PARP1 inhibitor compounds

Abstract

A compound of the formula (I) where y is 0, 1 or 2, each XD is independently C, N, O or S, XET and XEB are independently C or N, R1, R2 and R3 are as defined herein, and L is: Wherein ring C is an aro

Description

Technical Field The present invention relates to PARP1 inhibitor compounds, and in particular to PARP1 inhibitor compounds for use in medicine. The inhibitors of the invention may be used in pharmaceutical compositions, and in particular pharmaceutical compositions for treating a cancer. The invention also relates to methods of manufacture of such inhibitors, and methods of treatment using such inhibitors. Background The family of poly(ADP-ribose) polymerases (PARPs) consists of 17 PARP proteins that catalyse the transfer of ADP-ribose to target proteins, a posttranslational process termed PARylation. Target protein modification by PARylation causes significant changes to function and as such PARPs play an important role in many cellular processes such as chromatin remodelling, transcription, replication, recombination, cell cycle progression and DNA damage repair (Kamaletdinova, T. et al. Cell. 2019; 8: 1625). PARP1 and 2 are the most widely studied PARP enzymes, primarily due to their role in DNA damage repair, in particular in the base excision repair (BER) process of DNA single-strand breaks (Ngoi, YL. et al. Cancer J. 2021; 27: 521-528). PARP1 is activated by DNA damage breaks, and the subsequent PARylation of target proteins leads to recruitment of additional factors that initiate repair of DNA lesions. Auto-PARylation of PARP triggers the release of bound PARP from the DNA allowing other DNA repair proteins access to complete lesion repair. This highlights the critical role PARP plays in enabling a cancer cell to repair DNA damage caused by exogenous agents such as radiation therapy and chemotherapeutic agents. Inhibition of PARP enzymes has been utilised as a strategy to selectively kill cancer cells that harbour genetic defects in complementary DNA damage repair pathways (Farmer, H. et al. Nature. 2005; 434: 917-921). This synthetic lethality approach has been demonstrated successfully in tumours with epigenetic modifications or deleterious mutations in BRCA1 and BRCA2, two functionally redundant tumour suppressor proteins involved in DNA doublestrand break (DSB) repair by homologous recombination (HR) (Lord, CJ. and Ashworth, A. Science. 2017; 355: 1152-1158). Such tumours with HR deficiency (HRD) are dependent on PARP function for survival - following PARP inhibition in these tumours, DSB breaks will be processed by alternative error-prone repair pathways leading to genomic instability and cancer cell death. The inhibition of PARP can trap the inactivated PARP at the sites of DNA damage. This leads to replication fork stalling and subsequent collapse in S-phase when the fork reaches the site of the trapped PARP, resulting in the generation of genotoxic DNA double-strand breaks. It is believed that this PARP1-DNA trapping can lead to the selective death of cancer cells harbouring HRD (Farmer, H. et al. Nature. 2005; 434: 917-921). This strategy has led to the successful approval of several PARP inhibitors for the treatment of cancers with HRD, such as in BRCAl / 2-mutated breast, ovarian and prostate cancer, as well as in ovarian and prostate cancer harbouring genomic consequences of HRD, and ovarian cancer in the maintenance setting where platinum sensitivity acts as a surrogate for HRD (Fong, PC. et al. N. Engl. J. Med. 2009; 361:123-134). It has recently been shown that genomic instability, in the form of unrepaired DNA doublestrand breaks or micronuclei disruption can trigger innate immune system activation via the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS), leading to generation of cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) and induction of dimerization of stimulator of interferon genes (STING). STING subsequently translocates from the endoplasmic reticulum to the Golgi where it recruits and activates TANK-binding kinase 1 (TBK1). TBK1 phosphorylates interferon regulatory transcription factor 3 (IRF3) which drives the production of type I interferons and supports the induction of an adaptive immune response (Zhu, Y. etal. Mol. Cancer. 2019,18:152). For example, PARP inhibitor-induced STING pathway activation and anti-tumour immune responses have been demonstrated in multiple tumour models, providing rationale for exploiting combinations of PARP inhibitors with immunotherapies for improved therapeutic efficacy (Sen, T. et al. Cancer Discov. 