square Plexiglas enclosure (measuring 40 x 40 x 40 cm) in which the rats' movement trajectories are recorded using an activity monitor (Med. Associates Inc.). Before the start of the test period, the rats are habituated to their test cage for 60 minutes. After habituation is complete, the animals are treated with the compound or vehicle and then... 233230 2757082 of 82 P 18 01 03436 were placed back in the open field apparatus. The primary trial parameter measured was walking distance (recorded in 5-minute segments). The overall measurement time after receiving the initial treatment was 360 minutes. The total follow-up period in the study was 420 minutes, including 60 minutes of habituation. Results Oral administration of compound (Id-ia) was assessed in the locomotor activity assay in rats, and this functional reading was subsequently correlated with plasma concentrations of compound (I). Apomorphine and pramipexole were also tested concomitantly in this assay as comparators (i.e., a known standard of care (SoC) in the field of Parkinson's disease), and the plasma concentration of apomorphine was analyzed for apomorphine. As shown in Figure 3, compound (Id-ia) (10 to 300 pg / kg, orally) increases locomotor activity with an effect that begins approximately 2 hours post-administration (around time 180 minutes) and lasts until the end of the recording (at time 415 minutes). In contrast, the hyperactivity induced by apomorphine (3 mg / kg subcutaneously) is immediate but short-lived, as the effect disappears 1.5 hours post-administration (at time 150 minutes). Pramipexole (0.3 mg / kg, subcutaneously) also induces an increase in activity, but its effect appears approximately 1 hour post-administration and disappears 2.5 hours later (at time 270 minutes). The total distance traveled as seen in Figure 4 demonstrates a significantly increased activity for both the compound (Id-ia) and the two comparators tested, and this effect is one that is to be expected from dopamine agonists. 233230 2757082 of 82 P 18 01 03436 In parallel with the assessment of locomotor activity, blood samples were taken from satellite animals at six different time points (0.5, 1, 2, 3, 4, and 6 hours post-dose for animals treated with compound (Idia)). Pharmacokinetic analysis demonstrates that the behavioral effects of compound (Id-ia) (100 pg / kg, po) correlate with plasma concentrations of compound (I) (see Figure 5), showing that the behavioral effect of compound (Id-ia) is driven by compound (I) rather than by compound (Id-ia) itself. The corresponding apomorphine exposure analysis (at 0.25, 0.5, 1, 2, 4, and 6 hours post-dose) resulted in a correlation between plasma concentrations and hyperactive behavior (see Figure 6). It is hereby stated that, as of this date, the best method known to the applicant for putting the aforementioned invention into practice is the one that is clear from the present description of the invention. 233230 2757082 of 82 20225952036 CRISTIAN DANIEL BITTEL - 20225952036 Digitally signed by PORTALTRAMITES - INPI Date: 2024.05.17 15:33:05 -03:00 Reason: Digitally Signed by the INPI Location: Buenos Aires, Argentina 2757082

Claims

1. A compound according to formula (Id), FOLLOWING FORMULA 1, characterized in that R1 is H and R2 is selected from one of the substituents (i) and (ii) listed below; or R1 is selected from one of the substituents (i) and (ii) listed below and R2 is H; or R1 and R2 are both represented by the substituent (i) listed below; or R1 and R2 are both represented by the substituent (ii) listed below; or R1 is substituent (i) and R2 is substituent (ii); or R1 is substituent (ii) and R2 is substituent (i); FOLLOWING FORMULAS 2 AND 3, wherein * indicates the point of attachment; and wherein the carbon atom at the point of attachment in the substituent (i) is in the S configuration; or a pharmaceutically acceptable salt thereof. 12 Claims follow