Compounds for cell migration

Abstract

The invention provides a compound of formula (I) and the salts, solvates and protected forms thereof, together with their use in methods of treatment, including methods for regeneration and / or repair, such as promoting tissue regeneration and / or repair, wherein the compound of formula (I) is: where each of A, -XA-, -RA, -RB and -RQ are as defined herein. Also provided are methods for the preparation of the compounds of formula (I).

Description

Related Application The present case claims the benefit of, and priority to, GB 2402939.9 filed on 29 February 2024 (29.02.2024), the contents of which are hereby incorporated by reference in their entirety. Field of the Invention The present invention relates to novel IGD peptidomimetic compounds, pharmaceutical compositions comprising the compounds, and the use of the compounds and the pharmaceutical compositions for medical treatment, for example tissue regeneration and wound treatment. Background The formation of vasculature (angiogenesis) is a tightly regulated process which plays an important role in many biological functions. Angiogenesis is regulated by transmembrane glycoproteins known as integrins. The matching of integrins and ligands, particularly on integrin avp3, plays a crucial role in the sprouting ability of endothelial cells during angiogenesis (see Weis et al., Brooks et al.). Fibronectin (FN) is a ubiquitous adhesive protein which interacts with cells mainly through integrins and plays a significant role in vascular remodelling. MSF (migration stimulating factor) is a genetically truncated form of FN which displays activities - such as motogenesis -which are not displayed by full length FN. It stimulates the migration of epithelial (normal and tumour) and non-epithelial (tumour) cells, as well as the induction of angiogenesis. Although it is not typically found in healthy tissue, MSF may be detected during the wound healing process (see Ellis et al, Schor etal.). Investigation into the activities of fibronectin fragments of varying lengths has indicated that the difference in activities displayed by MSF and full-length FN can be explained by their different tertiary conformations, with the full-length protein occluding motogenic activity sites (see Vakonakis et al.). The motogenic activity of MSF has been attributed to a tripeptide motif of Isoleucine-Glycine-Aspartic acid (IGD). Synthetic IGD peptides subjected to migration assays gave positive results, with scrambled isoforms (DGI) not showing any activity. Peptide mutations (i.e., isoleucine for valine (VGD) or arginine (RGD)) were also inactive. A study of the tertiary conformation of this motif in MSF was undertaken with NMR, showing the IGD sequence as a highly conserved turn with limited conformational mobility (see Shpiro et al.). From this work, it was postulated that a peptidomimetic able to mimic this turn would have the potential to bind the same receptor as MSF (ibid.). Modelling studies were used to measure the dihedral angles of the IGD motif in native MSF. Small molecules which could mimic these geometrical features were then selected. It was found that the benzodiazepinone bicyclic ring structure could closely mimic the backbone structure of the IGD motif while limiting the conformational mobility of the molecule. Benzodiazepinone 4 was reported by Shpiro etal. to be a particularly promising candidate for development of an IGD-mimicking drug. Earlier work from one of the inventors generated both enantiomers of the peptidomimetic 4 (see Shpiro etal.). The (F?)-IGD peptidomimetic (R)-4 displayed increased motility on fibroblasts and endothelial cells, meanwhile, its enantiomer (S / -4 was found to be inactive (see Czosnyka, 2010). In-vivo testing on C57BLKs / Bom diabetic mice demonstrated that IGD peptidomimetic (R)-4 promoted wound healing, affecting wound contraction, wound closure, re-epithelialization, and cellular maturity (see Czosnyka, 2010). The patent application WO 2007 / 23273 also describes the use of the IGD peptidomimetic (R)-4 for modulating cell migration and wound treatment. Margery et al., Agnew Chem Int Ed. (2017), 56, 15644 describes the preparation of benzene derivatives having amino substituents. However, the use of such compounds in treating wounds or any other method of treatment is not described. Clement et al., Synlett, (2001), 2001, 1423 describes a method for preparing the GPIIb / llla receptor antagonist Lotrafiban, including the attachment of an aspartic acid to a benzene moiety as an intermediate step in the synthesis. However, there is no suggestion to use product of this reaction in treating wounds, or indeed in any other method of treatment. Summary of the Figures Figure 1 shows the results of cell viability experiments on HDFs (Human Dermal Fibroblasts) and HLIVECs (Human Umbilical Vein Endothelial Cells). Four example compounds of formula (I) (compounds 87, 88, 89 and 97) were tested. Figure 2 shows the results of a wound healing assay in HUVECs using the same set of example compounds as the cell viability experiments shown in Figure 1. * Denotes significant difference (p < 0.05) as compared to the control group. Figure 3 shows the results of a cell migration assay in HDFs using compound 87 as well as four further example compounds (compounds 8, 13, 17 and 18) at various concentrations. Summary of the Invention The inventors have established that flexible IGD peptidomimetic compounds are useful in wound treatment as an alternative to the known benzodiazepinone compounds. The flexible IGD peptidomimetic compounds have comparable wound healing and cell migratory activity to the benzodiazepinone compound 4, whilst beneficially not displaying the stereochemical specificity seen with these compounds. The impressive cell migration stimulating ability of these compounds indicates that they also have potential for wider use in treatments involving tissue regeneration and / or repair, for example in the treatment of bone fractures and in promoting nerve regeneration (Thiel et al, Nieuwenhius et al). The compounds may also be beneficial in the post-transplant healing process, scar reduction, and treatment of auto-immune diseases, as well as in promoting vascularisation within tissue-engineered constructs. In a general aspect, the invention provides IGD peptidomimetic compounds, which are flexible analogues of a benzodiazepinone compound. Such analogues are formally derived from benzodiazepinone compounds by ring-opening of the 7-membered diazepinone ring between the tertiary amine and methylene (-CH2-) groups, and loss of the methylene group connected to the benzene ring. In a first aspect of the invention, there is provided a compound of formula (I), and pharmaceutically acceptable salts, solvates, protected forms and prodrug forms thereof. The compound of formula (I) is represented thus: (I) wherein: Ais C(RE) orN, where -RE is -H, -F or Me; -XA- is -O-, -S-, or-NH-; -RA is optionally substituted Ci-w alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl; -RQ is -CH(RC)(RD), or-Rp, wherein -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH, -C(O)NH2, -C(O)NHRcb and -C(O)NRCBRCC, where each of -RCA, -RCB and -Rcc is independently Cm alkyl; -RD is -XD-RDD, C1-10 alkyl or -H, where -XD- is a C1-4 alkylene linker or a covalent bond, and -RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH -C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC, where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; or -Rp is phenyl or C5-6 heteroaryl, such as pyridinyl, optionally substituted with one or more groups -Rz, where each -Rz is independently selected from -C(O)ORZA, -C(O)OH, -C(O)NH2, -C(O)NHRzb, -C(O)NRzbRzc, -C(O)NHOH, -C(O)N(Rzd)OH and -C(O)S(RZE), where each of -RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl; wherein -RQ contains at least one -C(O)- carbon which is a,y-related to the group -NH- to which -RQ is attached; -RB is-H or -XB-RBB, where -XB- is a covalent bond, -0-, -S-, or -NH-, and -RBB is optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl; or -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz, and the salts, solvates and protected forms thereof. In one embodiment, -RQ is -CH(RC)(RD) and -Rc is independently selected from -C(O)ORCA, -C(O)OH, -CH2OH, -C(O)NH2, -C(O)NHRCB and -C(O)NRCBRCC, where each of -RCA, -RCB and -Rcc is independently C1-4 alkyl; -RD is -H, C1-10 alkyl or -XD-RDD, where -XD- is methylene (-CH2-), ethylene (-CH2-CH2-) or a covalent bond, and -RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH, -C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC, where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; -RB is -H or -XB-RBB, where -XB- is a covalent bond, -O-, -S-, or -NH-, and -RBB is an optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl; or -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz, The invention also provides a pharmaceutical composition comprising a compound of formula (I), optionally together with one or more pharmaceutically acceptable carriers. In a further aspect there is provided a compound of formula (I), or a pharmaceutical composition comprising a compound of formula (I), for use in a method of treatment or prophylaxis. In a further aspect there is provided a compound of formula (I), or a pharmaceutical composition comprising a compound of formula (I), for use in a method of tissue regeneration and / or repair, such as promoting tissue regeneration and / or repair. In yet a further aspect there is provided a compound of formula (I), or a pharmaceutical composition comprising a compound of formula (I), for use in a method of treating a wound. The present invention also provides a method of treatment, the method comprising the step of administering a compound of formula (I), ora pharmaceutical composition comprising a compound of formula (I), to a subject in need thereof. The method may be for the treatment of a wound. In yet a further aspect, there is provided a method of treatment, the method comprising contacting integrin avPa with a compound of formula (I). The present invention also provides methods for the preparation of compounds of formula (I) as well as intermediate compounds for use in the preparation of the compounds of formula (I). These and other aspects and embodiment of the invention are described in further detail below. Detailed Description of the Invention The present invention provides compounds of formula (I) for use in medical treatment. The compounds are peptidomimetics of the IGD motif found in migration stimulating factor (MSF). Previous work by the Marquez group has shown that the IGD sequence is a highly structured turn with limited conformational mobility and that this turn is seemingly important for receptor binding (see Shpiro et al.). It was found that peptidomimetics containing a benzodiazepinone bicyclic ring structure can closely mimic this geometry and hence bind the same receptors as MSF, triggering motogenesis. In contrast, the present inventors have shown that MSF activities can also be triggered by flexible IGD peptidomimetics which do not mimic the rigid geometry of the native IGD motif. These flexible mimetics do not contain a benzodiazepinone ring structure. As described herein, compounds of formula (I) are built around a simple monocyclic scaffold and contain isoleucine and aspartic acid bioisoteres. An in vitro wound healing assay on endothelial cells demonstrated that compounds of formula (I) are able to stimulate motogenesis. Both enantiomers of several flexible mimetics were tested alongside those of the previously described benzodiazepinone mimetic compound 4. The results indicate that the flexible mimetics enhance endothelial cell migration to a similar extent to R-4 and that both enantiomers of the flexible mimetics display motogenic activity. In order to assess potential for use as a drug, the flexible peptidomimetics were tested for toxicity in cell viability assays with both HLIVECs (Human Umbilican Vein Endothelial Cells) and HDFs (Human Dermal Fibroblasts). No significant effect on cell metabolic activity was observed. The simpler core structure of the compounds of the present invention compared to those described in prior art reduces the number of synthetic steps. The overall yield in the synthesis of the flexible compounds was significantly higher, and this is before the synthesis has been optimised. The motogenic activity displayed by both enantiomers of the flexible peptidomimetics means that there is no need for the synthesis of enantiomerically pure compounds. This means that the synthesis of compounds of formula (I) should be easier to up-scale than those described previously. Compounds The compounds of formula (I) are flexible IGD peptidomimetics. The compound of formula (I) typically comprises a benzene core having an isoleucine bioisostere group attached to a benzene ring atom via a heteroatom, such as oxygen or sulfur. The benzene core is further ort / 7o-substituted, with an aspartic acid bioisostere group attached to a benzene ring atom via a heteroatom, such as nitrogen. The benzene core may be yet further substituted. The present invention provides a compound of formula (I), and the use of this compound in a method of treatment. The compound of formula (I) is represented thus: (I) wherein: Ais C(RE) orN, where -RE is -H, -F or Me; -XA- is -O-, -S-, or-NH-; -RA is optionally substituted Ci-w alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl; -RQ is -CH(RC)(RD), or-Rp, wherein -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH, -C(O)NH2, -C(O)NHRcb and -C(O)NRCBRCC, where each of -RCA, -RCB and -Rcc is independently Cm alkyl; -RD is -H, C1-10 alkyl or -XD-RDD, where -XD- is a C1-4 alkylene, such as methylene (-CH2-), ethylene (-CH2-CH2-) or dimethyl methylene (-C(CH3)2-), or a covalent bond, and -RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH, -C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC, where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; or -Rp is phenyl or C5-6 heteroaryl, such as pyridinyl, optionally substituted with one or more groups -Rz, where each -Rz is independently selected from -C(O)ORZA, -C(O)OH, -C(O)NH2, -C(O)NHRzb, -C(O)NRzbRzc, -C(O)NHOH, -C(O)N(Rzd)OH and -C(O)S(RZE), where each of -RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl; -RB is -H or -XB-RBB, where -XB- is a covalent bond, -O-, -S-, or -NH-, and -RBB is an optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl, such as C2-10 alkyl; or -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz. References to the compound of formula (I) include references to the salts, solvates and protected forms thereof. A The group A is part of the core ring structure of the compound. A is C(RE) or N. When A is C(RE), the core of the compound of the invention is or contains a benzene ring. When A is N, the core of the compound of the invention is or contains a pyridine ring. -XA- and -Ra The group -XA- together with -RA forms an isoleucine bioisotere. This feature is generally conserved in known IGD peptidomimetics. The group -XA- is selected from -O-, -S-, and -NH-. In one embodiment, -XA- is -0-. In the worked examples of the present case, the group -XA- is -0-. The group -RA is optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl. The alkyl group may be C2-6 alkyl, such as C5 alkyl. The alkyl group may be linear or branched, such as branched. Where, the alkyl group is branched, there may be one or more branch points. A branch point may be at any position on the alkyl chain and is preferably at the position furthest from the group -XA-. The alkenyl group may be C2-6 alkenyl, such as C5 alkenyl. The alkenyl group may be linear or branched. The alkenyl group may contain one or two carbon-carbon doubled