2019; 9: 646-661). For example, the PARP inhibitor Olaparib was also recently shown to induce synthetic lethal effects in combination with a synthetic cyclic dinucleotide STING agonist in DNA damage repair deficient cancer cells and a BRCA-deficient breast cancer model (Pantelidou, C. et al. 2021: bioRxiv 2021.01.26.428337vl). Overall, modulation of nucleic acid sensing pathways via multiple mechanisms has been shown to promote anti-tumour efficacy in a variety of cell and animal models thus demonstrating therapeutic potential for augmenting efficacy of immunotherapies and overcoming resistance to immune checkpoint blockade through use of PARP inhibitors. There are numerous clinical trials ongoing combining PARP inhibitors with immunotherapies (reviewed in Chabanon, RM, et al. Nat. Rev. Cancer. 2021; 21: 701-717). Recently, PARP1 has also been shown to bind the Epstein Barr Virus (EBV) genome and that PARP1 inhibition can alter EBV chromatin structure and latent gene expression (Morgan, SM. et al. Nat. Commun. 2022; 13:187). Hence, PARP1 inhibitors may play a role in cancers where EBV plays a contributing role such as Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal and gastrointestinal cancers. Interestingly, EBV has also been shown to be a causative factor in multiple sclerosis (MS) whereby EBV infection greatly increases the risk of subsequent MS (Bjornevik, K. et al. Science (2021); 375: 296-301). First-generation PARP inhibitors generally demonstrate non-selective activity at PARP1 and 2. Haematological toxicities such as anaemia, neutropenia and thrombocytopenia are associated with clinical use of these molecules which restricts their use in combination with cytotoxic chemotherapies and other targeted agents due to dose-limiting cytopenias (LaFargue, CJ. et al. Lancet Oncol. 2019, 20, el5-e28). Evidence from pre-clinical mouse studies strongly suggests that PARP2 inhibition is a major driver of these haematological toxicities, with PARP2 being particularly linked to erythrogenesis in mice (Farres, J. et al. Blood. 2013; 122: 44-54). In addition, PARP2 function has been shown to be dispensable for anti-tumour activity in HRD mouse cancer models (Ronson, G E. etal. Nat. Commun. 2018, 9: 746). Taken together, these data suggest an unmet medical need for the development of inhibitors with improved selectivity for PARP1 over PARP2 and other PARPs, thus providing expanded therapeutic utility (1) as single agents and (2) in combination with other anti-cancer agents. To date, two PARPl-selective inhibitors, AZD5305 and AZD9574, have entered clinical development. AZD5305 was described as a potent PARP1 inhibitor and trapper with 500-fold selectivity over PARP2 and less off-target activity against secondary pharmacology targets than first-generation PARP inhibitors (Johannes, JW. et al. J. Med. Chern. 2021; 64: 14498-14512). Importantly, significantly less haematotoxicity was observed for AZD5305 in rodent models than with first-generation PARP inhibitors, confirming the reported pathogenic role of PARP2 in haematologic toxicity (111uzzi, G. et al. Clin. Cancer Res. 2022; CCR-22-0301). Having regard to the above, it is an aim of the present invention to provide PARP1 inhibitors, and in particular PARP1 inhibitors for use in medicine. It is a further aim to provide pharmaceutical compositions comprising such inhibitors, and in particular to provide compoundsand pharmaceutical compositions for treating a cancer. It is also an aim to provide methods of synthesis of the compounds. Summary In one aspect, the present invention provides a PARP1 inhibitor compound having a structure of: wherein: a dotted line represents a bond selected from a single bond and a double bond; y is 0,1, or 2; each XD is independently selected from C, N, O and S; XET and XEB are each independently selected from C and N; each R1 is independently absent or selected from H and a substituted or unsubstituted organic group; 5 each R4 is independently absent or selected from H and a substituted or unsubstituted organic group, with the proviso that the R4 groups are not fused to form a ring; R3 is H or a substituted or unsubstituted organic group; L is a group having a structure of: 10 wherein: ring C is an aromatic ring; XA1 is C or N; each XA2 is independently selected from C, N, O and S; each XB2 is independently selected from C, N, O and S; 15 XB3 is selected from C and N; each Xc is independently selected from C, N, O, and S, with the proviso that ring C is a heterocycle; each R5A, R5B, and R5C is independently absent or selected from H and a substituted or unsubstituted organic group; R6 is selected from H and a substituted or unsubstituted organic group; n is 0,1, 2, 3, 4, or 5; m is 0,1, 2, 3, 4, or 5, with the proviso that n + m is in the range 2 to 5; p is 1, 2 or 3; q is 1, 2 or 3, with the proviso that p + q is in the range 2 to 5; r is 0,1, 2, 3, or 4; and s is 0,1, 2, 3, or 4, with the proviso that r + s is 3 or 4; Q is a bond ora linking group having a structure selected from: wherein: t is 0, 1, 2, 3, 4 or 5; u is 0,1, 2, 3, 4 and 5, with the proviso that t + u is in the range 0 to 6; and each R7 and R8 is independently selected from H and a substituted or unsubstituted organic group. The PARP1 inhibitor compound may be for use in medicine. For instance, the PARP1 inhibitor compound may be for use in treating a cancer. Another aspect of the invention provides a pharmaceutical composition comprising a PARP1 inhibitor compound as defined herein. A further aspect of the invention provides a pharmaceutical kit for treating a cancer. The pharmaceutical kit comprises a PARP1 inhibitor compound as defined herein, and a further agent for treating cancer. The PARP1 inhibitor compound and the further agent are suitable for administration simultaneously, sequentially or separately. Still another aspect of the invention provides a method of treating a disease and / or a condition and / or a disorder, which method comprises administering to a patient a PARP1 inhibitor compound, a composition or a kit as defined herein. Another aspect of the invention provides a method of synthesising a PARP1 inhibitor compound as defined herein. The method comprises conducting a reaction between: i) a first reactant comprising rings D and E and bearing a first portion of group L, and ii) a second reactant comprising a remainder of group L, to form the PARP1 inhibitor compound. This Summary is provided to introduce a selection of concepts in a simplified form that are further described below in the Detailed Description. This Summary is not intended to identify key features or essential features of the claimed subject matter, nor is it intended to be used to limit the scope of the claimed subject matter. Nor is the claimed subject matter limited to implementations that solve any or all of the disadvantages noted herein. Detailed Description General Definitions The verb 'to comprise' is used herein as shorthand for 'to include or to consist of'. In other words, although the verb 'to comprise' is intended to be an open term, the replacement of this term with the closed term 'to consist of' is explicitly contemplated, particularly where used in connection with chemical compositions. It will be appreciated that some compounds disclosed herein may be ionisable, i.e. some compounds may be weak acids, weak bases, or ampholytes. Representations of the free forms of ionisable compounds are intended to encompass the corresponding ionised forms. lonisable compounds may be in free form, or in the form of a pharmaceutically-acceptable salt. A compound is considered to be a PARP1 inhibitor if its presence is capable of preventing or reducing the ability of immobilised PARP1 to undergo auto-poly-ADP ribosylation (AutoPARylation) following incubation with biotinylated-NAD+ as compared to the same process in its absence. Typically, the compound is considered to be a PARP1 inhibitor if it has an IC50 <10 pM in a suitable assay. A suitable assay may be conducted using 2 nM PARP1, 2 pM biotin-NAD+ assay solution in 20 mM HEPES (pH 7.5), 100 mM NaCI, 2 mM DTT, 0.1 % BSA (w / v), 0.02 % Tween (v / v) assay buffer. PARylation may take place for 2 h at room temperature and may be detected using a dissociation-enhanced lanthanide fluorescence immunoassay (DELFIA) readout. A particularly suitable assay is described in the Examples below. Preferably, the compound has an IC50 <1 pM, more preferably <100 nM and most preferably <10 nM in the PARP1 inhibitor assay. A compound is considered to be a selective PARP1 inhibitor if its presence is capable of displacing or reducing the ability of a high affinity Cy5 fluorescent dye-labelled chemical probe to bind to PARP1 whilst displacing the same chemical probe at PARP2 with at least 10-fold weaker activity. Typically, the compound is considered to be a selective PARP1 inhibitor if it has an IC50 <10 pM in this assay at PARP1 with at least 10-fold selectivity preference over PARP2. A suitable such assay may be conducted for 1 h at room temperature using 10 nM PARP1 or PARP2, Tb-cryptate antibody and PARP1 / 2 binding probe in 20 mM HEPES (pH 7.5), 100 mM NaCI, 2 mM DTT, 0.1 % BSA (w / v), 0.02 % Tween (v / v) assay buffer. Probe binding displacement may be detected using homogeneous time-resolved fluorescence. A particularly suitable assay is described in the Examples below. Preferably the selectivity preference of PARP1 over PARP2 is at least 50-fold, more preferably at least 100-fold. A compound is also considered to be a selective PARP1 inhibitor if it has an IC50 <10 pM at PARP1 with at least 10-fold selectivity preference over PARP2 in NanoBRET assays demonstrating cellular target engagement. These assays are based on bioluminescence resonance energy transfer (BRET) between a Nano-luc-tagged protein (e.g. PARP1 or PARP2) and a fluorescent group on a high affinity NAD+ competitive binding probe. Such cellular probe displacement assays can be utilised to measure inhibitor affinities