bonds, such as one. A double bond may not be a,p to the group -XA-. The alkynyl group may be C2-6 alkynyl, such as C5 alkynyl. The alkynyl group may be linear or branched. The alkynyl group may contain a single carbon-carbon triple bond. Each of the alkyl, alkenyl and alkynyl is optionally substituted, such as optionally substituted with one or more groups -RM, where each -RM is independently selected from C5-6 aryl, halo, -OH, -SH, -NH2, -NHRAC, -NRACRAD, -CN, -NO2, -C(O)OH, -C(O)ORAB, -C(O)NH2, -C(O)NHRac, -C(O)NRacRad, C5-6cycloalkyl and C5-6 heterocyclyl, where each of -RAB, -RAC and -RAD is independently C1-4 alkyl; Where an alkyl, alkenyl or alkynyl group is substituted, the substituent may not be provided at the carbon atom that is a to the group -XA-, for example where -RM is -OH, -SH, -NH2, -NHRac, or -NRACRAD Where an alkyl, alkenyl or alkynyl group is substituted with Cs-earyl, C5-6 cycloalkyl or C5-6 heterocyclyl, this group is optionally substituted at each ring carbon with a group -RAE, where each -RAE is independently selected from -CH3, -CH2CH3, -OH, -NH2, -C(O)OH, -C(O)OCH3, -C(O)NH2, -F, -Cl and -Br. The C5-6cycloalkyl may be cyclohexyl. The Cs-earyl may be phenyl. The C5-6 heterocyclyl may be pyridine. Each of the alkyl, alkenyl and alkynyl groups may be unsubstituted. In one embodiment, -RA is C4-10 alkyl, such as Cs alkyl. In one embodiment, -RA is / -pentyl (3-methylbutyl). In the worked examples of the present case, the group -RA is / -pentyl. -Rq The group -RQ may form the aspartic acid bioisotere. -RQ may be -CH(RC)(RD), or -Rp. In one embodiment, -RQ is -CH(RC)(RD). In one embodiment, -RQ is -Rp. In some embodiments, the group -RQ contains at least one -C(O)- carbon which is a,p-related to the group -NH- to which -RQ is attached. This group may act as a bioisotere for the carboxylic acid side chain of the aspartic acid. -Rc and -RD Where present, the groups -Rc and -RD together form the aspartic acid bioisotere. In the benzodiazepinone IGD mimetics previously described in the art, -Rc is incorporated into the 7-membered ring and the stereochemistry of the chiral carbon at the branch point between -Rc and -RD was found to be important for the activity of the compounds. In the compounds of the present invention, the stereochemistry at this carbon was found to have no impact on wound healing or cell migratory activity. The group -Rc is connected to the carbon atom that is a to the amino group of the aspartic acid isostere. The group -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH, -C(O)NH2, -C(O)NHRCB and -C(O)NRCBRCC Each of the groups -RCA, -RCB and -Rcc is independently C1-4 alkyl. The C1-4 alkyl group may be C1-3 alkyl, such as methyl or ethyl, such as methyl. In one embodiment, -Rc is -C(O)ORCA or -C(O)OH. In one embodiment, -Rc is -C(O)ORCA, such as -C(O)OMe or -C(O)OEt. In one embodiment, -Rc is -C(O)OMe. In the worked examples of the present case, the group -Rc is -C(O)OMe. In one embodiment, -Rc is -H. The group -RD is also connected to the carbon atom that is a to the amino group of the isostere. The group -RD is -H, C1-10 alkyl or -XD-RDD where -XD- is C1-4 alkylene, such as methylene (-CH2-), ethylene (-CH2-CH2-), or dimethyl methylene (-C(CH3)2-), or a covalent bond, and -RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH, -C(O)NH2, -C(O)NHRDB and -C(O)NRDBRDC. Preferably, -RD is -XD-RDD. Each of the groups -RDA, -RDB and -RDC is independently C1-4 alkyl. The C1-4 alkyl group may be C1-3 alkyl, such as methyl or ethyl, such as methyl. In one embodiment, -XD- is C1-4 alkylene. The alkylene group may be straight or branched. In one embodiment, -XD- is methylene. In some worked examples of the present case, -XD-is methylene. In one embodiment, -XD- is methyl methylene -C(CH3)H-. In one embodiment, -XD- is dimethyl methylene -C(CH3)2-. In a worked example of the present case, -XD- is dimethyl methylene. In one embodiment, -XD- is ethylene. In one embodiment, -RDD is independently selected from -C(O)ORDA, -C(O)OH, -C(O)NH2, -C(O)NHRDB and -C(O)NRDBRDC. In one embodiment, -RDD is selected from -C(O)ORDA and -C(O)OH. In one embodiment, -RDD is selected from -C(O)NH2, -C(O)NHRDB and -C(O)NRDBRDC. In one embodiment, -RDD is -C(O)OH. In one embodiment, -RDD is -C(O)ORDA, where -RDA is methyl or ethyl. In one embodiment, -RDD is -C(O)OMe. In the some worked examples of the present case, the group -RDD is -C(O)OMe. Each group -RG is independently selected from -C(O)ORGA, -C(O)OH, -CH2OH, -C(O)NH2, -C(O)NHRGB and -C(O)NRGBRGC Each of the groups of-RGA, -RGB and -RGC is independently Cm alkyl. The C1-4 alkyl group may be C1-3 alkyl, such as methyl or ethyl, such as methyl. In one embodiment, each -RG is independently selected from -C(O)ORGA and -C(O)OH. In one embodiment, each -RG is independently selected from -C(O)NH2, -C(O)NHRGB and -C(O)NRGBRGC. -Rp Where present, the group -Rp forms the aspartic acid bioisotere. -Rp is phenyl or C5-6 heteroaryl, such as pyridinyl, optionally substituted with one or more groups -Rz, such as one or two (mono- or disubstituted), such as one (monosubstituted). The heteroaryl group contains one, two or three ring heteroatoms independently selected from O, S and N(H). The heteroaryl group may have one or two, such as one, heteroatom. At least one, or each, of the heteroatoms may be N(H). Preferably, the C5-6 heteroaryl is a nitrogen-containing C5-6 heteroaryl, such as a heteroaryl selected from pyridinyl, pyrimidinyl, pyrrolyl, pyrazolyl and imidazolyl. Where -Rp is C5-6 heteroaryl, -Rp is preferably attached to the group -NH- via a ring carbon atom of the heteroaryl group. In one embodiment, -Rp is phenyl. In some worked examples of the present invention, -Rp is phenyl. In one embodiment, -Rp is C5-6 heteroaryl, such as a nitrogen-containing C5-6 heteroaryl. In one embodiment, -Rp is pyridinyl. Each -Rz is independently selected from -C(O)ORZA, -C(O)OH, -C(O)NH2, -C(O)NHRZB, -C(O)NRZBRZC, -C(O)NHOH, -C(O)N(RZD)OH and -C(O)S(RZE). Where -Rp is C5-6 heteroaryl, each group -Rz is attached via a ring carbon atom of the heteroaryl group. Each of-RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl, such as methyl or ethyl, such as methyl. In one embodiment, -Rz is -C(O)ORZA or -C(O)OH, such as -C(O)O(CH3). In some worked examples of the present invention, -Rz is -C(O)O(CH3). In one embodiment, -Rz is -C(O)NH2, -C(O)NH(CH3) or -C(O)N(CH3)2. In one embodiment, -Rz is -C(O)NHOH or-C(0)N(CH3)0H. In one embodiment, -Rz is -C(O)S(RZE), such as -C(O)S(CH3). A group -Rz may be attached at the 2-, 3- or 4- positions of the phenyl or C5-6 heteroaryl relative to the group -NH-, such as at the 2-position. In one embodiment, the phenyl group or C5-6 heteroaryl is monosubstituted with -Rz, such as where -Rz is provided at the 2-position relative to the group -NH-. In one embodiment, -Rp is phenyl or pyridinyl group which is monosubstituted with -Rz, where -Rz is provided at the 2-position (ort / 70-position) relative to the group -NH-. In some worked examples of the present invention, -Rp is a phenyl group which is monosubstituted with -Rz, where -Rz is provided at the 2- position (orf / 70-position). In one embodiment, -Rp is monosubstituted with -Rz, where -Rz is provided at the 2-position relative to -NH- and where -Rz is -C(O)OCH3 or-C(O)OH, such as -C(O)OCH3. -RB and -Re The groups -RB and -RE are optional benzene ring substituents. The group -RB is in the position where the methylene (-CH2-) group of the 7-membered ring in the benzodiazepinone mimetic compound 4 is connected to the benzene ring. The group -RE is not present in the benzodiazepinone IGD mimetics previously described in the art. The group -RE is only present when A is C(RE). The group -RB is -H or -XB-RBB. Here, -XB- is a covalent bond, -O-, -S-, or -NH-, and -RBB is an optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl, such as C2-10 alkyl. In one embodiment, -RB is -H. In one embodiment, -RB is -XB-RBB. In one embodiment, -XB- is -O- or a covalent bond. In one embodiment, -XB- is -0-. In one embodiment, -XB- is a covalent bond. The group -RBB is optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl. Each of the alkyl, alkenyl and alkynyl is optionally substituted, such as optionally substituted with one or more groups -RBC, where each -RBC is independently selected from Cs-earyl, halo, -OH, -SH, -NH2, -NHRBD, -NRBDRBE, -ON, -NO2, -C(O)OH, -C(O)ORBD, -C(O)NH2, -C(O)NHRBD, -C(O)NRBDRBE, C5-6cycloalkyl and Cs-eheterocyclyl, where each of-RBD and -RBE is independently Cm alkyl. Where an alkyl, alkenyl or alkynyl group is substituted, the substituent may not be provided at the carbon atom that is a to the group -XB-, for example where -RBC is -OH, -SH, -NH2, -NHRbd, or -NRBDRBE. Each of the alkyl, alkenyl and alkynyl groups may be unsubstituted. The alkyl group may be Ci-6 alkyl, such as methyl or ethyl, such as methyl. The alkyl group may be C2-6 alkyl, such as C5 alkyl. The alkyl group may be linear or branched. Where the alkyl group is branched, there may be one or more branch points. A branch point may be at any position on the alkyl chain. Preferably, the branch is a methyl group, and this may be a substitute on the penultimate carbon atom in the parent main chain. The alkenyl group may be C2-6 alkenyl, such as C5 alkenyl. The alkenyl group may be linear or branched. The alkenyl group may contain one or two carbon-carbon doubled bonds, such as one. A double bond may not be a,p to the group -XB-. The alkynyl group may be C2-6 alkynyl, such as C5 alkynyl. The alkynyl group may be linear or branched. The alkynyl group may contain a single carbon-carbon triple bond. Where an alkyl, alkenyl or alkynyl group is substituted with Cs-earyl, C5-6 cycloalkyl or C5-6 heterocyclyl, this group is optionally substituted at each ring carbon with a group -RBF, where each -RBF is independently selected from -CH3, -CH2CH3, -OH, -NH2, -C(O)OH, -C(O)OCH3, -C(O)NH2, -F, -Cl and -Br. In one embodiment, -RBB is C4-10 alkyl, such as C5 alkyl. In one embodiment, -RBB is / -pentyl (3-methylbutyl). In some of the worked examples of the present case, the group -RBB is / -pentyl. In one embodiment, -RBB is 3-phenyl-n-propyl-1-ene. In one embodiment, -RBB is methyl or ethyl. In one embodiment, -RBB is methyl. In some of the worked examples of the present case, -RBB is methyl. Where -RB is -H or -XB-RBB, -RE may be -H, -F or Me. In one embodiment, -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRFA and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz, When -RB together with -RE form a fused C5-6 aryl ring, the core may be indole, naphthalene, quinoline or isoquinoline. When -RB together with -RE form a fused C5-6 carbocyclic or heterocyclic ring, such a ring is non-aromatic. The ring may be partially saturated. When -RB together with -RE form a fused C5-6 carbocyclic or heterocyclic ring, the core may be 2,3-dihydroindene, tetralin, indoline or tetrahydroquinoline. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is unsubstituted. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is optionally monosubstituted with -RF, where -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRFA and -NRFARFB; where -RFA and -RFB are C1-4alkyl, Boc or Cbz. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted with -RF, where -RF is independently selected from -NH2, -NHRFA and -NRFARFB; where -RFA and -RFB are -CH3, Boc or Cbz. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted with -RF, where -RF is -NHC(O)CH3 or -OC(O)CH3. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted with -RF, where -RF is -NHC(O)CH3. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted in the position C6 with -RF, where -RF is -NHC(O)CH3. Preferred Compounds In one embodiment, the compound of formula (I) is a compound of formula (II): wherein A is C(RE), where -RE is H; -RQ is -CH(RC)(RD), or-Rp, wherein -Rc is -C(O)OCH3, C(O)OH, or -H; -RD is -XD-RDD, where -XD- is methylene (-CH2-), methyl methylene (-C(CH3)H-) or dimethyl methylene (-C(CH3)2-), and -RDD is -C(O)ORDA or-C(O)OH, where -RDA is C1-2 alkyl; or -Rp is phenyl monosubstituted with -Rz, where -Rz is selected from -C^OR^, -C(O)OH, -C(O)NH2, -C(O)NHRZB, -C(O)NRZBRZC, -C(O)NHOH, -C(O)N(RZD)OH and -C(O)S(RZE); and wherein -RQ contains at least one -C(O)- carbon which is a,p-related to the group -NH- to which -RQ is attached; -RB is -H or -XB-RBB, where -XB- is a covalent bond, -O-, -S-, or -NH-, where -RBB is C1-10 alkyl; or -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz, In one embodiment, -Rc is -C(O)OCH3. In one embodiment, -Rc is -H. In one embodiment, -RD is -CH2C(O)OCH3. In one embodiment, -RD is -C(CH3)HC(O)OCH3. In one embodiment, -RD is -C(CH3)2C(O)OCH3. In one embodiment, -Rp is the group: where * represents the point of attachment to -NH- and -Rz is selected from -C(O)O(CH3), -C(O)OH, -C(O)NH2, -C(O)NH(CH3) and -C(O)N(CH3)2. In one embodiment, both -RB and -RE are -H. In one embodiment, -RB is -XB-RBB, where -XB- is a covalent bond and -RBB is methyl. In one embodiment, -RB is -ORBB where -RBB is / -pentyl, and -RE is -H. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is unsubstituted. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted with -RF, where -RF is selected from -NHC(O)CH3, -H, -OC(O)CH3, -NH2, -NHRFA and -NRFARFB, where -RFA and -RFB are C1-4alkyl, Boc or Cbz. In one embodiment, -RB together with -RE and the carbon ring atoms to which they are attached form a fused benzene ring, which ring is monosubstituted in the position C6 with -RF, where -RF is -NHC(O)CH3. The compounds of the invention may be selected from: and the salts, solvates and protected forms thereof. Intermediates and Methods of Preparation Compounds of formula (I) and (II) may be prepared by conventional organic synthesis, using methods known to those skilled in the art. The worked examples in the present case provide examples methods of preparation. In general, the compounds of formula (I), including the compounds of formula (II), are prepared from the intermediate compounds of formula (III), for example by the reaction of the compound of formula (III) with an activated malate derivative, such as a compound of formula (IV) or an activated benzene derivative or aromatic heterocycle, such as a compound of formula (V). Thus, in one aspect there is provided the compounds of formula (III) and the salts, solvates and protected forms thereof. The compound of formula (III) is represented thus: wherein: Ais C(RE) orN; -XA- is -O-, -S-, or-NH-; -RA is optionally substituted Ci-w alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl; -RB is H or -X-RBB, where -X- is a covalent bond, -0-, -S-, or -NH-, and -RBB is C1-10 alkyl; and where present, -RE is -H, -Me or F, or -RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB, and each of-RFA and -RFB is independently C1-4alkyl, Boc orCbz, In one aspect of the invention, there is provided a method for the preparation of a compound of formula (I), the method comprising the step of reacting a compound of formula (III) with a compound of formula (IV) or (V) represented thus: (IV) (V) wherein: -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH, -C(O)NH2, -C(O)NHRCB and -C(O)NRCBRCC, where each of -RCA, -RCB and -Rcc is independently Cm alkyl; -RD is -H, C1-10 alkyl or -XD-RDD, where -XD- is C1-4 alkylene, such as methylene (-CH2-), ethylene (-CH2-CH2-) or dimethyl methylene (-C(CH3)2-), or a covalent bond, and -RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH, -C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC, where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; -Rp is phenyl or a 5- to 6-membered aromatic heterocyclyl, such as pyridinyl, optionally substituted with one or more groups -Rz, where each -Rz is independently selected from -C(O)ORZA, -C(O)OH, -C(O)NH2, -C(O)NHRzb, -C(O)NRzbRzc, -C(O)NHOH, -C(O)N(Rzd)OH and -C(O)S(RZE), where each of -RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl; -LA is independently selected from -OTs, -OTf, -OMs, -Cl, -Br, and -I. -LB is independently selected from -F, -Cl, -Br and -I. Protected Forms Compounds of the invention, such as compounds of formula (I) and (II), may be provided in a protected form. Here, reactive functionality, such as amino functionality, may be masked in order to prevent its reaction during a synthesis step. A protecting group is provided to mask the reactive functionality, and this protecting groups may be removed at a later stage of the synthesis to reveal the original reactive functionality. In one embodiment, the protected form is a compound where amino, hydroxyl, and / or carboxyl functionality is protected (masked) by a protecting group. Protecting groups, such as those for amino acid residues, are well known and well described in the art. Amino acids having side group protection, optionally together with amino and carboxy protection, are commercially available. Thus, a protected IGD peptidomimetic compound may be prepared from appropriately protected amino acid starting materials. Where a protecting group is used is it is removable under conditions that do not substantially disrupt the structure of the IGD core. In one embodiment, the protecting groups are acid-labile, base labile, or are removable under reducing conditions. Example protecting groups for amino functionality include Boc (tert-butoxycabonyl), Bn (benzyl, Bzl), CbZ (benzyloxycarbonyl, Z), 2-CL-Z (2-chloro), ivDde (1-[4,4-dimethyl-2,6-dioxocylcohex-1-ylidene]-3-methylbutyl), Fmoc (fluorenylmethyloxycarbonyl), HSOs-Fmoc (sulfonylated Fmoc, such as 2-sulfo-Fmoc, as described in e.g. Schechter et al, J.Med Chem 2002, 45 (19) 4264), Dde (1-[4,4-dimethyl-2,6-dioxocylcohex-1-ylidene]ethyl), Mmt (4-methoxytrityl), Mtt (4-methyltrityl), Nvoc (6-nitroveratroyloxycarbonyl), Tfa (trifluroacetyl), and Alloc (allyloxycarbonyl). Example protecting groups for aromatic nitrogen functionality includes Boc, Mtt, Trt and Dnp (dinitrophenyl). Example protecting groups for hydroxyl functionality include Trt (trityl), Bn (benzyl), and tBu (tert-butyl). Further example protecting groups include silyl ether protecting groups, such as TMS, TES, TBS, TIPS, TBDMS, and TBDPS. Such protecting groups are removable with TBAF, for example. Example protecting groups for carboxyl functionality include Bn (benzyl, Bz), tBu (tert-butyl), TMSET (trimethylsilylethyl) and Dmab ({1-[4,4-dimethyl-2,6-dioxocylcohex-1-ylidene]-3-methylbutyljamino benzyl). In some embodiments, only some types of functionality are protected. For example, only amino groups may be protected. In one embodiment, amino groups and hydroxyl groups, where present, are protected. Salts, Solvates and Other Forms Examples of salts of compound of formula (I) and (II) include all pharmaceutically acceptable salts, such as, without limitation, acid addition salts of strong mineral acids such as HCI and HBr salts and addition salts of strong organic acids such as a methanesulfonic acid salt. Further examples of salts include sulfates and acetates such as acetate itself, trifluoroacetate or trichloroacetate. Base addition salts of strong bases such as NaOH or KOH are also included. A compound of formula (I) and (II) can also be formulated as a prodrug. Prodrugs can include a compound herein described in which one or more functional groups are protected with a group which can be cleaved in vivo, to liberate the biologically active compound. In one embodiment the prodrug is an “amine prodrug”. Examples of amine prodrugs include sulphomethyl, as described in e.g., Bergen etal, Antimicrob. Agents and Chemotherapy, 2006, 50, 1953 or HSO3-FMOC, as described in e.g. Schechter etal, J.Med Chern 2002, 45(19) 4264, and salts thereof. Further examples of amine prodrugs are given by Krise and Oliyai in Biotechnology: Pharmaceutical Aspects, 2007, 5(2), 101-131. In one embodiment a compound of formula (I) or (II) is provided as a prodrug. A reference to a compound of formula (I) or (II), or any other compound described herein, is also a reference to a solvate of that compound. Examples of solvates include hydrates. A compound of formula (I) or (II), or any other compound described herein, includes a compound where an atom is replaced by a naturally occurring or non-naturally occurring isotope. In one embodiment the isotope is a stable isotope. Thus, a compound described here includes, for example deuterium containing compounds and the like. For example, H may be in any isotopic form, including 1H, 2H (D), and 3H (T); C may be in any isotopic form, including 12C, 13C, and 14C; O may be in any isotopic form, including 16O and 18O; and the like. Certain compounds of formula (I) or (II), or any other compound described herein, may exist in one or more particular geometric, optical, enantiomeric, diasteriomeric, epimeric, atropic, stereoisomeric, tautomeric, conformational, or anomeric forms, including but not limited to, cis- and trans-forms; E- and Z-forms; c-, t-, and r- forms; endo- and exo-forms; R-, S-, and meso-forms; D- and L-forms; d- and l-forms; (+) and (-) forms; keto-, enol-, and enolateforms; syn- and anti-forms; synclinal- and anticlinal-forms; a- and p-forms; axial and equatorial forms; boat-, chair-, twist-, envelope-, and halfchair-forms; and combinations thereof, hereinafter collectively referred to as “isomers” (or “isomeric forms”). Note that, except as discussed below for tautomeric forms, specifically excluded from the term “isomers,” as used herein, are structural (or constitutional) isomers (i.e., isomers which differ in the connections between atoms rather than merely by the position of atoms in space). For example, a reference to a methoxy group, -OCH3, is not to be construed as a reference to its structural isomer, a hydroxymethyl group, -CH2OH. Similarly, a reference to ortho-chlorophenyl is not to be construed as a reference to its structural isomer, metachlorophenyl. However, a reference to a class of structures may well include structurally isomeric forms falling within that class (e.g., Ci-ealkyl includes n-propyl and iso-propyl; butyl includes n-, iso-, sec-, and tert-butyl; methoxyphenyl includes ortho-, meta-, and paramethoxyphenyl). Unless otherwise specified, a reference to a particular compound includes all such isomeric forms, including mixtures (e.g., racemic mixtures) thereof. Methods for the preparation (e.g., asymmetric synthesis) and separation (e.g., fractional crystallisation and chromatographic means) of such isomeric forms are either known in the art or are readily obtained by adapting the methods taught herein, or known methods, in a known manner. One aspect of the present invention pertains to compounds in substantially purified form and / or in a form substantially free from contaminants. In one embodiment, the substantially purified form is at least 50% by weight, e.g., at least 60% by weight, e.g., at least 70% by weight, e.g., at least 80% by weight, e.g., at least 90% by weight, e.g., at least 95% by weight, e.g., at least 97% by weight, e.g., at least 98% by weight, e.g., at least 99% by weight. Unless specified, the substantially purified form refers to the compound in any stereoisomeric or enantiomeric form. For example, in one embodiment, the substantially purified form refers to a mixture of stereoisomers, i.e., purified with respect to other compounds. In one embodiment, the substantially purified form refers to one stereoisomer, e.g., optically pure stereoisomer. In one embodiment, the substantially purified form refers to a mixture of enantiomers. In one embodiment, the substantially purified form refers to an equimolar mixture of enantiomers (i.e., a racemic mixture, a racemate). In one embodiment, the substantially purified form refers to one enantiomer, e.g., optically pure enantiomer. In one embodiment, the contaminants represent no more than 50% by weight, e.g., no more than 40% by weight, e.g., no more than 30% by weight, e.g., no more than 20% by weight, e.g., no more than 10% by weight, e.g., no more than 5% by weight, e.g., no more than 3% by weight, e.g., no more than 2% by weight, e.g., no more than 1% by weight. Unless specified, the contaminants refer to other compounds, that is, other than stereoisomers or enantiomers. In one embodiment, the contaminants refer to other compounds and other stereoisomers. In one embodiment, the contaminants refer to other compounds and the other enantiomer. In one embodiment, the substantially purified form is at least 60% optically pure (i.e., 60% of the compound, on a molar basis, is the desired stereoisomer or enantiomer, and 40% is the undesired stereoisomer or enantiomer), e.g., at least 70% optically pure, e.g., at least 80% optically pure, e.g., at least 90% optically pure, e.g., at least 95% optically pure, e.g., at least 97% optically pure, e.g., at least 98% optically pure, e.g., at least 99% optically pure. Methods of Treatment The compounds of formula (I) or (II) or pharmaceutical formulations containing these compounds, are suitable for use in methods of treatment and prophylaxis. The compounds may be administered to a subject in need thereof. The compounds of formula (I) or (II) are for use in a method of treatment of the human or animal body by therapy. In some aspects of the invention, a compound of formula (I) or (II) may be administered to a mammalian subject, such as a human, for use in a method of tissue regeneration and / or repair, such as promoting tissue regeneration and / or repair. In another aspect of the invention, a compound of formula (I) or (II) may be administered to a mammalian subject, such as a human, in order to treat a wound, a bone fracture or an autoimmune disease, to stimulate nerve regeneration, or to assist in the post-transplant healing process. In another aspect of the invention, a compound of formula (I) or (II) is for use in the promotion of vascularisation of tissue-engineered constructs, such as those for use in a mammalian subject, such as a human. In one embodiment, a compound of formula (I) or (II) is used in a method of treatment of a wound wherein the compound of formula (I) or (II) binds the integrin avPa and initiates a signal transduction cascade involving the tyrosine phosphorylation of ppFAK125, induction of new RNA synthesis and cell activation. A compound of formula (I) or (II) may be used in a method of treatment of a bone fracture, such as a treatment where the compound of the invention promotes osteoblast migration. A compound of formula (I) or (II) may be for use in a method of stimulating nerve regeneration. Another aspect of the present invention pertains to use of a compound of formula (I) or (II) in the manufacture of a medicament for use in treatment. In one embodiment, the medicament comprises a compound of formula (I) or (II). In one embodiment, the medicament is for use in a method of tissue regeneration and / or repair. In one embodiment, the medicament is for use in the treatment of a wound. The compounds of formula (I) or (II), or compositions comprising the same may be used together with an active agent in methods of treatment. Treatment The term “treatment,” as used herein in the context of treating a condition, pertains generally to treatment and therapy, whether of a human or an animal (e.g., in veterinary applications), in which some desired therapeutic effect is achieved, for example, acceleration of a healing process, the inhibition of the progress of the condition, and includes a reduction in the rate of progress, a halt in the rate of progress, alleviation of symptoms of the condition, amelioration of the condition, and cure of the condition. Treatment as a prophylactic measure (i.e., prophylaxis) is also included. For example, use with patients who have not yet developed the condition, but who are at risk of developing the condition, is encompassed by the term “treatment.” The term “therapeutically-effective amount,” as used herein, pertains to that amount of a compound, or a material, composition or dosage form comprising a compound, which is effective for producing some desired therapeutic effect, commensurate with a reasonable benefit / risk ratio, when administered in accordance with a desired treatment regimen. The term “treatment” includes combination treatments and therapies, in which two or more treatments or therapies are combined, for example, sequentially or simultaneously. Here, a compound of the invention may be used together with another agent, or the combination may include a plurality of the compounds of the invention. Formulations In one aspect, the present invention provides a pharmaceutical composition comprising a compound of formula (I) or (ll)together with a pharmaceutically acceptable carrier. The pharmaceutical composition may additionally comprise a second active agent. While it is possible for the compound of formula (I) or (II) to be administered alone or together with the second active agent, it is desirable to present it as a pharmaceutical formulation (e.g., composition, preparation, medicament) comprising at least one compound of formula (I) or (II), as described herein, together with one or more other pharmaceutically acceptable ingredients well known to those skilled in the art, including, but not limited to, pharmaceutically acceptable carriers, diluents, excipients, adjuvants, fillers, buffers, preservatives, anti-oxidants, lubricants, stabilisers, solubilisers, surfactants (e.g., wetting agents), masking agents, colouring agents, flavouring agents, and sweetening agents. The formulation may further comprise other active agents, for example, other therapeutic or prophylactic agents. Thus, the present invention further provides pharmaceutical compositions, as defined above, and methods of making a pharmaceutical composition comprising admixing at least one compound of formula (I) or (II), as described herein, together with one or more other pharmaceutically acceptable ingredients well known to those skilled in the art, e.g., carriers, diluents, excipients, etc. If formulated as discrete units (e.g., tablets, etc.), each unit contains a predetermined amount (dosage) of the compound. The composition optionally further comprises the second active agent in a predetermined amount. The term “pharmaceutically acceptable,” as used herein, pertains to compounds, ingredients, materials, compositions, dosage forms, etc., which are, within the scope of sound medical judgment, suitable for use in contact with the tissues of the subject in question (e.g., human) without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit / risk ratio. Each carrier, diluent, excipient, etc. must also be “acceptable” in the sense of being compatible with the other ingredients of the formulation. Suitable carriers, diluents, excipients, etc. can be found in standard pharmaceutical texts, for example, Remington’s Pharmaceutical Sciences, 18th edition, Mack Publishing Company, Easton, Pa., 1990; and Handbook of Pharmaceutical Excipients, 5th edition, 2005. The formulations may be prepared by any methods well known in the art of pharmacy. Such methods include the step of bringing into association the compound of formula (I) or (II) with a carrier which constitutes one or more accessory ingredients. In general, the formulations are prepared by uniformly and intimately bringing into association the compound with carriers (e.g., liquid carriers, finely divided solid carrier, etc.), and then shaping the product, if necessary. The formulation may be prepared to provide for rapid or slow release; immediate, delayed, timed, or sustained release; or a combination thereof. Formulations may suitably be in the form of liquids, solutions (e.g., aqueous, non-aqueous), suspensions (e.g., aqueous, non-aqueous), emulsions (e.g., oil-in-water, water-in-oil), elixirs, syrups, drops, tablets (including, e.g., coated tablets), granules, powders, capsules (including, e.g., hard and soft gelatin capsules), pills, ampoules, boluses, suppositories, pessaries, tinctures, gels, pastes, ointments, creams, lotions, oils, foams, sprays, mists, or aerosols. Formulations may suitably be provided as a patch, adhesive plaster, bandage, dressing, or the like which is impregnated with one or more compounds and optionally one or more other pharmaceutically acceptable ingredients, including, for example, penetration, permeation, and absorption enhancers. Formulations may also suitably be provided in the form of a depot or reservoir. The compound may be dissolved in, suspended in, or admixed with one or more other pharmaceutically acceptable ingredients. The compound may be presented in a liposome or other microparticulate which is designed to target the compound, for example, to blood components or one or more organs. Where a liposome is used, it is noted that the liposome may contain both the compound of formula (I) or (II) and a second active agent. Formulations suitable for buccal administration include mouthwashes, losenges, pastilles, as well as patches, adhesive plasters, depots, and reservoirs. Losenges typically comprise the compound in a flavoured basis, usually sucrose and acacia or tragacanth. Pastilles typically comprise the compound in an inert matrix, such as gelatin and glycerin, or sucrose and acacia. Mouthwashes typically comprise the compound in a suitable liquid carrier. Formulations suitable for oral transmucosal administration include liquids, solutions (e.g., aqueous, non-aqueous), suspensions (e.g., aqueous, non-aqueous), emulsions (e.g., oil-in-water, water-in-oil), mouthwashes, losenges, pastilles, as well as patches, adhesive plasters, depots, and reservoirs. Formulations suitable for non-oral transmucosal administration include liquids, solutions (e.g., aqueous, non-aqueous), suspensions (e.g., aqueous, non-aqueous), emulsions (e.g., oil-in-water, water-in-oil), suppositories, pessaries, gels, pastes, ointments, creams, lotions, oils, as well as patches, adhesive plasters, depots, and reservoirs. Formulations suitable for transdermal administration include gels, pastes, ointments, creams, lotions, and oils, as well as patches, adhesive plasters, bandages, dressings, depots, and reservoirs. Tablets may be made by conventional means, e.g., compression or moulding, optionally with one or more accessory ingredients. Compressed tablets may be prepared by compressing in a suitable machine the compound in a free-flowing form such as a powder or granules, optionally mixed with one or more binders (e.g., povidone, gelatin, acacia, sorbitol, tragacanth, hydroxypropylmethyl cellulose); fillers or diluents (e.g., lactose, microcrystalline cellulose, calcium hydrogen phosphate); lubricants (e.g., magnesium stearate, talc, silica); disintegrants (e.g., sodium starch glycolate, cross-linked povidone, cross-linked sodium carboxymethyl cellulose); surface-active or dispersing or wetting agents (e.g., sodium lauryl sulfate); preservatives (e.g., methyl p-hydroxybenzoate, propyl p-hydroxybenzoate, sorbic acid); flavours, flavour enhancing agents, and sweeteners. Moulded tablets may be made by moulding in a suitable machine a mixture of the powdered compound moistened with an inert liquid diluent. The tablets may optionally be coated or scored and may be formulated so as to provide slow or controlled release of the compound therein using, for example, hydroxypropylmethyl cellulose in varying proportions to provide the desired release profile. Tablets may optionally be provided with a coating, for example, to affect release, for example an enteric coating, to provide release in parts of the gut other than the stomach. Ointments are typically prepared from the compound and a paraffinic or a water-miscible ointment base. Creams are typically prepared from the compound and an oil-in-water cream base. If desired, the aqueous phase of the cream base may include, for example, at least about 30% w / w of a polyhydric alcohol, i.e., an alcohol having two or more hydroxyl groups such as propylene glycol, butane-1,3-diol, mannitol, sorbitol, glycerol and polyethylene glycol and mixtures thereof. The topical formulations may desirably include a compound which enhances absorption or penetration of the compound through the skin or other affected areas. Examples of such dermal penetration enhancers include dimethylsulfoxide and related analogues. Emulsions are typically prepared from the compound and an oily phase, which may optionally comprise merely an emulsifier (otherwise known as an emulgent), or it may comprise a mixture of at least one emulsifier with a fat or an oil or with both a fat and an oil. A hydrophilic emulsifier may be included together with a lipophilic emulsifier which acts as a stabiliser. It is also possible to include both an oil and a fat. Together, the emulsifier(s) with or without stabiliser(s) make up the so-called emulsifying wax, and the wax together with the oil and / or fat make up the so-called emulsifying ointment base which forms the oily dispersed phase of the cream formulations. Suitable emulgents and emulsion stabilisers include Tween 60, Span 80, cetostearyl alcohol, myristyl alcohol, glyceryl monostearate and sodium lauryl sulfate. The choice of suitable oils or fats for the formulation is based on achieving the desired cosmetic properties, since the solubility of the compound in most oils likely to be used in pharmaceutical emulsion formulations may be very low. Thus the cream should be a non-greasy, non-staining and washable product with suitable consistency to avoid leakage from tubes or other containers. Straight or branched chain, mono- or dibasic alkyl esters such as di-isoadipate, isocetyl stearate, propylene glycol diester of coconut fatty acids, isopropyl myristate, decyl oleate, isopropyl palmitate, butyl stearate, 2-ethylhexyl palmitate or a blend of branched chain esters known as Crodamol CAP may be used. These may be used alone or in combination depending on the properties required. Alternatively, high melting point lipids such as white soft paraffin and / or liquid paraffin or other mineral oils can be used. Formulations suitable for ocular administration include eye drops wherein the compound is dissolved or suspended in a suitable carrier, especially an aqueous solvent for the compound. Formulations suitable for rectal administration may be presented as a suppository with a suitable base comprising, for example, natural or hardened oils, waxes, fats, semi-liquid or liquid polyols, for example, cocoa butter or a salicylate; or as a solution or suspension for treatment by enema. Formulations suitable for vaginal administration may be presented as pessaries, tampons, creams, gels, pastes, foams or spray formulations containing in addition to the compound, such carriers as are known in the art to be appropriate. Formulations suitable for parenteral administration (e.g., for example by injection or infusion, intravenously or subcutaneously), include aqueous or non-aqueous, isotonic, pyrogen-free, sterile liquids (e.g., solutions, suspensions), in which the compound is dissolved, suspended, or otherwise provided (e.g., in a liposome or other microparticulate). Such liquids may additional contain other pharmaceutically acceptable ingredients, such as anti-oxidants, buffers, preservatives, stabilisers, bacteriostats, suspending agents, thickening agents, and solutes which render the formulation isotonic with the blood (or other relevant bodily fluid) of the intended recipient. Examples of excipients include, for example, water, alcohols, sugars, polyols, glycerol, vegetable oils, and the like. Examples of suitable isotonic carriers for use in such formulations include Sodium Chloride Injection, Ringer’s Solution, or Lactated Ringer’s Injection. Typically, the concentration of the compound in the liquid is from about 1 ng / mL to about 100 ng / mL. The formulations may be presented in unit-dose or multi-dose sealed containers, for example, ampoules and vials, and may be stored in a freeze-dried (lyophilised) condition requiring only the addition of the sterile liquid carrier, for example water for injections, immediately prior to use. Extemporaneous injection solutions and suspensions may be prepared from sterile powders, granules, and tablets. The pharmaceutical composition may additionally comprise a second active agent. In an alternative embodiment, where a second active agent is provided for use in therapy, the second active agent may be separately formulated from the compound of formula (I) or (II). The comments below above in relation to the compound of formula (I) or (II) may therefore also apply to the second active agent, as separately formulated. Dosage Generally, the methods of the invention may comprise administering to a subject an effective amount of a compound of formula (I) or (II) so as to provide a wound healing effect. It will be appreciated by one of skill in the art that appropriate dosages of the compound of formula (I) or (II), and compositions comprising the compound of formula (I) or (II), can vary from patient to patient. Determining the optimal dosage will generally involve the balancing of the level of therapeutic benefit against any risk or deleterious side effects. The selected dosage level will depend on a variety of factors including, but not limited to, the activity of the particular compound of formula (I) or (II), the route of administration, the time of administration, the rate of excretion of the compound, the duration of the treatment, other drugs, compounds, and / or materials used in combination, the severity of the condition, and the species, sex, age, weight, condition, general health, and prior medical history of the patient. The amount of compound of formula (I) or (II) and route of administration will ultimately be at the discretion of the physician, veterinarian, or clinician, although generally the dosage will be selected to achieve local concentrations at the site of action which achieve the desired effect without causing substantial harmful or deleterious side-effects. Administration can be effected in one dose, or intermittently (e.g., in divided doses at appropriate intervals) throughout the course of treatment. Methods of determining the most effective means and dosage of administration are well known to those of skill in the art and will vary with the formulation used for therapy, the purpose of the therapy, the target cell(s) being treated, and the subject being treated. Single or multiple administrations can be carried out with the dose level and pattern being selected by the treating physician, veterinarian, or clinician. Kits One aspect of the invention pertains to a kit comprising (a) a compound of formula (I) or (II), or a composition comprising a compound as defined in any one of formula (I) or (II), e.g., typically provided in a suitable container and / or with suitable packaging; and (b) instructions for use, e.g., written instructions on how to administer the compound or composition. The written instructions may also include a list of indications for which the compound of formula (I) or (II) is a suitable treatment. In one embodiment, the kit further comprises a second active agent, or a composition comprising the second active agent. Here, the written instructions may also include a list of indications for which the second active agent, together with the compound of formula (I) or (II), is suitable for treatment. The second active agent may be selected from an antimicrobial, a coagulant, and a debridement agent. Routes of Administration A compound of formula (I) or (II) or a pharmaceutical composition comprising the compound of formula (I) or (II), may be administered to a subject by any convenient route of administration, whether systemically / peripherally or topically (i.e., at the site of desired action). Routes of administration include, but are not limited to, oral (e.g., by ingestion); buccal; sublingual; transdermal (including, e.g., by a patch, plaster, etc.); transmucosal (including, e.g., by a patch, plaster, etc.); rectal (e.g., by suppository or enema); vaginal (e.g., by pessary); parenteral, for example, by injection or infusion, including subcutaneous, intradermal, intramuscular, intravenous, intraarterial, intracardiac, intrathecal, intraspinal, intracapsular, subcapsular, intraorbital, intraperitoneal, intratracheal, subcuticular, intraarticular, subarachnoid, and intrasternal; by implant of a depot or reservoir, for example, subcutaneously or intramuscularly. The Subject / Patient The subject / patient may be a chordate, a vertebrate, a mammal, a placental mammal, a marsupial (e.g., kangaroo, wombat), a rodent (e.g., a guinea pig, a hamster, a rat, a mouse), murine (e.g., a mouse), a lagomorph (e.g., a rabbit), avian (e.g., a bird), canine (e.g., a dog), feline (e.g., a cat), equine (e.g., a horse), porcine (e.g., a pig), ovine (e.g., a sheep), bovine (e.g., a cow), a primate, simian (e.g., a monkey or ape), a monkey (e.g., marmoset, baboon), an ape (e.g., gorilla, chimpanzee, orang-utan, gibbon), or a human. Furthermore, the subject / patient may be any of its forms of development, for example, a foetus. In one embodiment, the subject / patient is a horse. In one embodiment, the subject / patient is a horse at risk of developing proud flesh. In one embodiment, the subject / patient is a human. In one embodiment, the subject / patient is a human suffering from a chronic wound. In one embodiment, the subject / patient is a human subject having diabetes, or at risk of diabetes. Recent work by Harman et al. has demonstrated that chronic wounds in humans due to impaired wound healing are akin to the limb wounds of horses. It is also envisaged that the invention may be practised on a non-human animal having a wound. A non-human mammal may be a rodent. Rodents include rats, mice, guinea pigs, chinchillas and other similarly-sized small rodents used in laboratory research. Other Options Each and every compatible combination of the embodiments described above is explicitly disclosed herein, as if each and every combination was individually and explicitly recited. Various further aspects and embodiments of the present invention will be apparent to those skilled in the art in view of the present disclosure. “and / or” where used herein is to be taken as specific disclosure of each of the two specified features or components with or without the other. For example, “A and / or B” is to be taken as specific disclosure of each of (i) A, (ii) B and (iii) A and B, just as if each is set out individually herein. Unless context dictates otherwise, the descriptions and definitions of the features set out above are not limited to any particular aspect or embodiment of the invention and apply equally to all aspects and embodiments which are described. Where technically appropriate embodiments may be combined and thus the disclosure extends to all permutations and combinations of the embodiments provided herein. Certain aspects and embodiments of the invention will now be illustrated by way of example and with reference to the figures described above. Examples The following examples are provided solely to illustrate the present invention and are not intended to limit the scope of the invention, as described herein. Synthesis Examples Chemistry General Information All reagents and starting materials were purchased from commercially available sources (Sigma Aldrich, Merck & Co., AKscientific), and used without purification unless stated