and selectivity ratios at PARP1 and 2. A particularly suitable assay is described in the Examples below. Preferably the selectivity preference of PARP1 over PARP2 is at least 50-fold, more preferably at least 100-fold. The expression "substituted or unsubstituted organic group" is used herein as a synonym for "substituent". Example organic groups are discussed in more detail hereinbelow. Where it is said that an organic group is "substituted", it is meant that an H in the organic group is replaced by a further organic group. A dotted line in a structural formula represents a covalent bond of any appropriate non-zero order, most typically a single bond or a double bond. As will be appreciated, systems comprising multiple double bonds may be conjugated or aromatic. Except where the configuration of a particular bond is directly illustrated, all formulae herein are shown in non-stereoisomeric form and are intended to represent all possible stereoisomers of a particular structure, including all possible isolated enantiomers corresponding to the formula, all possible mixtures of enantiomers corresponding to the formula, all possible mixtures of diastereomers corresponding to the formula, all possible mixtures of epimers corresponding to the formula and all possible racemic mixtures corresponding to the formula. In addition to this, all formulae herein are intended to represent all tautomeric forms equivalent to the corresponding formula. The term "aliphatic ring" is used herein in the broad sense of a non-aromatic ring. An aliphatic ring may be carbocylic or heterocyclic, saturated or partially unsaturated, and substituted or unsubstituted. Where a general formula depicts an element in the format (X)i, where X is variable element and i is a number, the parentheses are expanded before assigning each X. For example, if variable X may be C or N, then (X)z encompasses C-C, C-N, and N-N. Where stereochemistry is depicted, the stereochemistry shown is relative stereochemistry rather than absolute stereochemistry. Compound numbering Various ones of the compounds provided herein are enantiomeric or diastereomeric. Where a suffix is applied to a compound number, the suffix indicates stereochemistry. A compound number without a suffix denotes a compound having the indicated structural formula without defining stereochemistry. The suffix 'rac' in a compound number denotes a racemic mixture. The suffixes 'cis' and 'trans' denotes compounds which are A ring cis and A ring trans, as explained in the section "stereochemistry" hereinbelow. In the case of diastereomeric compounds, the cis and trans suffixes may refer to pairs of diastereomers having the indicated configuration of the A ring. Nuclear Overhauser Effect nuclear magnetic resonance spectroscopy ("NOE NMR") may be used to determine the stereochemistry of compounds as described herein. The suffix 'a' in a compound number denotes an enantiomer eluted as a first fraction when a mixture of two enantiomers is separated by supercritical fluid chromatography ("SFC") using a chiral column. The suffix 'b' in a compound number denotes an enantiomer eluted as a second fraction when a mixture of two enantiomers is separated by supercritical fluid chromatography ("SFC") using a chiral column. Discussion Provided herein are PARP1 inhibitor compounds having a structure of: a dotted line represents a bond selected from a single bond and a double bond; y is 0,1, or 2; each XD is independently selected from C, N, O and S; XE and XEB are each independently selected from C and N; 10 each R1 is independently absent or selected from H and a substituted or unsubstituted organic group; each R4 is independently absent or selected from H and a substituted or unsubstituted organic group, with the proviso that the R4 groups are not fused to form a ring; R3 is H ora substituted or unsubstituted organic group; 15 ring C is an aromatic ring; XA1 is C or N; each XA2 is independently selected from C, N, O and S; each XB2 is independently selected from C, N, O and S; XB3 is selected from C and N; each Xc is independently selected from C, N, O, and S, with the proviso that ring C is a heterocycle; each R5A, R5B, and R5C is independently absent or selected from H and a substituted or unsubstituted organic group; R6 is selected from H and a substituted or unsubstituted organic group; n is 0, 1, 2, 3, 4, or 5; m is 0,1, 2, 3,4, or 5, with the proviso that n + m is in the range 2 to 5; p is 1, 2 or 3; q is 1, 2 or 3, with the proviso that p + q is in the range 2 to 5; r is 0,1, 2, 3, or 4; s is 0,1, 2, 3, or 4, with the proviso that r + s is 3 or 4; and Q is a bond ora linking group having a structure selected from: where: t is 0,1, 2, 3, 4 or 5; u is 0,1, 2, 3, 4 and 5, with the proviso that t + u is in the range 0 to 6; and each R7 and R8 is independently selected from H and a substituted or unsubstituted organic group. Various aspects of the above general structure will now be discussed in more detail. Stereochemistry Some of the PARP1 inhibitor compounds provided herein include one or more chiral centres. 