otherwise. Solvents were laboratory reagent grade unless specified. Anhydrous solvents were dried in-house by passing over sealed column of activated alumina. Reactions involving air sensitive reagents and dry solvents were performed in glassware dried in an oven (110°C) and were carried out with the exclusion of air using a nitrogen atmosphere. Microwave reactions were performed in a domestic microwave (Samsung I Timesaver 800W) adapted with a reflux system, or in a CEM Discover SP microwave reactor. Solvents were evaporated under reduced pressure at 40°C using a Buchi Rotavapor. Column chromatography was performed under pressure using silica gel (Chem-supply Silica LC 60 A) as the stationary phase, and HPLC grade solvents as eluent. Reactions were monitored by thin layer chromatography. TLC was performed on aluminium sheets precoated with silica gel (Merck Silica Gel 60 F254). The plates were visualized by the quenching of UV fluorescence (Amax 254 nm) and / or by staining with a vanillin and / or anisaldehyde and / or KMnO4 solution dips. Proton magnetic resonance spectra (1H NMR) and carbon magnetic resonance spectra (13C NMR) were recorded at using 400 MHz and 101 MHz or at 600 MHz and 151 MHz using either a Jeol JNM-ECZ600R 600 MHz spectrometer NMR with a ASC30 Autosampler or a Jeol JNM-ECZ400S 400 MHz spectrometer NMR with a ASC64 Autosampler. Chemical shifts (6) are reported in parts per million (ppm) and are referenced to the residual solvent peak. NMR signals are described by multiplicity as singlet (s), doublet (d), triplet (t), quartet (q), quintet (quint) septet (sept) or multiplet (m) and broad (br) or by a combination of these terms which refer to the spin-spin coupling pattern observed, J values reported to 1 decimal place. Two-dimensional (COSY, HSQC, HMQC, HMBC) NMR spectroscopy was used to assist in the assignment of signals in the 1H and 13C NMR spectra. Structures have been given an arbitrary numbering system to facilitate 1H and 13C NMR assignments. IR spectra were obtained employing a Perkin-Elmer Spectrum One FTIR instrument operating in transmittance mode with liquid samples pressed between KBr discs (neat). Only representative absorptions are reported in wavenumbers for the molecule’s functional groups. High resolution mass spectra were recorded on a Bruker MaXis 4G spectrometer operating in ESMS+. Melting points were obtained using samples isolated after purification without further recrystallization, unless stated, on a METTLER Toledo MP 90. Optical rotations were measured in DCM on a Perkin Elmer 341 polarimeter with a 10 cm cell. Each optical rotation measurement was done five times and the mean value is reported. (S)-2-Trifluoromethanesulfonyloxy-succinic acid dimethyl ester (fSJ-12) (5)-12 The compound may be prepared according to the procedure described by Matheson etal. (2015). ( / ?)-2-Trifluoromethanesulfonyloxy-succinic acid dimethyl ester (fRJ-12) W-12 The compound may be prepared according to the procedure described by Matheson etal. (2015). (E)-] -(Phenyldiazenyl)naphthalen-2-ol (51) 51 Aniline (630 pL, 6.93 mmol, 1.0 eq.) was dissolved in dilute H2SO4 (10% aq., 10 mL), and the mixture was stirred and heated gently (30°C) until homogeneous. In a separate round bottom flask, sodium nitrite (470 mg, 6.93 mmol, 1.0 eq.) was dissolved in water (5 mL). The solution containing the amine was cooled down to 0 °C and was treated dropwise with the sodium nitrite solution to generate a diazonium solution. p-Naphthol (1.0 g, 6.93 mmol, 1.0 eq.) was dissolved in a NaOH aq. solution (20%, 20 mL), and cooled down to 0 °C. The P-naphthol solution was then treated dropwise with the freshly generated diazonium solution, resulting in the formation of a red precipitate. Once the addition was complete, the reaction mixture was filtered, and the crude red solid residue dried overnight under vacuum. The dry solid was recrystallized from absolute EtOH to give the desired product as red needles (1.33 g, 77%). The spectral data matched that reported in the literature (see Di Donna et al.). M.p. 136.6-137.1 °C. 1H NMR (CDCI3,600 MHz) 6: 8.55 (1H, d, J= 7.8 Hz), 7.73 (1H, d, J = 9.0 Hz), 7.72 (2H, dd, J= 8.4, 1.2 Hz), 7.60 (1H, d, J= 8.4 Hz), 7.54 (1H, ddd, J= 7.8, 6.6, 1.2 Hz), 7.47 (2H, dd, J= 8.4, 7.2 Hz), 7.39 (1H, ddd, J= 9.0, 7.8, 1.2 Hz), 7.29 (1H, tt, J = 7.8, 1.2 Hz), 6.86 (1H, d, J= 9.6 Hz). 1,6-Dinitronaphthalen-2-ol (59) 5     4 59 Calcium nitrate (2.78 g, 16.97 mmol, 1.5 eq) was dissolved in acetic acid (5 mL), and the solution was then treated with diazo compound 51 (2.80 g, 11.31 mmol, 1.0 eq). The resulting mixture was sonicated until homogeneous, and then heated in a domestic microwave in 4 runs of 1 min each at 350 MW, with 1 min cool down period between each run. Once the runs were completed, the mixture was poured in ice cold water (20 mL), filtered, and the resulting solid was dried under vacuum overnight. The resulting orange solid was used without further purification (2.17 g, 82%). M.p. 249.1-250.1 °C. 1H NMR (CDCI3,600 MHz) 6: 12.21 (1H, s), 9.07 (1H, d, J= 9.6 Hz), 8.75 (1H, d, J= 2.4 Hz), 8.48 (1H, dd, J= 9.6, 3.0 Hz), 8.18 (1H, d, J= 9.0 Hz), 7.45 (1H, d, J= 9.0 Hz). 13C NMR (CDCI3, 151 MHz) 6: 160.6, 144.7, 139.7, 130.4, 128.4, 127.8, 125.1, 125.0, 124.1, 122.2. HRMS (ESI) calculated forCioH7N205 [M]+: m / z 235.0340, found m / z 235.0349. 2-(3-Methylbutoxy)-1,6-dinitronaphthalene (60) 60 A solution of alcohol 59 (2.88 g, 12.3 mmol, 1.0 eq) in dry DMF (50 mL) was treated with potassium carbonate (3.40 g, 24.6 mmol, 2.0 eq) and 1-bromo-3-methyl butane (3.0 mL, 24.6 mmol, 2.0 eq). The reaction mixture was heated up to 60 °C, and stirred for 36 h. The reaction was cooled down to r.t. and quenched with a sat. aq. solution of ammonium chloride (50 mL). The resulting solution was extracted with EtOAc (50 mL x 3). The combined organic phases were washed with water (70 mL x 5), brine (70 mL x 2), dried (Na2SO4) and concentrated in vacuo. The crude product was then purified using FCC (Hex: EtOAc 8:2) giving the title compound as an orange solid (2.63 g, 70%). M.p. 75.8-80 °C. 1H NMR (CDCI3,600 MHz) 6: 8.80 (1H, d, J = 2.4 Hz), 8.34 (1H, dd, J= 9.6, 2.4 Hz), 8.15 (1H, d, J= 9.6 Hz), 7.79 (1H, d, J= 9.0 Hz), 7.50 (1H, d, J= 9.0 Hz), 4.30 (2H, t, J = 6.6 Hz), 1.84 (1H, app sept, J = 6.6 Hz), 1.75 (2H, q, J = 6.6 Hz), 0.97 (6H, d, J = 6.6 Hz). 13C NMR (CDCI3, 151 MHz) 6: 151.3, 144.6, 136.0, 134.2, 128.4, 126.2, 124.9, 122.5, 122.3, 116.1, 69.0, 37.6, 24.9, 22.5. HRMS (ESI) calculated for C15H17N2O5 [M]+: m / z 305.1128, found m / z 305.1132. 2-(3-Methylbutoxy)-1-nitronaphthalen-6-amine (61) 61 A homogenous solution of nitro compound 60 (1.65 g, 5.43 mmol, 1.0 eq) in EtOH (250 mL), was treated with a solution of sodium sulphide nonahydrate (4.34 g, 10.85 mmol, 2.0 eq) and sodium bicarbonate (46 mg, 0.54 mmol, 0.1 eq) in water (80 mL) over 30 min. The reaction was allowed to stir at r.t. and monitored by TLC until completion (5 h), before being concentrated under reduced pressure. The resulting residue was dissolved in EtOAc (200 mL) and washed with water (150 mL x 2) and brine (150 mL). The organic phases were then dried (Na2SO4), filtered and concentrated in vacuo. The crude product was purified with FCC (PE:EtOAc 6:4) to give the desired product as an orange solid (708 mg, 48%). M.p. 96.8 °C 1H NMR (CDCI3,600 MHz) 5: 7.65 (1H, d, J = 9.0 Hz, ArC(4)H), 7.49 (1H, d, J = 9.0 Hz, ArC(3)H), 7.21 (1H, d, J = 9.0 Hz, ArC(8)H), 7.05 (1H, dd, J = 9.0, 2.4 Hz, ArC(7)H), 6.96 (1H, d, J= 1.8 Hz, ArC(5)H), 4.16 (2H, t, J=Q.Q Hz, C(9)H2), 1.80 (1H, app sept, J = Q.Q Hz, C(n)H), 1.68 (2H, q, J = 6.6 Hz, C(io)H2), 0.94 (6H, d, J = 6.6 Hz, 2x C(i2)H3). 13C NMR (CDCI3, 101 MHz) 5: 145.7 (C(6)), 143.6 (C(2)), 130.0 (C(d), 129.7 (C(4)), 121.9 (C(3)), 121.3 (C(7)), 119.8 (C(4a)), 115.3 (C(8)), 108.5 (C(5)), 69.0 (C(9)), 37.9 (C(i0)), 24.8 (C(n)), 22.5 (2x C(12)). One unresolved carbon. HRMS (ESI) calculated for C15H17N2O5 [M]+: m / z 275.1390, found m / z 275.1390. (E)-] -(2-(lsopentyloxy)naphthalen-1 -yl)-phenyldiazene (74) N 74 A homogeneous solution of 51 (940 mg, 3.79 mmol, 1.0 eq) in DMSO (25 mL) was treated with potassium hydroxide (320 mg, 5.68 mmol, 1.5 eq), the mixture was allowed to stir for 15 min, before 1-bromo-3-methyl butane (680 pL, 5.68 mmol, 1.5 eq) was added. The reaction mixture was warmed up to 80 °C and stirred at this temperature for 72 h. The mixture was then diluted with water (25 mL) and extracted with EtOAc (50 mL x 3). The combined organic layers were washed with brine (50 mL x 2), dried (Na2SO4), filtered and concentrated in vacuo. The crude product was purified using FCC (DCM) to yield the product as a red oil (996 mg, 83%). 1H NMR (CDCI3,400 MHz) 5: 8.36 (1H, d, J= 8.4 Hz), 8.01 (2H, dd, J =6.8, 1.6 Hz), 7.84 (1H, d, J= 9.2 Hz), 7.81 (1H, d, J= 8.4 Hz), 7.56 (2H, m), 7.53-7.49 (2H, m), 7.42 (1H, ddd, J= 8.0, 6.8, 0.8 Hz), 7.39 (1H, d, J= 9.2 Hz), 4.19 (2H, t, J = 6.4 Hz), 1.82 (1H, app sept, J = 6.8 Hz), 1.68 (2H, q, J = 6.8 Hz), 0.91 (6H, d, J = 6.8 Hz).13C NMR (CDCI3, 101 MHz) 5: 153.5, 147.4, 136.8, 130.9, 129.3, 129.2, 129.1, 127.9, 127.6, 124.5, 123.2, 122.7, 116.4, 69.3, 38.2, 25.0, 22.6. HRMS (ESI) calculated for C21H23N2O [M]+: m / z 390.2178, found m / z 390.2176. 2-(lsopentyloxy)naphthalen-1-amine (75) 75 A solution of azo derivative 74 (50 mg, 0.16 mmol, 1.0 eq) in dry MeOH (4 mL) was cooled down to 0°C, and treated with palladium on carbon 10wt % (5 mg). The reaction mixture was flushed with N2, and the N2 atmosphere was then replaced with a hydrogen atmosphere and the reaction was stirred at r.t. for 16 h. The mixture was then filtered through celite, and concentrated in vacuo onto silica gel. The crude product was purified by FCC (PE:EtOAc 8:2) to give the desired product as a white solid (8 mg, 22%). 1H NMR (CDCI3,400 MHz) 5: 7.76 (1H, dd, J = 8.0, 0.8 Hz), 7.74 (1H, dd, J = 8.0, 0.8 Hz), 7.42 (1H, ddd, J= 8.4, 6.8, 1.6 Hz), 7.34-7.30 (2H, m), 7.24 (1H, d, J= 9.2 Hz), 4.14 (2H, t, J = 6.8 Hz), 1.88 (1H, app sept, J = 6.8 Hz), 1.75 (2H, q, J = 6.8 Hz), 0.98 (6H, d, J = 6.8 Hz). 13C NMR (CDCI3, 101 MHz) 5: 142.0, 129.4, 128.4, 125.0, 124.1, 123.6, 120.4, 118.7, 118.6, 114.8, 68.1, 38.5, 25.2, 22.7. HRMS (ESI) calculated forCi5H20NO [M]+: m / z 230.1538, found m / z 230.1539. ( / ?9-Dimethyl (2-(isopentyloxy)naphthalen-1-yl)aspartatl( / ?9-89) (^)-89 A solution of amine 75 (55 mg, 0.24 mmol, 1.0 eq) in dry DCM (10 mL) was treated with 2,6-lutidine (60 pL, 0.48 mmol, 2.0 eq) and stirred for 20 min before the addition of a solution of triflate (SJ-12 (211 mg, 0.72 mmol, 3.0 eq) in dry DCM (5 mL). The reaction was heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t. and quenched with water (10 mL). The layers were separated, and the aq. layer was extracted with DCM (10 mL x 2). The organic layers were combined and washed with a sat. solution of copper sulfate (20 mL x 3), water (20 mL), and brine (20 mL x 2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a purple oil (34 mg, 38%). 1H NMR (CDCI3,400 MHz) 5: 8.06 (1H, dd, J = 8.4, 0.8 Hz), 7.74 (1H, dd, J = 8.0, 0.8 Hz), 7.51 (1H, d, J = 8.8 Hz), 7.45 (1H, ddd, J= 8.4, 6.8, 1.2 Hz), 7.32 (1H, ddd, J= 8.0, 6.8, 1.2 Hz), 7.22 (1H, d, J = 8.8 Hz), 4.50 (1H, t, J = 5.6 Hz), 4.12 (2H, q, J = 6.8 Hz), 3.72 (3H, s), 3.63 (3H, s), 2.88 (2H, d, J = 6.0 Hz), 1.85 (1H, app sept, J = 6.8 Hz), 1.73 (2H, q, J = 6.8 Hz), 0.99 (3H, d, J = 6.4 Hz) 0.97 (3H, d, J= 6.4 Hz). 13C NMR (CDCI3, 101 MHz) 5: 173.4, 171.5, 148.6, 129.7, 128.4, 126.1, 123.9, 123.7, 122.0, 114.2, 67.9, 57.4, 52.4, 51.9, 38.3, 37.3, 25.1, 22.7, 22.7. One unresolved carbon. HRMS (ESI) calculated for C21H28NO5 [M]+: m / z 374.1970, found m / z 374.1962. [a]D22 7: 14.6 (c = 0.002 g / mL, DCM) (SJ-Dimethyl (2-(isopentyloxy)naphthalen-1-yl)aspartate ((S / -89) (5)-89 A solution of amine 75 (55 mg, 0.24 mmol, 1.0 eq) in dry DCM (10 mL) was treated with 2,6-lutidine (60 pL, 0.48 mmol, 2.0 eq) and stirred for 20 min before the addition of a solution of trilte (R)-12 (211 mg, 0.72 mmol, 3.0 eq) in dry DCM (5 mL). The reaction was heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t. and quenched with water (10 mL). The layers were separated, and the aq. layer was extracted with DCM (10 mL x 2). The organic layers were combined and washed with a sat. solution of copper sulfate (20 mL x 3), water (20 mL), and brine (20 mL x 2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a purple oil (25 mg, 28%). [a]D22 7: -10.2 (c = 0.0019 g / mL, DCM) A / -(6-(lsopentyloxy)-5-nitronaphthalen-2-yl)acetamide (99) A solution of amine 61 (300 mg, 1.1 mmol, 1.0 eq) in chloroform (5 mL) was treated with 4-dimethylaminopyridine (10 mg, 0.1 mmol, 0.1 eq) and acetic anhydride (124 pL, 1.3 mmol, 1.2 eq) before being heated up to 60 °C for 4 h. The reaction was then cooled down to r.t. and diluted with chloroform (20 mL). The solution was then washed with water (20 mL x 2) and brine (20 mL). The organic layer was recuperated, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc (elution gradient 5:5 to 4:6)) to yield the desired product as a yellow solid. (255 mg, 74%) M.p.: 139.9 °C; 1H NMR (CDCI3,400 MHz) 5: 8.38 (1H, d, J = 1.6 Hz), 7.86 (1H, d, J= 9.2 Hz), 7.60 (1H, d, J= 9.2 Hz), 7.44 (1H, s), 7.37 (1H, dd, J= 9.2, 2.0 Hz), 7.30 (1H, d, J= 9.2 Hz), 4.22 (2H, t, J = 6.8 Hz), 2.24 (3H) 1.83 (1H, app sept, J = 6.4 Hz), 1.70 (2H, q, J = 6.8 Hz), 0.95 (6H, d, J = 6.8 Hz).13C NMR (CDCh, 101 MHz) 5: 168.7, 147.8, 136.3, 134.7, 131.9, 128.7, 122.8, 122.7, 121.5, 116.7, 115.1,68.8, 37.9, 24.9, 24.8, 22.6.HRMS (ESI) calculated for C17H21N2O4 [M]+: m / z 317.1498, found m / z 317.1496. A / -(5-Amino-6-(isopentyloxy)naphthalen-2-yl)acetamide (98) A solution of nitro compound 99 (100 mg, 0.32 mmol, 1.0 eq) in dry MeOH (3 mL) was treated with ammonium formate (400 mg), and palladium on carbon 10wt % (10 mg). The mixture was heated up to 60 °C and stirred at this temperature for 5 h before being allowed to cool back down to r.t. The reaction was filtered through celite, and the celite plug was washed with EtOAc (20 mL). The filtrate was washed with water (15 mL x 2), brine (15 mL), dried (Na2SO4), filtered and concentrated in vacuo. The crude product was purified through a plug of silica (Hex:EtOAc 4:6) to yield the desired compound as a white solid (56 mg, 62%). M.p. 126.0 °C; 1H NMR (MeOD4, 400 MHz) 5: 8.03 (1H, d, J = 2.0 Hz), 7.87 (1H, d, J= 9.2 Hz), 7.47 (1H, dd, J= 9.2, 2.0 Hz), 7.25 (1H, d, J= 8.8 Hz), 7.20 (1H, d, J= 8.8 Hz), 4.14 (2H, t, J = 6.4 Hz), 2.16 (3H, s), 1.91 (1H, app sept, J = 6.4 Hz), 1.74 (2H, q, J = 6.8 Hz), 1.01 (6H, d, J= 6.8 Hz). 13C NMR (MeOD4, 101 MHz) 5: 171.7, 143.0, 135.4, 131.4, 131.2, 122.9, 122.8, 120.2, 119.2, 118.3, 116.7, 69.2, 39.6, 26.3, 23.8, 23.0. HRMS (ESI) calculated for C17H23N2O2 [M]+: m / z 287.1763, found m / z 287.1754. ( / ?9-Dimethyl (6-acetamido-2-(isopentyloxy)naphthalen-1 -yl I part ate ((R)-97) A solution of amine 98 (60 mg, 0.21 mmol, 1.0 eq) in dry DCM (7 mL) was treated with a solution of triflate (SJ-12 (197 mg, 0.63 mmol, 3.0 eq) in dry DCM (7 mL) followed by 2,6-lutidine (49 pL, 0.42 mmol, 2.0 eq). The resulting mixture was warmed up to 40 °C, and stirred at this temperature for 48 h, before being allowed to cool down to r.t. The reaction was quenched with water (10 mL), and the biphasic mixture was separated. The aqueous phase was extracted with DCM (10 mL), and the organic layers were combined and washed With a sat aq. solution of copper sulfate (15 mL x 3), water (15 mL), and brine (15 mL). The solution was dried (MgSO4), filtered and concentrated in vacuo. The crude product was purified using FCC (DCM:MeOH (elution gradient 100:0 to 95:5)) to yield the title compound as a yellow oil (34 mg, 38%). 