5 Such compounds may be provided in the form of an isolated enantiomer; a mixture of two or more enantiomers; a mixture of two or more diastereomers or epimers; or a racemic mixture. Some PARP1 inhibitor compounds may be capable of tautomerism. Such compounds may be 10 provided in the form of any possible tautomer. When ring A of the PARP1 inhibitor compounds is a cycloalkane, the compound may exhibit cis-trans isomerism. In the context of the present disclosure, unless expressly stated 15 otherwise, a "cis" compound has a cis configuration across ring A: 14 And a "trans" compound has a trans configuration across ring A: Substituents - general 5 The expression "R5 group" refers generically to groups R5A, R5B, and R5C. An "R5A" group is an R5 group which is attached to ring A, and so on. Some of the formulae presented herein use more specific identifiers for R5 groups. For example, "R5A1" identifies a subset of R5A groups. 10 The expression "X atom" refers generically to any variable ring atom (XD, Xr, XEB, XA1, XA2, XB2, XB3, Xc). In the compounds provided herein, various ones of the R1, R4, and R5 groups may be absent. Dotted lines in the structural formulae presented herein representing covalent bonds of any 15 non-zero order. As will be appreciated, the number of ring bonds and the number of substituents are selected such that the atoms of the rings maintain a stable valency. Maintaining a stable valency means ensuring that an atom has its normal (typically most common) valency in organic compounds (i.e. 2 for oxygen; 2 or 6 for sulfur; 3 or 4 for nitrogen; and 4 for carbon). When an X atom is N, that atom most preferably has a valency of 3. Compounds containing tetravalent N atoms are also contemplated. Preferably, the PARP1 inhibitor compound includes at most one tetravalent N, and more preferably no tetravalent N atoms. Each R1, R4 and R5 group may independently be absent or present, and may be the same or different. For the avoidance of doubt, where the number of R groups attached to an atom may vary according to the choice of corresponding X group, the following provisos typically apply: i) When an X atom is O, its corresponding R groups are both absent. ii) When an X atom is S, its corresponding R groups are both absent or are both selected from =0 and =NR10, where R10 is H or a substituted or unsubstituted organic group, preferably a Cl to C3 alkyl group. iii) When an X is N and is double bonded to an adjacent ring atom, its corresponding R groups are absent. iv) When an X is N and is not double bonded to an adjacent ring atom, exactly one corresponding R group is present. v) When an X is C and is double bonded to an adjacent ring atom, exactly one corresponding R group is present. vi) When an X is C and is not double bonded to an adjacent ring atom, both corresponding R5 groups or both the corresponding R5 and R6 groups are present. Atom XA1 of ring A is a special case, since this atom connects rings E and A. XA1 bears an R5 substituent only if XA1 is C and does not form a double bond to another ring atom. The substituents (i.e. R groups; R1, R3, R4, R5, R6, R7, and R8) are not especially limited, provided that they do not prevent the PARP1 inhibitory function from occurring. The substituents are selected from H and a substituted or unsubstituted organic group. Thus, both above and in the following, the terms 'substituent' and 'organic group' are not especially limited and may be any functional group or any atom, especially any functional group or atom common in organic chemistry. Any R5 or R6 group may form a ring with any other R5 or R6 group on an adjacent and / or proximal atom, although in most embodiments this is not preferred, except where explicitly stated. Thus, the following substituents may together form a ring: an R5A with another R5A; an R5B with another R5B; an R5C with another R5C; or an R5C with R6. In the present context, an adjacent and / or proximal atom may mean another atom directly bonded to an atom (adjacent) or may be two atoms with only a single atom in between (proximal), or may mean two atoms close enough sterically to be capable of forming a ring (proximal). Preferably R5 / R6 groups attached to the same atom do not together form a ring, although this is not excluded. A single R1, R4, R5 or R6 group on an atom, or two R1 / R4 / R5 groups on the same atom, may form a group which is double bonded to that atom. Accordingly, an R1, R4, R5 or R6 group, or two R1 / R4 / R5 groups attached to the same atom, may together form a =0 group, or a =C(R')2 group (wherein each R' group is the same or different and is H or an organic group, preferably H or a linear or branched Ci-Ce alkyl group). This is more typical in cases where the R groups are attached to a C atom, such that together they form a C=O group ora C=C(R')2 group. Thus, in some cases an XD, XA2 or XB2 atom which is C may bear a =0 group. 'Substituent' and 'organic group' may have any of the following meanings. The organic group may comprise any one or more atoms from any of groups IHA, IVA, VA, VIA or VIIA of the Periodic Table, such as a B, Si, N, P, O, or S atom (e.g. OH, OR, NH2, NHR, NR2, SH, SR, SO2R, SO3H, PO4H2) or a halogen atom (e.g. F, Cl, Br or I) where R is a linear or branched lower hydrocarbon (1-6 C atoms) or a linear or branched higher hydrocarbon (7 C atoms or more, e.g. 7-40 C atoms). The organic group preferably comprises a hydrocarbon group. The hydrocarbon group may comprise a straight chain, a branched chain or a cyclic group. Independently, the hydrocarbon group may comprise an aliphatic or an aromatic group. Also independently, the hydrocarbon group may comprise a saturated or unsaturated group. When the hydrocarbon comprises an unsaturated group, it may comprise one or more alkene functionalities and / or one or more alkyne functionalities. When the hydrocarbon comprises a straight or branched chain group, it may comprise one or more primary, secondary and / or tertiary alkyl groups. When the hydrocarbon comprises a cyclic group it may comprise an aromatic ring, a nonaromatic ring, an aliphatic ring, a heterocyclic group, and / or fused ring derivatives of these groups. The ring may be fully saturated, partially saturated, or fully unsaturated. The cyclic group may thus comprise a benzene, naphthalene, anthracene, phenanthrene, phenalene, biphenylene, pentalene, indene, as-indacene, s-indacene, acenaphthylene, fluorene, fluoranthene, acephenanthrylene, azulene, heptalene, pyrrole, pyrazole, imidazole, 1,2,3-triazole, 1,2,4-triazole, tetrazole, pyrrolidine, furan, oxetane, tetrahydrofuran, 2-aza-tetrahydrofuran, 3-aza-tetrahydrofuran, oxazole, isoxazole, furazan, 1,2,4-oxadiazol, 1,3,4-oxadiazole, thiophene, isothiazole, thiazole, thiolane, pyridine, pyridazine, pyrimidine, pyrazine, piperidine, 2-azapiperidine, 3-azapiperidine, piperazine, pyran, tetra hydro pyran, 2-azapyran, 3-azapyran, 4-azapyran, 2-aza-tetrahydropyran, 3-aza-tetrahydropyran, morpholine, thiopyran, 2-azathiopyran, 3-azathiopyran, 4-azathiopyran, thiane, indole, indazole, benzimidazole, 4-azaindole, 5-azaindole, 6-azaindole, 7-azaindole, isoindole, 4-azaisoindole, 5-azaisoindole, 6-azaisoindole, 7-azaisoindole, indolizine, 1-azaindolizine, 2-azaindolizine, 3-azaindolizine, 5-azaindolizine, 6-azaindolizine, 7-azaindolizine, 8-azaindolizine, 9-azaindolizine, purine, carbazole, carboline, benzofuran, isobenzofuran, benzothiophene, isobenzothiophene, quinoline, cinnoline, quinazoline, quinoxaline, 5-azaquinoline, 6-azaquinoline, 7-azaquinoline, isoquinoline, phthalazine, 6-azaisoquinoline, 7-azaisoquinoline, pteridine, chromene, isochromene, acridine, phenanthridine, perimidine, phenanthroline, phenoxazine, xanthene, phenoxanthiin, and / or thianthrene, as well as regioisomers of the above groups. These groups may generally be attached at any point in the group, and also may be attached at a hetero-atom or at a carbon atom. In some instances particular attachment points are preferred, such as at 1-yl, 2-yl and the like, and these are specified explicitly where appropriate. All tautomeric ring forms are included in these definitions. For example pyrrole is intended to include 1 / 7-pyrrole, 2 / 7-pyrrole and 3H-pyrrole. The number of carbon atoms in the hydrocarbon group is not especially limited, but preferably the hydrocarbon group comprises from 1-40 C atoms. The hydrocarbon group may thus be a lower hydrocarbon (1-6 C atoms) or a higher hydrocarbon (7 C atoms or more, e.g. 7-40 C atoms). The lower hydrocarbon group may be a methyl, ethyl, propyl, butyl, pentyl or hexyl group or regioisomers of these, such as isopropyl, isobutyl, tert-butyl, etc. The number of atoms in the ring of the cyclic group is not especially limited, but preferably the ring of the cyclic group comprises from 3-10 atoms, such as 3, 4, 5, 6, 7, 8, 9 or 10 atoms. The groups comprising heteroatoms described above, as well as any of the other groups defined above, may comprise one or more heteroatoms from any of groups IHA, IVA, VA, VIA or VIIA of the Periodic Table, such as a B, Si, N, P, O, or S atom or a halogen atom (e.g. F, Cl, Br or I). Thus, the substituent may comprise one or more of any of the common functional groups in organic chemistry, such as hydroxy groups, carboxylic acid groups, ester groups, ether groups, aldehyde groups, ketone groups, amine groups, amide groups, imine groups, thiol groups, thioether groups, sulfate groups, sulfonic acid groups, sulfonyl groups, and phosphate groups etc. The substituent