1H NMR (MeOD4, 400 MHz) 5: 8.11 (1H, d, J = 2.0 Hz), 7.99 (1H, d, J= 8.8 Hz), 7.49 (1H, dd, J= 9.2, 2.4 Hz), 7.46 (1H, d, J= 9.6 Hz), 7.31 (1H, d, J= 9.2 Hz), 4.48 (1H, t, J= 6.0 Hz), 4.13 (2H, m), 3.66 (3H, s), 3.64 (3H, s), 2.86 (1H, d, J= 5.6 Hz), 2.85 (1H, d, J= 5.6 Hz), 2.17 (3H, s), 1.90 (1H, app sept, J = 6.8 Hz), 1.73 (2H, q, J = 6.8 Hz), 1.01 (3H, d, J = 6.4 Hz), 1.00 (3H, d, J = 6.4 Hz).13C NMR (MeOD4, 151 MHz) 5: 174.7, 173.1, 171.8, 148.7, 135.5, 131.4, 130.1, 126.7, 124.4, 123.7, 121.2, 118.5, 116.2, 68.9, 58.5, 52.6, 52.3, 39.5, 37.9, 26.2, 23.8, 23.1, 23.0.HRMS (ESI) calculated for C23H31N2O6 [M]+: m / z 431.2182, found m / z 431.2177. [a]D22 7: 22.5 (c = 0.018 g / mL, DCM) (SJ-Dimethyl (6-acetamido-2-(isopentyloxy)naphthalen-1-yl)aspartate ((SJ-97) A solution of amine 98 (55 mg, 0.19 mmol, 1.0 eq) in dry DCM (7 mL) was treated with a solution of triflate (SJ-12 (173 mg, 0.59 mmol, 3.0 eq) in dry DCM (7 mL) followed by 2,6-lutidine (44 pL, 0.38 mmol, 2.0 eq). The resulting mixture was warmed up to 40 °C, and stirred at this temperature for 48 h, before being allowed to cool down to r.t. The reaction was quenched with water (10 mL), and the biphasic mixture was separated. The aqueous phase was extracted with DCM (10 mL), and the organic layers were combined and washed With a sat aq. solution of copper sulfate (15 mL x 3), water (15 mL), and brine (15 mL). The solution was dried (MgSO4), filtered and concentrated in vacuo. The crude product was purified using FCC (DCM:MeOH (elution gradient 100:0 to 95:5)) to yield the title compound as a yellow oil (25 mg, 31%). [a]D22 7: -25.6 (c = 0.0034 g / mL, DCM) 1 -(lsopentyloxy)-2-nitrobenzene (93) 93 A solution of 2-nitrophenol (700 mg, 5.03 mmol, 1.0 eq) in dry DMF (30 mL) was treated with potassium carbonate (1.04 g, 7.56 mmol, 1.5 eq), and the mixture was allowed to stir at r.t. for 15 min before the addition of 1-bromo-3-methyl butane (1.26 mL, 7.56 mmol, 1.5 eq). The reaction mixture was heated up to 60°C, and stirred for 36 h. The reaction was cooled down to r.t. and quenched with a sat. aq. solution of ammonium chloride (50 mL). The mixture was extracted with EtOAc (40 mL x 3). The combined organic phases were washed with water (70 mL x 2), brine (70 mL x 2), dried (Na2SO4), filtered and concentrated in vacuo. The crude product was purified through a plug of silica gel (Hex:EtOAc 85:15) giving the title compound as a yellow oil (915 mg, 87%). 1H NMR (CDCI3,400 MHz) 6: 7.80 (1H, dd, J= 8.0, 1.6 Hz), 7.49 (1H, ddd, J= 8.8, 7.6, 2.0 Hz), 7.06 (1H, dd, J= 8.4, 0.8 Hz), 6.99 (1H, ddd, J= 8.4, 7.2, 1.2 Hz), 4.11 (2H, t, J= 6.4 Hz), 1.86 (1H, app sept, J = 6.8 Hz), 1.72 (2H, q, J = 6.8 Hz), 0.95 (6H, d, J = 6.4 Hz). 13C NMR (CDCI3,101 MHz) 5: 152.5, 140.0, 134.0, 125.6, 120.0, 114.4, 68.0, 37.6, 24.9, 22.5. HRMS (ESI) calculated forCnHi6NO3 [M]+: m / z 210.1123, found m / z 210.1125. 2-(lsopentyloxy)aniline (91) 91 A 0°C solution of nitro benzene 93 (486 mg, 2.32 mmol, 1.0 eq) in EtOAc (10 mL) was treated with palladium on carbon 10wt % (49 mg), and the reaction mixture was flushed with N2. The N2 atmosphere was then replaced with a hydrogen atmosphere, and the reaction was stirred at r.t. for 12 h. The mixture was then filtered through celite, dried (Na2SO4), filtered and concentrated in vacuo to give the desired amine 91 as a magenta oil (351 mg, 84%). 1H NMR (DMSO-D6,400 MHz) 6: 6.74 (1H, dd, J = 8.4, 0.8 Hz), 6.61 (1H, ddd, J = 8.8, 7.6, 1.2 Hz), 6.57 (1H, dd, J= 8.0, 2.0 Hz), 6.45 (1H, ddd, J= 7.6, 6.8, 2.0 Hz), 4.56 (2H, s), 3.90 (2H, t, J = 6.8 Hz), 1.78 (1H, app sept, J = 6.8 Hz), 1.59 (2H, q, J = 6.8 Hz), 0.89 (6H, d, J = 6.8 Hz). 13C NMR (DMSO-D6,101 MHz) 5 146.1, 138.2, 121.3, 116.7, 114.3, 112.0, 66.5, 38.1,25.1, 23.0. HRMS (ESI) calculated forCnHisNO [M]+: m / z 180.1395, found m / z 180.1383. ( / ?9-Dimethyl (2-(isopentyloxy)phenyl)aspartate ((R)-87) (Rys’? A solution of amine 91 (163 mg, 0.91 mmol, 1.0 eq) in dry DCM (20 mL) was treated with 2,6-lutidine (218 pL, 1.82 mmol, 2.0 eq), and the reaction was allowed to stir for 20 min before the addition of triflate (S / -12 (535 mg, 1.82 mmol, 2 eq) in dry DCM (5 mL). The reaction mixture was then heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t. and quenched with water (20 mL). The layers were separated, and the aqueous layer was extracted with DCM (20 mL x 2). The organic layers were combined and washed with a sat. aq. solution of copper sulfate (50 mL x 3), water (50 mL) and brine (50 mL x2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a yellow oil (149 mg, 43%). 1H NMR (CDCI3,400 MHz) 5: 6.82 (1H, tt, J= 7.2, 1.2 Hz), 6.77 (1H, dt, J= 8.0, 1.6 Hz), 6.69 (1H, tt, J = 8.0, 1.2 Hz), 6.61 (1H, dt, J= 8.0, 1.2 Hz), 4.48 (1H, t, J= 6.8 Hz), 4.00 (2H, t, J = 6.8 Hz), 3.73 (3H, s), 3.69 (3H, s), 2.89 (2H, d, J = 6.0 Hz), 1.83 (1H, app sept, J = 6.4 Hz), 1.73 (2H, q, J = 6.8 Hz), 0.97 (6H, d, J = 6.8 Hz). 13C NMR (CDCI3, 101 MHz) 5: 172.9, 171.0, 146.8, 136.2, 121.0, 118.0, 111.0, 110.6, 66.9, 53.2, 52.6, 52.0, 38.0, 37.4, 25.3, 22.7. HRMS (ESI) calculated for C17H26NO5 [M]+: m / z 324.1816, found m / z 324.1805. [a]D22 7: 4.7 (c = 0.0012 g / mL, DCM) (SJ-Dimethyl (2-(isopentyloxy)phenyl)aspartate ((SJ-87) (5)-87 A solution of amine 91 (153 mg, 0.85 mmol, 1.0 eq) in dry DCM (20 mL) was treated with 2,6-lutidine (200 pL, 1.71 mmol, 2.0 eq), and the reaction was allowed to stir for 20 min before the addition of triflate (R)-^2 (503 mg, 1.71 mmol, 2.0 eq) in dry DCM (5 mL). The reaction mixture was then heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t. and quenched with water (20 mL). The layers were separated, and the aqueous layer was extracted with DCM (20 mL x 2). The organic layers were combined and washed with a sat. aq. solution of copper sulfate (50 mL x 3), water (50 mL) and brine (50 mL x x2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a yellow oil (186 mg, 67%). [a]D22 7: -3.7 (c = 0.001 g / mL, DCM) 1,3-Bis(3-methylbutoxy)-2-nitrobenzene (31) A solution of 2-nitroresorcinol (1.14 g, 7.36 mmol, 1.0 eq) in dry DMF (20 mL) was treated with potassium carbonate (2.54 g, 18.39 mmol, 2.5 eq). The mixture was left to stir for 15 min, and then 1-bromo-3-methyl butane (2.2 mL, 18.39 mmol, 2.5 eq) was added. The reaction mixture was warmed up to 60 °C and allowed to stir at this temperature for 24 h. The mixture was then cooled down to r.t.,and diluted with EtOAc (30 mL). The biphasic mixture was washed with water (30 mL x 5), and brine (30 mL x 2). The organic phase was recovered, dried (Na2SO4), filtered and concentrated in vacuo to give the desired product as a yellow oil (1.85 g, 95%). The product was used in the next reaction without further purification. 1H NMR (CDCI3, 600 MHz) 5: 7.25 (1H, t, J= 9.0 Hz), 6.57 (2H, d, J= 9.0 Hz), 4.04 (4H, t, J = 6.6 Hz), 1.75 (2H, app sept, J = 6.6 Hz), 1.63 (4H, q, J = 6.6 Hz), 0.91 (12H, d, J = 6.6 Hz). 13C NMR (CDCI3, 151 MHz) 5: 151.4, 132.6, 130.9, 105.1,67.9, 37.5, 24.9, 22.5. HRMS (ESI) calculated for Ci6H26NO4 [M+H]+: m / z 296.1851, found m / z 296.1856. 2,6-Bis(isopentyloxy)aniline (94) A 0 °C solution of nitro benzene 31 (700 mg, 2.37 mmol, 1 eq) in dry MeOH (12 mL) was treated with ammonium formate (1.5 g) and palladium on carbon 10wt % (70 mg). The reaction was heated up to 60 °C and stirred at this temperature for 16 h. The mixture was then cooled back down to r.t., filtered through celite, and concentrated in vacuo. The residue was dissolved in EtOAc (30 mL), washed with water (20 mL x 3) and brine (20 mL x 2). The organic layer was dried (Na2SO4), filtered and concentrated in vacuo to yield the product as a dark brown oil (545 mg, 87%). The product was used without further purification. 1H NMR (CDCI3,400 MHz) 5: 6.66 (1H, t, J = 8.4 Hz), 6.50 (2H, d, J = 8.4 Hz), 4.01 (4H, t, J = 6.4 Hz), 1.84 (2H, app sept, J = 6.8 Hz), 1.70 (4H, q, J = 6.4 Hz), 0.95 (12H, d, J = 6.8 Hz). 13C NMR (CDCI3, 101 MHz) 5 147.2, 125.1, 117.3, 104.9, 67.0, 38.2, 25.2, 22.7. HRMS (ESI) calculated for Ci6H28NO2 [M]+: m / z 266.2141, found m / z 266.2115. ( / ?9-Dimethyl (2,6-bis(isopentyloxy)phenyl)aspartate ((R)-88) 0 (^)-88 A solution of amine (94) (227 mg, 0.85 mmol, 1.0 eq) in dry DCM (20 mL) was treated with 2,6-lutidine (198 pL, 1.71 mmol, 2.0 eq) the reaction was allowed to stir for 20 min, before the addition of triflate (SJ-12 (502 mg, 1.71 mmol, 2.0 eq) in dry DCM (5 mL). The solution was heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t., quenched with water (20 mL), and the layers were separated. The aqueous layer was extracted with DCM (20 mL x 2), and the organic phases were combined and washed with a sat. aq. solution of copper sulfate (50 mL x 3), water (50 mL) and brine (50 mL x 2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a yellow oil (157 mg, 45%). 1H NMR (CDCI3,400 MHz) 6: 6.76 (1H, t, J = 8.0 Hz), 6.49 (2H, d, J = 8.4 Hz), 4.80 (1H, t, J = 5.2 Hz), 3.97 (4H, t, J = 6.8 Hz), 3.70 (3H, s), 3.64 (3H, s), 2.84 (1H, dd, J = 16.0, 4.8 Hz), 2.77 (1H, dd, J = 16.0, 4.8 Hz), 1.82 (2H, app sept, J = 6.8 Hz), 1.69 (4H, q, J = 6.4 Hz), 0.95 (12H, d, J = 6.4 Hz). 13C NMR (CDCI3, 101 MHz,) 5: 173.8, 171.5, 150.3, 125.0, 120.5, 105.3, 67.2, 55.0, 52.2, 51.8, 38.2, 38.1,25.2, 22.7. HRMS (ESI) calculated for C22H35NO6 [M]+: m / z 410.2541, found m / z 410.2537. [a]D22 7: 5.1 (c= 0.002 g / mL, DCM) (SJ-Dimethyl (2,6-bis(isopentyloxy)phenyl)aspartate ((S / -88) 0 14 U 12 (5)-88 A solution of amine (94) (280 mg, 1.05 mmol, 1.0 eq) in dry DCM (20 mL) was treated with 2,6-lutidine (245 pL, 2.11 mmol, 2.0 eq) the reaction was allowed to stir for 20 min, before the addition of triflate (R)-^2 (620 mg, 2.11 mmol, 2.0 eq) in dry DCM (5 mL). The solution was heated up to 40 °C, and allowed to stir at this temperature for 36 h. The reaction was then cooled down to r.t., quenched with water (20 mL), and the layers were separated. The aqueous layer was extracted with DCM (20 mL x 2), and the organic phases were combined and washed with a sat. aq. solution of copper sulfate (50 mL x 3), water (50 mL) and brine (50 mL x 2). The organic layer was recovered, dried (MgSO4), filtered and concentrated in vacuo. The crude product was then purified using FCC (Hex:EtOAc 9:1) to yield the desired product as a yellow oil (243 mg, 57%). [a]D227: -6.4 (c = 0.001 g / mL, DCM) Additional Examples 1 -(lsopentyloxy)-2-nitrobenzene (4) 4 2-nitrophenol (501 mg, 3.59 mmol, 1.0 eq) was dissolved in dry DMF (21 mL) and treated with potassium carbonate (745 mg, 5.39 mmol, 1.5 eq), and the mixture was left to stir at r.t. for 17 min before the addition of 1-bromo-3-methyl butane (646 pL, 5.39 mmol, 1.5 eq). The reaction mixture was left to stir at 60 °C for 25 h. The reaction was cooled down to r.t. and quenched with water (50 mL). The mixture was extracted with EtOAc (40 mL x 3). The combined organic phases were washed with water (50 mL x 5) and brine (50 mL x 2), then dried (Na2SO4), filtered, and concentrated in vacuo. The crude product was purified through a plug of silica gel (Hex:EtOAc 85:15) to give the title compound as a yellow oil (681 mg, 91%). 1H NMR (CDCI3, 400 MHz) 5: 7.80 (1H, dd, J= 8.0, 1.7 Hz), 7.50 (1H, ddd, J= 8.5, 7.4, 1.7 Hz), 7.07 (1H, dd, J= 8.4, 1.0 Hz), 6.99 (1H, ddd, J= 8.1, 7.4, 1.1 Hz), 4.13 (2H, t, J= 6.5 Hz), 1.87 (1H, app sept, J = 6.7 Hz), 1.73 (2H, q, J = 6.6 Hz), 0.96 (6H, d, J = 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 5: 152.6, 140.2, 134.0, 125.6, 120.1, 114.5, 68.1, 37.7, 25.0, 22.6. \ / max / cnT1: 2956, 1607, 1470, 1522, 1350, 1279. 2-(lsopentyloxy)aniline (5) A solution of nitrobenzene 4 (614 mg, 2.39 mmol, 1.0 eq) in EtOAc (12 mL) was cooled down to 0 °C. The mixture was then treated with palladium on carbon 10 wt% (61 mg) and flushed with nitrogen. The nitrogen atmosphere was replaced with a hydrogen atmosphere, and the reaction was allowed to stir at r.t. for 20 h. The mixture was then filtered through a celite plug, dried (MgSO4), filtered, and concentrated in vacuo to give the title compound as a magenta oil (415 mg, 96%). The compound was used without any further purification. The spectral data matches that reported in the literature. 1H NMR (CDCI3, 400 MHz) 5: 6.91-6.85 (1H, m), 6.83-6.78 (3H, m), 4.03 (2H, t, J = 6.6 Hz), 1.85 (1H, app sept, J = 6.8 Hz), 1.72 (2H, q, J = 6.6 Hz), 0.95 (6H, d, J = 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 5: 147.7, 133.8, 121.0, 120.3, 116.6, 111.6, 66.8, 38.2, 25.2, 22.7. HRMS (ESI) calculated for C11H17NO [M]+: m / z 180.1383, found m / z 180.1376. \ / max / cm-1: 3472, 3375, 2955, 1613, 1460, 1504, 1217. Methyl 3-((2(isopentyloxy)phenyl)amino)propanoate (8) OMe Aniline 5 (654 mg, 3.62 mmol, 1.0 eq) was added to methyl 3-bromo-propionate (395 pL, 3.62 mmol, 1.0 eq) and the mixture was heated at 100°C in a microwave for 25 min. The progress of the reaction was assessed by 1H NMR. Upon completion, the reaction was diluted with DCM (15 mL) and washed with water (25 mL x 3) and brine (25 mL x 2). The reaction was then dried (MgSO4), filtered, and concentrated in vacuo. The crude product was purified by flash column chromatography (silica gel, elution gradient: 100% Hexanes to Hex:EtOAc 50:50), to give the title compound as a light-yellow oil (250 mg, 26%). 1H NMR (CDCI3, 400 MHz) 5: 6.86 (1H, dt, J =7.7, 1.5 Hz), 6.76 (1H, dd, J = 8.0, 1.5 Hz), 6.68-6.62 (2H, m), 4.00 (2H, t, J= 6.6 Hz), 3.70 (3H, s), 3.49 (2H, t, J= 6.8 Hz), 2.65 (2H, t, J = 6.6 Hz), 1.83 (1H, app sept, J = 6.6 Hz), 1.70 (2H, q, J = 6.4 Hz), 0.97 (6H, d, J = 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 5: 172.8, 146.6, 137.7, 121.2, 116.9, 110.7, 110.0, 66.8, 51.8, 39.3, 38.2, 34.1, 25.3, 22.7. HRMS (ESI) calculated forCi5H23NO3 [M]+: m / z 266.1751, found m / z 266.1748. \ / max / cm-1: 3438, 2951, 1731, 1599, 1509, 1449, 1246, 1212, 1173, 1019. Methyl 2,2-dimethyl-3-(((trifluoromethyl)sulfonyl)oxy)propanoate (16) 0 TfO^^^OMe 16 Methyl 3-hydroxy-2,2-dimethyl propanoate (193 pL, 1.51 mmol, 1.0 eq) was dissolved in dry DCM (0.6 mL) and treated with 2,6-lutidine (350 pL, 3.03 mmol, 2.0 eq). The reaction was cooled to -78 °C and allowed to stir for 20 min. Trifluoromethane sulfonic anhydride (373 pL, 2.27 mmol, 1.5 eq) was dissolved in dry DCM (0.3 mL) and added dropwise to the reaction. The reaction was left to stir at -78 °C for 1 h 30 min. The reaction was allowed to warm to room temperature before being quenched with water (5 mL). The reaction was then washed with water (25 mL x 3), a sat. solution of copper sulfate (25 mL), and brine (25 mL x 2). The crude product was dried (MgSO4), filtered, and concentrated in vacuo. This yielded the title compound as a yellow oil (280 mg, 70%). The compound was used without further purification. 1H NMR (CDCI3, 400 MHz) 5: 4.50 (2H, s), 3.74 (3H, s), 1.30 (6H, s). 13C NMR (CDCI3, 101 MHz) 5: 174.3, 117.1, 81.1, 52.6, 43.1, 21.9. HRMS (ESI) calculated for C7H11F3O5S [M+ Na]: m / z 264.8279, found m / z 264.0283. \ / max / cm-1: 2984, 1735, 1412, 1197, 1141, 941. Methyl 3-((2-(isopentyloxy)phenyl)amino)-2,2-dimethylpropanoate (13) Aniline 5 (25.6 mg, 0.14 mmol, 1.9 eq) was added to an inseparable mix of methyl 3-hydroxy-2,2- dimethyl propanoate and dimethyl propanoate 16, within this mixture the proportions of dimethyl propanoate 16 as calculated by 1H NMR were: (19.8 mg, 75 mmol, 1.0 eq). The reaction was heated to 100 °C in the microwave for 13 min. The reaction was then diluted with EtOAc (15 mL) and washed with water (25 mL x 3) and brine (25 mL x 2). The reaction was then dried (MgSO4), filtered, and concentrated in vacuo. The crude product was purified in a column of silica gel (Hex:EtOAc 90:10). This afforded the title compound as a dark yellow oil (10.8 mg, 49%). 1H NMR (CDCh, 400 MHz) 5: 6.84 (1H, dt, J= 7.9, 1.4 Hz), 6.75 (1H, dd, J = 7.9, 1.5 Hz), 6.67-6.61 (2H, m), 4.01 (2H, t, J= 13.1,6.6 Hz), 3.67 (3H, s), 3.25 (2H, s), 1.84 (1H, app sept., J= 7.2 Hz), 1.70 (2H, q, J = 6.4 Hz), 1.28 (6H, s), 0.97 (6H, d, J=Q.Q Hz). 13C NMR (CDCI3, 101 MHz) 5: 177.4, 146.3, 138.7, 121.2, 116.4, 110.7, 110.0, 66.8, 52.5, 52.0, 43.8, 38.3, 25.4, 23.6, 22.8. HRMS (ESI) calculated for C17H27NO3 [M]+: m / z 294.2064, found m / z 294.2059. \ / max / cm-1: 3426, 2954, 1730, 1602, 1472, 1249, 1212, 1147. Methyl 2-((2-(isopentyloxy)phenyl)amino)benzoate (17) Aniline 5 (157 mg, 0.84 mmol, 1.2 eq) in toluene (10 mL) was treated with methyl-2-bromobenzote (98 pL, 0.70 mmol, 1.0 eq), CS2CO3 (315 mg, 0.97 mmol, 1.4 eq), and BINAP (37 mg, 0.06 mmol, 0.08 eq). The reaction mixture was then bubbled under argon for 10 min. Pd(OAc)2 (9.5 mg, 0.04 mmol, 0.05 eq) was added to the reaction mixture, which was then heated to 120°C and allowed to stir for 23 h. The reaction was taken off heat and cooled to r.t. before being quenched with water (50 mL) and brine (20 mL). The reaction was extracted with EtOAc and the organic phase then washed with 1M aq. HCI (60 mL x 2) and brine (50 mL x 2). The reaction was then dried (Na2SO4), filtered, and concentrated in vacuo. The crude product was filtered through a plug of silica gel (Hex: EtOAc 80:20) giving the title compound as a yellow oil (189 mg, 60%). 1H NMR (CDCI3, 400 MHz) 6: 7.97-7.95 (1H, m), 7.43 (1H, dd, J =7.7, 1.6 Hz), 7.34-7.29 (2H, m), 7.00 (1H, ddd, J= 8.2, 7.1, 1.6 Hz), 7.02-6.88 (2H, m), 6.73 (1H, ddd, J= 8.1, 5.5, 2.7 Hz), 4.04 (2H, t, J = 6.6 Hz), 3.90 (3H, s), 1.86 (1H, app sept, J = 6.9 Hz), 1.71 (2H, q, J = 6.6 Hz), 0.93 (6H,d, J = 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 6: 168.6, 151.0, 147.3, 133.9, 131.7, 130.6, 123.1, 120.5, 120.4, 117.2, 114.5, 113.0, 112.4, 67.0, 51.8, 38.1, 25.0, 22.7. HRMS (ESI) calculated for C19H23NO3 [M]+: m / z 314.1751, found m / z 314.1742. \ / max / cm-1: 3329, 2952, 1692, 1594, 1453,1524, 1257, 1226, 1083. 1 -(lsopentyloxy)-3-methyl-2-nitrobenzene (21) 2 3-Methyl-2-nitrophenol (203 mg, 1.31 mmol, 1.0 eq) was dissolved in dry DMF (10 mL), treated with potassium carbonate (283 mg, 1.96 mmol, 1.5 eq), and the mixture was left to stir at r.t. for 30 min before the addition of 1-bromo-3-methyl butane (234 pL, 1.96 mmol, 1.5 eq). The reaction mixture was left to stir at 60 °C for 68 h. The reaction was cooled down to r.t. and quenched with a sat. solution of ammonium chloride (10 mL). The mixture was extracted with EtOAc (30 mL x 3). The combined organic phases were washed with water (30 mL x 3) and brine (25 mL x 3), then dried (MgSO4), filtered, and concentrated in vacuo. The crude product was purified through a plug of silica gel (Hex: EtOAc 80:20) to give the title compound as a yellow oil (263 mg, 89%). 1H NMR (CDCI3, 400 MHz) 5: 7.26 (1H, t, J= 8.1 Hz), 6.86-6.81 (2H, m), 4.06 (2H, t, J= 7.8 Hz), 2.29 (3H, s), 1.78 (1H, app sept, J = 6.6 Hz), 1.65 (2H, q, J = 6.4 Hz), 0.93 (6H, d, J = 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 5: 150.4, 142.6, 131.0, 130.6, 122.4, 111.0, 67.9, 37.6, 25.0, 22.6, 17.0. \ / max / cm-1: 2956, 1612, 1469, 1522, 1369, 1287. 2-(lsopentyloxy)-6-methylaniline (19) Nitrobenzene 21 (236 mg, 1.06 mmol, 1.0 eq) was dissolved in MeOH (10 mL). Ammonium formate (1.14 g, 18.1 mmol, 17 eq) and palladium on carbon 10 wt% (25 mg) were added to the solution which was then left to stir under reflux at 50 °C for 24 h. The reaction was allowed to cool down to r.t. The reaction was filtered through celite (with EtOAc) and then washed with water (50 mL x 2) and brine (25 mL x 3). The reaction was then dried (MgSO4), filtered, and concentrated in vacuo. This gave the desired product as an orange oil (204 mg, 90%), which was used without any further purification. 1H NMR (CDCh, 400 MHz) 5: 6.71-6.69 (3H, m), 4.02 (2H, t, J= 6.6 Hz), 2.23 (3H, s), 1.85 (1H, app sept, J = 6.8 Hz), 1.72 (2H, q, J = 6.6 Hz), 0.97 (6H, d, J = 6.6 Hz). 13C NMR (CDCh, 101 MHz) 5: 147.0, 133.1, 122.6, 109.2, 66.9, 38.3, 25.3, 22.7, 17.4, two unresolved carbons. HRMS (ESI) calculated for C12H19NO [M]+: m / z 193.1539, found m / z 194.1540. \ / max / cm-1: 3476, 3380, 2955, 1615, 1487, 1278. Methyl 2-((2-(isopentyloxy)-6-methylphenyl)amino)benzoate (18) Aniline 19 (195 mg, 1.01 mmol, 1.2 eq) in dry toluene (8 mL) was treated with methyl 2-bromobenzoate (118 pL, 0.84 mmol, 1.0 eq), CS2CO3 (384 mg, 1.17 mmol, 1.4 eq), and BINAP (42.7 mg, 0.07 mmol, 0.08 eq). The reaction was stirred under argon for 10 min. Pd(OAc)2 (11.1 mg, 0.04 mmol, 0.05 eq) was added and the reaction was left to stir under reflux at 120 °C for 4 days. Reaction progress was assessed by TLC. Upon completion, the reaction was allowed to cool down to room temperature. The reaction was quenched with water (20 mL) and brine (20 mL) and then extracted with EtOAc (15 mL x 3). The combined organic phase was washed with 1M aq. HCI (20 mL x 2) and brine (50 mL x 3). The reaction was then dried (MgSO4), filtered, and concentrated in vacuo. The crude product was purified by flash column chromatography (silica gel, Hex:EtOAc 9:1). This gave the title compound as a light orange oil (29.8 mg, 11%). 1H NMR (CDCh, 400 MHz) 5: 7.93 (1H, dd, J= 8.0, 1.3 Hz), 7.19 (1H, ddd, J= 8.6, 6.1, 1.7 Hz), 7.12 (1H, t, J= 7.9 Hz), 6.89-6.79 (2H, m), 6.63 (1H, ddd, J= 8.1, 5.7, 1.2 Hz), 6.31 (1H, dd, J = 8.5, 1.2 Hz,), 3.93-3.90 (5H, m), 2.23 (3H, s), 1.58 (1H, app sept, J = 6.4 Hz), 1.49 (2H, q, J= 6.4 Hz), 0.79 (6H, d, J= 6.6 Hz). 13C NMR (CDCI3, 101 MHz) 5: 169.1, 155.1, 152.0, 137.4, 133.9, 131.3, 128.2, 126.4, 122.6, 115.8, 113.8, 110.9, 110.4, 66.9, 51.6, 38.0, 24.9, 22.5, 18.3. HRMS (ESI) calculated forC2oH25N03 [M]+: m / z 328.1907, found m / z 328.1916 Biological Results The compounds of the invention were tested, and the results were compared to compounds (R)-4 and (SJ-4, which are previously reported in the art. Table 1. Cell viability assay of HDFs (Human Dermal Fibroblasts) with the compounds of the invention. Cell viability HDFs Conditions % growth inhibition Control vehicle -0.7149 (R)-4 (100 ng / mL) -14.0704 (S)-4 (100 ng / mL) -5.7358 (R)-87 (100 ng / mL) -2.7230 (S)-87 (100 ng / mL) -0.8538 (R)-97 (100 ng / mL) -0.1835 (S)-97 (100 ng / mL) 2.3341 (R)-89 (100 ng / mL) 3.0593 (S)-89 (100 ng / mL) -0.1649 (R)-88 (100 ng / mL) -1.2352 (S)-88 (100 ng / mL) 5.7511 The control group are cells treated with vehicle (DMSO). Table 2. Cell viability assay in HLIVECs (Human Umbilical Vein Endothelial Cells) with the compounds of the invention. Cell viability HUVECs Conditions Growth inhibition (%) Control vehicle 1.2643 (R)-4 (100 ng / mL) 8.5627 (S)-4 (100 ng / mL) 2.9760 (R)-87 (100 ng / mL) 2.8033 (S)-87 (100 ng / mL) 4.5807 (R)-97 (100 ng / mL) 1.8232 (S)-97 (100 ng / mL) 1.5822 (R)-89 (100 ng / mL) -3.9463 (S)-89 (100 ng / mL) -4.3883 (R)-88 (100 ng / mL) -7.9022 (S)-88 (100 ng / mL) -7.4439 5 The control group are cells treated with vehicle (DMSO). Table 3. Wound closure effect in HLIVECs with the compounds of the invention. Wound healing assay in HUVECs Conditions Wound closure (%) Control + 56.4021 Control - 27.5988 Control (vehicle) 33.6526 (R)-4 (5 ng / mL) 49.2952 (S)-4 (5 ng / mL) 37.0614 (R)-87 (5 ng / mL) 48.0163 (S)-87 (5 ng / mL) 48.4937 (R)-97 (5 ng / mL) 47.9463 (S)-97 (5 ng / mL) 47.9725 (R)-89 (5 ng / mL) 47.4996 (S)-89 (5 ng / mL) 47.6883 (R)-88 (5 ng / mL) 50.1130 (S)-88 (5 ng / mL) 48.2610 Quantification of wound healing in the HLIVEC assay was undertaken after 8 hours of exposure of the cells to the compound at a 5 ng / mL concentration. The positive control group used full EGM media, and in the negative control EGM media serum and GF free were used. The control group used serum free EGM with vehicle (DMSO). Table 4. Cell migration effect in HDFs with additional compounds of the invention. Compound Distance migrated (%) Control (Vehicle) 100.0 Compound 17 (1 ng / mL) 95.0 Compound 17 (10 ng / mL) 127.4 Compound 17 (100 ng / mL) 124.1 Compound 17 (1000 ng / mL) 126.6 Compound 8 (1 ng / mL) 123.8 Compound 8 (10 ng / mL) 130.3 Compound 8 (100 ng / mL) 141.7 Compound 8 (1000 ng / mL) 128.3 Compound (R)-87 (1 ng / mL) 133.4 Compound (R)-87 (10 ng / mL) 140.6 Compound (R)-87 (100 ng / mL) 152.7 Compound (R)-87 (1000 ng / mL) 145.0 Compound 18 (1 ng / mL) 138.6 Compound 18 (10 ng / mL) 152.5 Compound 18 (100 ng / mL) 145.0 Compound 18 (1000 ng / mL) 169.0 Compound 13 (1 ng / mL) 134.3 Compound 13 (10 ng / mL) 131.4 Compound 13 (100 ng / mL) 131.6 Compound 13 (1000 ng / mL) 145.2 5 Quantification of cell migration in HDFs was undertaken after 24 hours of exposure of the cells to the compound at the stated concentration. The control group used DMEM media with vehicle (DMSO). Biology General Information. 0 Dimethyl sulfoxide and Phosphate buffered saline (PBS) were purchased from Sigma-Aldrich and used as received. bFGF was purchased from R&D Systems (P09038). Human umbilical vein endothelial cells (HLIVEC), vascular cell basal medium, endothelial cell growth kit-VEGF, trypsin for primary cells and trypsin neutralizing solution were purchased from ATCC. Fetal bovine serum (FBS), AlamarBlue®, Dulbecco’s Modified Eagle Medium (DMEM), trypsin, and Penicillin / streptomycin were purchased from Gibco. The fluorescence of the 96 well plates was recorded using a SpectrMax® iD3 Multi-Mode Microplate Reader, Molecular Devices. The quantification of the wound areas from the scratch assay was done using Imaged with the Wound healing size tool plugin written by Suarez-Arnedo etal. For the statistical analysis, data are presented as mean ± standard deviation. Individual differences between groups and time points were assessed using one-way ANOVA (GraphPad Prism 9). Statistical significance was accepted at p<0.05. Media Composition. For Human Dermal Fibroblast (HDF) culturing and experimental: DMEM supplemented with 10% FBS, and 1% P / S. For HLIVEC culturing and metabolic activity assays: Endothelial Basal Media supplemented with endothelial Cell growth Kit-VEGF, and 1% P / S. To starve HLIVEC for the wound healing assay: Endothelial Basal Media supplemented with endothelial Cell growth Kit-VEGF, 1% FBS, and 1% P / S. For HLIVEC wound healing assay: either Endothelial Basal Media supplemented with endothelial Cell growth Kit-VEGF without GFs, and without FBS and 1% P / S. Or Endothelial Basal Media supplemented with endothelial Cell growth Kit-VEGF without FBS and 1% P / S. Metabolic Activity Assays HLIVECs or HDFs were cultured in growth media (Endothelial Basal Media supplemented with ATCC endothelial Cell Growth Kit-VEGF and 1% P / S for HUVEC, or DMEM supplemented with 10% FBS, and 1% P / S), when the cells were at 80% confluency, they were trypsined. The cells were then seeded in 48 well plates at a density of 50,000 cells / cm2 and allowed to attach overnight. The media was then replaced to the media containing the compounds in different concentrations (300 pL) and incubated for 48 h. After exposure, AlamarBlue® was used to measure the metabolic activity of cells. Briefly, each sample was incubated for 4 h with 400 pL media containing 10% AlamarBlue® solution, diluted according to manufacturer’s instructions. After the incubation period, 100 pL samples in triplicate were taken from the wells into a 98 well plate. The reduction of AlamarBlue® in the solution was determined by reading fluorescence at an excitation wavelength at 560 nm and an emission wavelength at 590 nm using a spectrophotometer. The % of growth inhibition was calculated with Formula 1: % growth inhibition = 100 x (l-(well fluorescence / control fluorescence)) All the samples were tested in triplicate and each experiment was repeated 3 times (n = 9). According to the ISO 10993-5:2009, 30% cell growth inhibition was used as threshold for cytotoxicity (indicated by red line). The results are shown in Figure 1. None of the enantiomers have a significant effect on either HDFs or HLIVECs metabolic activity at the concentrations tested. Wound Healing Assay (HUVECs) HLIVECs were trypsinised, seeded in a 48 well-plate at a density of 42,000 cells / well. Cells were allowed to attach for 18 h before being starved overnight in EGM media with 1% FBS. Linear scratches were generated using 200 pL tips, and the cell debris generated was washed with warm EGM media. Pictures of the wound are (to) were taken. Cells were then exposed to 250 pL of either assay EGM media with DMSO, with the compounds, without GF, and with 2% FBS for 8 h. Pictures of the wound are (tf) were taken after the exposure. Wound closure (%) was calculated following Formula 2: Wound closure (%) = ((Wound area(to) - Wound area(tf)) I (Wound area(to)) x 100 All the samples were tested in quadruplicate and each experiment was repeated 3 times (n = 12). The results are presented in Figure 2, and they show that at the concentration tested all the flexible, acyclic peptidomimetics enhance endothelial cell migration. Cell Migration Assay (HDFs) with Additional Example Compounds HDFs were trypsinised, seeded in a 48 well-plate at a density of 50,000 cells / well. Cells were allowed to attach for 18 h before being starved overnight in DM EM without FBS. Linear scratches were generated using 200 pL tips, and the cell debris generated was washed with warm DMEM media. Photos of the wound area (to) were taken. Cells were then exposed to 300 pL of either assay DMEM media with DMSO, with the compounds for 24 h. Photos of the wound area (tf) were taken after the exposure, and measurements assessed from the photos. Wound closure (%) was calculated following Formula 2, then the migration relative to control was calculated following Formula 3: Migration relative to control = (Wound closure (%)) I (Wound closure (%) of the control) The results are presented in Figure 3, and they show that all the tested flexible, acyclic peptidomimetics enhance endothelial cell migration. General Procedure for Making IGD Gels. 1. The IGD compound was dissolved in DMSO to a 10 mg / mL concentration (Solution A). 2. Serial dilution* in Millipore water until a concentration of 5 ng / mL is achieved (DMSO content should be 0.00005%) (Solution B). 3. To make 500 mL of 5 ng / mL IGD gel: a. On a 1 L beaker, 500 mL of Solution B were heated up to 80 °C. b. Under vigorous stirring add 25g of HPMC (hydroxypropyl methylcellulose), keep the stirring until complete dissolution of the HPMC c. Take the stirring bar out and allow to cool down to r.t. d. Transfer to primary container. Allow the gel to sit in the fridge overnight to obtain a homogeneous solution. *Serial dilution for 500 mL of 5ng / mL IGD gel (Solution B): • Take 10 pL of Solution A and make up to 1 L with Millipore water (Solution C). • Take 25 mL of Solution C and make up to 500 mL with Millipore water (Solution B). References All documents mentioned in this specification are incorporated herein by reference in their entirety. Brooks et al. Science 1994, 264, 569-571. DOI: 10.1126 / science.7512751 Clement etal., Synlett, 2001, 2001, 1423 Czosnyka, K. Studies Towards the Synthesis of Fibronectin-Based Peptidomimetics. University of Glasgow, 2010 Di Donna etal. Analytical Chemistry 2004, 76, 5104-5108. DOI: 10.1021 / ac0498821 Ellis etal. Cell Signal 2010, 22, 1655-9. DOI: 10.1016 / j.cellsig.2010.06.005 Harman et al. Adv Wound Care (New Rochelle) 2021, 7. DOI: 10.1089 / wound.2018.0883 Margery et al., Agnew Chem Int Ed. 2017, 56, 15644 Matheson, M. The investigation and Development of IGD Peptidomimetics as Wound Healing Agents. University of Glasgow, 2015. Nieuwenhuis et al. Biol. Rev 2018, 93; 1339-1362 Schoreta / . J Cell Sci 1988, 90 (Pt 3), 401-7. DOI: 10.1242 / jcs.90.3.401 Shpiro etal. Molecular BioSystems 2005, 1, 318-320. DOI: 10.1039 / B509023G Suarez-Arnedo, A. etal. PLCS ONE 2020, 15, e0232565. DOI: 10.137ournal.pone.0232565 Thiel etal. Biol. Rev. Camb. Philos. Soc. 2018, 93(1); 350-363 Vakonakis etal. J Biol Chem 2009, 284, 15668-75. DOI: 10.1074 / jbc.M109.003673 Weis et al. Cold Spring Harbor Perspective in Medicine 2011 WO 2007 / 23273 A1

Claims

1. A compound of formula (I):wherein:Ais C(RE) orN, where -RE is -H, -F or -CH3;-XA- is -O-, -S-, or-NH-;-RA is optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl;-RQ is -CH(RC)(RD), or-Rp,wherein -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH,-C(O)NH2, -C(O)NHRcb and -C(O)NRCBRCC, where each of -RCA, -RCB and -Rcc is independently Cm alkyl;-RD is -XD-RDD, C1-10 alkyl or -H, where-XD- is a C1-4 alkylene, such as methylene (-CH2-), ethylene (-CH2-CH2-) ordimethyl methylene (-C(CH3)2-), or a covalent bond, and-RDD is independently selected from -C(O)ORDA, -C(O)OH, OH,-C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC, where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; or-Rp is phenyl or C5-6 heteroaryl, such as pyridinyl, optionally substituted with one or more groups -Rz, whereeach -Rz is independently selected from -C(O)ORZA, -C(O)OH,-C(O)NH2, -C(O)NHRzb, -C(O)NRzbRzc, -C(O)NHOH, -C(O)N(Rzd)OH and -C(O)S(RZE),where each of -RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl;-RB is-H or -XB-RBB, where-XB- is a covalent bond, -O-, -S-, or -NH-, and-RBB is optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl, such as C2-10 alkyl; or-RB, together with -RE and the carbon ring atoms to which they are attached, form a fused ring selected from a fused C5-6 aryl ring, a fused C5-6 carbocyclic ring or a fused C5-6 heterocyclic ring, where the fused ring is optionally substituted at each ring carbon atom with -RF, whereeach -RF is independently selected from -NHC(O)CH3, -OC(O)CH3,-NH2, -NHRfa and -NRFARFB, andeach of-RFA and -RFB is independently C1-4alkyl, Boc orCbz,and the salts, solvates and protected forms thereof.

2. The compound according to claim 1, wherein -RA is C2-10 alkyl, such as C5 alkyl (pentyl), for example / -pentyl (3-methylbutyl).

3. The compound according to claim 1 or claim 2, wherein -RQ contains at least one -C(O)- carbon which is a,p-related to the group -NH- to which -RQ is attached.

4. The compound according to claim 1 or claim 2, wherein A is C(RE).

5. The compound according to any one of claims 1 to 4, wherein -RQ is -CH(RC)(RD).

6. The compound according to claim 5, wherein -Rc is selected from:-C(O)OCH3, -C(O)OH, -H, -C(O)NH2i -C(O)NHCH3 and -C(O)N(CH3)2.

7. The compound according to claim 6, wherein -Rc is -C(O)OCH3 or -C(O)OH.

8. The compound according to claim 6, wherein -Rc is -H.

9. The compound according to any one of claims 5 to 8, wherein -RD is -XD-RDD.

10. The compound according to claim 9, wherein -XD- is methylene (-CH2-), methylmethylene (-CH(CH3)-), or dimethyl methylene (-C(CH3)2-).

11. The compound according to claim 9 or 10, wherein -RDD is -C(O)OCH3 or-C(O)OH.

12. The compound according to any one of claims 1 to 4, wherein -RQ is -Rp.

13. The compound according to claim 12, wherein -Rp is phenyl.

14. The compound according to claim 12, wherein -Rp is phenyl ort / io-monosubstituted with -Rz.

15. The compound according to any one of claims claim 12 to 14, wherein -Rz is selected from -C(O)OCH3, -C(O)OH, -C(O)NH2i -C(O)NH(CH3) and -C(O)N(CH3)216.    The compound according to any one of claims 1 to 15, wherein -XA- is -O-.

17. The compound according to any one of claims 1 to 16, wherein -RB is -H.

18. The compound according to any one of claims 1 to 16, wherein -RB is -XB-RBB.

19. The compound according to claim 18, where -XB- is -O- or a covalent bond, and -RBBis optionally substituted C1-6 alkyl.

20. The compound according to claim 18 or claim 19, wherein -XB- is -O- and -RBB is Cs alkyl (pentyl), such as is / -pentyl (3-methylbutyl).

21. The compound according to claim 18 or claim 19 wherein -XB- is a covalent bond and -RBB is C1-6 alkyl, such as methyl.

22. The compound according to claim 18 or claim 19, wherein -RBB is C2-io alkyl substituted with -RBC, where each -RBC is independently selected from C5-6 aryl, such as phenyl, C5-6 cycloalkyl, C5-6 heterocyclyl, halo, -OH, -SH, -NH2, -NHRBD, -NRBDRBE, -ON, -NO2, -C(O)OH, -C(O)ORbd, -C(O)NH2i -C(O)NHRbd, and -C(O)NRBDRBE, where each of -RBD and -RBE is independently C1-4 alkyl.

23. The compound according to claim 4, wherein -RE is -H.

24. The compound according to claim 4, wherein -RB together with -RE and the carbonring atoms to which they are attached form a fused ring.

25. The compound according to claim 24, wherein -RE together with -RB forms a fused benzene ring which is optionally monosubstituted with the group -RF, such as monosubstituted with -NHC(O)CH3.

26. The compound according to any one of the claims 1-25, wherein the compound of formula (I) is represented by formula (V) or (VI):

27. A pharmaceutical composition comprising a compound according to any one of claims 1 to 26, optionally together with one or more pharmaceutically acceptable carriers.

28. A compound according to any one of the claims 1 to 26, or a pharmaceutical composition according to claim 27, for use in a method of treatment or prophylaxis.

29. A compound according to any one of claims 1 to 26 or a pharmaceutical composition according to claim 27 for use in a method of tissue regeneration and / or repair, such as promoting tissue regeneration and / or repair.

30. A compound according to any one of claims 1 to 26 or a pharmaceutical composition according to claim 27, for use in a method of treating a wound.

31. A method of preparing a compound of formula (I) by reacting the compound of formula (III) with a compound of formula (IV) or (V):wherein:A is C(RE) or N, where -RE is -H, -F or Me;-XA- is -O-, -S-, or-NH-;-RA is optionally substituted Ci-w alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C2-10 alkyl;-RB is -H or -XB-RBB, where -XB- is a covalent bond, -0-, -S-, or -NH-, and -RBB is an optionally substituted C1-10 alkyl, optionally substituted C2-10 alkenyl or optionally substituted C2-10 alkynyl, such as C1-10 alkyl, such as C2-10 alkyl; or-RB together with -RE and the carbon ring atoms to which they are attached form a fused C5-6 aryl ring, such as benzene, or a fused C5-6 carbocyclic or heterocyclic ring, which ring is optionally substituted at each ring carbon with -RF,where each -RF is independently selected from -NHC(O)CH3, -OC(O)CH3, -NH2, -NHRfa and -NRFARFB;where each of -RFA and -RFB is independently C1-4 alkyl, Boc or Cbz.RPwherein:wherein -Rc is independently selected from -C(O)ORCA, -C(O)OH, -H, -CH2OH, -C(O)ORCA,-C(O)NH2, -C(O)NHRcb and -C(O)NRCBRCC,where -RCA, -RCB and -Rcc are C1-4 alkyl;-RD is -H, C1-10 alkyl or -XD-RDD, where-XD- is C1-4 alkylene or a covalent bond and-RDD is independently selected from -C(O)ORDA, -C(O)OH, -OH,-C(O)NH2, -C(O)NHRdb and -C(O)NRDBRDC,where each of -RDA, -RDB and -RDC is independently C1-4 alkyl; or-Rp is phenyl or C5-6 heteroaryl, such as pyridinyl, optionally substituted with one or more groups -Rz, whereeach -Rz is independently selected from -C(O)ORZA, -C(O)OH,-C(O)NH2, -C(O)NHRzb, -C(O)NRzbRzc, -C(O)NHOH, -C(O)N(Rzd)OH and -C(O)S(RZE),where each of -RZA, -RZB, -Rzc, -RZD and -RZE is independently C1-4 alkyl;-LA is independently selected from -OTs, -OTf, -OMs, -Cl, -Br, and -I;5           -LB is independently selected from -F, -Cl, -Br and -I.

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