may also comprise derivatives of these groups, such as carboxylic acid anhydrides and carboxylic acid halides. In addition, any substituent may comprise a combination of two or more of the substituents and / or functional groups defined herein. Where it is said that a substituent (R1, R3, R4, R5A(e.g. R5A1, R5A2, R5A3), R5B, R5C, R6, R7, R8, R51, and / or R52) is a substituted or unsubstituted organic group, the or each substituted or unsubstituted organic group may in particular be independently selected from: deuterium; a halogen (such as -F, -Cl, -Br and -I); a nitrile group; a substituted or unsubstituted linear or branched Ci-Ce alkyl group (such as Me, Et, Pr, i-Pr, n-Bu, i-Bu, t-Bu, pentyl and hexyl); a substituted or unsubstituted linear or branched Ci-Ce alkyl-aryl group (such as -CH2Ph, -CH2(2,3 or 4)F-Ph, -CH2(2,3 or 4)CI-Ph, -CH2(2,3 or 4)Br-Ph, -CH2(2,3 or4)l-Ph, -CH2CH2Ph, -CH2CH2CH2Ph, -CH2CH2CH2CH2Ph, -CH2CH2CH2CH2CH2Ph, and -CH2CH2CH2CH2CH2CH2Ph); a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (such as -CH2F, -CH2CI, -CH2Br, -CH2I, -CHF2, -CF3, -CCI3 -CBr3, -Cl3, -CH2CH2F, -CH2CF3, -CH2CCI3, -CH2CBr3, and -CH2CI3); NH2 or a substituted or unsubstituted linear or branched primary secondary or tertiary Ci-Ce amine group (such as -NMeH, -NMe2, -NEtH, -NEtMe, -NEt2, -NPrH, -NPrMe, -NPrEt, -NPr2, -NBuH, -NBuMe, -NBuEt, -CH2-NH2, -CH2-NMeH, -CH2-NMe2, -CH2-NEtH, -CH2-NEtMe, -CH2-NEt2, -CH2-NPrH, -CH2-NPrMe, and -CH2-NPrEt); a substituted or unsubstituted amino-aryl group (such as -NH-Ph, -NH-(2,3 or4)F-Ph, -NH-(2,3 or4)CI-Ph, -NH-(2,3 or4)Br-Ph, -NH-(2,3 or 4)I-Ph, -NH-(2,3 or 4)Me-Ph, -NH-(2,3 or 4)Et-Ph, -NH-(2,3 or4)Pr-Ph, -NH-(2,3 or4)Bu-Ph, NH-(2,3 or4)OMe-Ph, -NH-(2,3 or 4)0Et-Ph, -NH-(2,3 or 4)0Pr-Ph, -NH-(2,3 or 4)OBu-Ph, -NH-2,(3,4,5 or 6)F2-Ph, -NH-2,(3,4,5 or 6)CI2-Ph, -NH-2,(3,4,5 or 6)Br2-Ph, -NH-2,(3,4,5 or 6)I2-Ph, -NH-2,(3,4,5 or 6)Me2-Ph, -NH-2,(3,4,5 or 6)Et2-Ph, -NH-2,(3,4,5, or 6)Pr2-Ph, -NH-2,(3,4,5 or 6)Bu2-Ph), a substituted or unsubstituted cyclic amine or amido group (such as pyrrolidin-l-yl, pyrrolidin-2-yl, pyrrolidin-3-yl, piperidin-l-yl, piperidin-2-yl, piperidin-3-yl, piperidin-4-yl, morpholin-2-yl, morpholin-3-yl, morpholin-4-yl, 2-keto-pyrrolidinyl, 3-keto-pyrrolidinyl, 2-keto-piperidinyl, 3-keto-piperidinyl, and 4-keto-piperidinyl); a substituted or unsubstituted cyclic C3-Cs alkyl group (such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl and cyclooctyl); an -OH group; a substituted or unsubstituted linear or branched Ci-Ce alcohol group (such as -CH2OH, -CH2CH2OH, -CH(CH3)CH2OH, -C(CH3)2OH, -CH2CH2CH2OH, -CH2CH2CH2CH2OH, -CH(CH3)CH2CH2OH, -CH(CH3)CH(CH3)OH, -CH(CH2CH3)CH2OH, -C(CH3)2CH2OH, -CH2CH2CH2CH2CH2OH, and -CH2CH2CH2CH2CH2CH2OH); a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid group (such as -COOH, -CH2COOH, -CH2CH2COOH, -CH2CH2CH2COOH, -CH2CH2CH2CH2COOH, and -CH2CH2CH2CH2CH2COOH); a substituted or unsubstituted linear or branched carbonyl group (such as -(CO)Me, -(CO)Et, -(CO)Pr, -(CO)iPr, -(CO)nBu, -(CO)iBu, -(CO)tBu, -(CO)Ph, -(CO)CH2Ph, -(CO)CH2OH, -(CO)CH2OCH3, -(CO)CH2NH2, -(CO)CH2NHMe, -(CO)CH2NMe2, -(CO)-cyclopropyl, -(CO)-l,3-epoxypropan-2-yl; -(CO)NH2, -(CO)NHMe, -(CO)NMe2, -(CO)NHEt, -(CO)NEt2, -(CO)-pyrollidine-N-yl, -(CO)-morpholine-N-yl, -(CO)-piperazine-N-yl, -(CO)-N-methyl-piperazine-N-yl, -(CO)NHCH2CH2OH, -(CO)NHCH2CH2OMe, -(CO)NHCH2CH2NH2, -(CO)NHCH2CH2NHMe, and -(CO)NHCH2CH2NMe2); a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid ester group (such as -COOMe, -COOEt, -COOPr, -COO-i-Pr, -COO-n-Bu, -COO-i-Bu, -COO-t-Bu, -CH2COOMe, -CH2CH2COOMe, -CH2CH2CH2COOMe, and -CH2CH2CH2CH2COOMe); a substituted or unsubstituted linear or branched Ci-Ce amide group (such as -CO-NH2, -CO-NMeH, -CO-NMe2, -CO-NEtH, -CO-NEtMe, -CO-NEt2, -CO-NPrH, -CO-NPrMe, and -CO-NPrEt); a substituted or unsubstituted linear or branched C1-C7 amino carbonyl group (such as -NH-CO-Me, -NH-CO-Et, -NH-CO-Pr, -NH-CO-Bu, -NH-CO-pentyl, -NH-CO-hexyl, -NH-CO-Ph, -NMe-CO-Me, -NMe-CO-Et, -NMe-CO-Pr, -NMe-CO-Bu, -NMe-CO-pentyl, -NMe-CO-hexyl, -NMe-CO-Ph); a substituted or unsubstituted linear or branched C1-C7 alkoxy or aryloxy group (such as -OMe, -OEt, -OPr, -O-i-Pr, -O-n-Bu, -O-i-Bu, -O-t-Bu, -O-pentyl, -O-hexyl, -OCH2F, -OCHF2, -OCF3, -OCH2CI, -OCHCb, -OCCI3, -O-Ph, -O-CH2-Ph, -O-CH2-(2,3 or 4)-F-Ph, -O-CH2-(2,3 or 4)-CI-Ph, -CH2OMe, -CH2OEt, -CH2OPr, -CH2OBu, -CH2CH2OMe, -CH2CH2CH2OMe, -CH2CH2CH2CH2OMe, and -CH2CH2CH2CH2CH2OMe); a substituted or unsubstituted linear or branched aminoalkoxy group (such as-OCH2NH2, -OCH2NHMe, -OCH2NMe2, -OCH2NHEt, -OCH2NEt2, -OCH2CH2NH2, -OCH2CH2NHMe, -OCH2CH2NMe2, -OCH2CH2NHEt, and -OCH2CH2NEt2); a substituted or unsubstituted sulfonyl group (such as -SO2Me, -SO2Et, -SO2Pr, -SO2iPr, -SO2Ph, -SO2-(2,3 or 4)-F-Ph, -SO2-cyclopropyl, -SO2CH2CH2OCH3, -SO2NH2, -SO2NHMe, -SO2NMe2, -SO2NHEt, -SO2NEt2, -SO2-pyrrolidine-N-yl, -SO2-morpholine-N-yl, -SO2NHCH2OMe, and -SO2NHCH2CH2OMe); a substituted or unsubstituted aminosulfonyl group (such as -NHSO2Me, -NHSO2Et, - NHSO2Pr, -NHSO2iPr, -NHSO2Ph, -NHSO2-(2,3 or4)-F-Ph, -NHSO2-cyclopropyl, -NHSO2CH2CH2OCH3); a substituted or unsubstituted aromatic group (such as Ph-, 2-F-Ph-, 3-F-Ph-, 4-F-Ph-, 2-CI-Ph-, 3-CI-Ph-, 4-CI-Ph-, 2-Br-Ph-, 3-Br-Ph-, 4-Br-Ph-, 2-l-Ph-, 3-l-Ph, 4-l-Ph-, 2,(3,4,5 or 6)-F2-Ph-, 2,(3,4,5 or 6)-CI2-Ph-, 2,(3,4,5 or 6)-Br2-Ph-, 2,(3,4,5 or 6)-l2-Ph-, 2,(3,4,5 or 6)-Me2-Ph-, 2,(3,4,5 or 6)-Et2-Ph-, 2,(3,4,5 or 6)-Pr2-Ph-, 2,(3,4,5 or 6)-Bu2-Ph-, 2,(3,4,5 or 6)-(CN)2-Ph-, 2,(3,4,5 or 6)-(NO2)2-Ph-, 2,(3,4,5 or 6)-(NH2)2-Ph-, 2,(3,4,5 or 6)-(MeO)2-Ph-, 2,(3,4,5 or 6)-(CF3)2-Ph-, 3,(4 or 5)-F2-Ph-, 3,(4 or 5)-CI2-Ph-, 3,(4 or 5)-Br2-Ph-, 3,(4 or 5)-12-Ph-, 3,(4 or 5)-Me2-Ph-, 3,(4 or 5)-Et2-Ph-, 3,(4 or 5)-Pr2-Ph-, 3,(4 or 5)-Bu2-Ph-, 3,(4 or 5)-(CN)2-Ph-, 3,(4 or 5)-(NO2)2-Ph-, 3,(4 or 5)-(NH2)2-Ph-, 3,(4 or 5)-(MeO)2-Ph-, 3,(4 or 5)-(CF3)2-Ph-, 2-Me-Ph-, 3-Me-Ph-, 4-Me-Ph-, 2-Et-Ph-, 3-Et-Ph-, 4-Et-Ph-, 2-Pr-Ph-, 3-Pr-Ph-, 4-Pr-Ph-, 2-Bu-Ph-, 3-Bu-Ph-, 4-Bu-Ph-, 2-(CN)-Ph-, 3-(CN)-Ph-, 4-(CN)-Ph-, 2-(NO2)-Ph-, 3-(NO2)-Ph-, 4-(NO2)-Ph-, 2-(NH2)-Ph-, 3-(NH2)-Ph-, 4-(NH2)-Ph-, 2-MeO-Ph-, 3-MeO-Ph-, 4-MeO-Ph-, 2-(NH2-CO)-Ph-, 3-(NH2-CO)-Ph-, 4-(NH2-CO)-Ph-, 2-CF3-Ph-, 3-CF3-Ph-, 4-CF3-Ph-, 2-CF3O-Ph-, 3-CF3O-Ph-, and 4-CF3O-Ph-); a saturated or unsaturated, substituted or unsubstituted, heterocyclic group, optionally an aromatic heterocyclic group or a non-aromatic heterocyclic group (such as pyrrole-l-yl, pyrrole-2-yl, pyrrole-3-yl, pyrazole-l-yl, pyrazole-3-yl, pyrazole-4-yl, pyrazole-5-yl, imidazole-l-yl, imidazole-2-yl, imidazole-4-yl, imidazole-5-yl, 1,2,3-triazole-l-yl, l,2,3-triazole-4-yl, l,2,3-triazole-5-yl, 1,2,4-triazole-l-yl, l,2,4-triazole-3-yl, l,2,4-triazole-5-yl, pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, pyridazine-3-yl, pyridazine-4-yl, pyrimidin-2-yl, pyrimidin-4-yl, pyrimidin-5-yl, pyrimidin-6-yl, pyrazine-2-yl, pyrrolidine-l-yl, pyrrolidine-2-yl, pyrrolidine-3-yl, piperidine-l-yl, piperidine-2-yl, piperidine-3-yl, piperidine-4-yl, 2-azapiperidine-l-yl, 2-azapiperidine-3-yl, 2-azapiperidine-4-yl, 3-azapiperidine-l-yl, 3-azapiperidine-2-yl, 3-azapiperidine-4-yl, 3-azapiperidine-5-yl, piperazine-l-yl, piperazine-2-yl, furan-2-yl, furan-3-yl, pyran-2-yl, pyran-3-yl, pyran-4-yl, 2-azapyran-2-yl, 2-azapyran-3-yl, 2-azapyran-4-yl, 2-azapyran-5-yl, 2-azapyran-6-yl, 3-azapyran-2-yl, 3-azapyran-4-yl, 3-azapyran-5-yl, 3-azapyran-6-yl, 4-azapyran-2-yl, 4-azapyran-3-yl, 4-azapyran-4-yl, 4-azapyran-5-yl, 4-azapyran-6-yl, oxetan-2-yl, oxetan-3-yl, tetrahydrofuran-2-yl, tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-2-yl, 2-aza-tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-4-yl, 2-aza-tetrahydrofuran-5-yl, 3-aza-tetrahydrofuran-2-yl, 3-aza-tetrahydrofuran-3-yl, 3-aza-tetrahydrofuran-4-yl, 3-aza-tetrahydrofuran-5-yl, tetrahydropyran-2-yl, tetrahydropyran-3-yl, tetrahydropyran-4-yl, 2-aza-tetrahydropyran-2-yl, 2-aza-tetrahydropyran-3-yl, 2-aza-tetrahydropyran-4-yl, 2-aza-tetrahydropyran-5-yl, 2-aza-tetrahydropyran-6-yl, 3-aza-tetrahydropyran-2-yl, 3-aza-tetrahydropyran-3-yl, 3-aza-tetrahydropyran-4-yl, 3-aza-tetrahydropyran-5-yl, 3-aza-tetrahydropyran-6-yl, morpholine-2-yl, morpholine-3-yl, morpholine-4-yl, thiophen-2-yl, thiophen-3-yl, isothiazole-3-yl, isothiazole-4-yl, isothiazole-5-yl, thiazole-2-yl, thiazole-4-yl, thiazole-5-yl, thiopyran-2-yl, thiopyran-3-yl, thiopyran-4-yl, 2-azathiopyran-2-yl, 2-azathiopyran-3-yl, 2-azathiopyran-4-yl, 2-azathiopyran-5-yl, 2-azathiopyran-6-yl, 3-azathiopyran-2-yl, 3-azathiopyran-4-yl, 3-azathiopyran-5-yl, 3-azathiopyran-6-yl, 4-azathiopyran-2-yl, 4-azathiopyran-3-yl, 4-azathiopyran-4-yl, 4-azathiopyran-5-yl, 4-azathiopyran-6-yl, thiolane-2-yl, thiolane-3-yl, thiane-2-yl, thiane-3-yl, thiane-4-yl, oxazol-2-yl, oxazol-4-yl, oxazol-5-yl, isoxazol-3-yl, isoxazol-4-yl, isoxazol-5-yl, furazan-3-yl, (l,3,4-oxadiazol)-2-yl, (l,3,4-oxadiazol)-5-yl, (l,2,4-oxadiazol)-3-yl, (l,2,4-oxadiazol)-5-yl; and tetrazole-l-yl, tetrazole-2-yl, tetrazole-5-yl). With the exception of R4, pairs of substituent groups with matching identifiers may together form a single group. For example, a pair of R5A groups attached to the same atom may together represent a carbonyl group. Alternatively or additionally, a pair of substituent groups attached to different atoms of the same ring may be connected to form a ring. A pair of R5A groups attached to different atoms may together form a ring with ring A atoms. A pair of R5B groups attached to different atoms may together form a ring with ring B atoms. A pair of R5C groups attached to different atoms may together form a ring with ring C atoms. It is also contemplated that an R5C group and an R6 group attached to different atoms may together form a ring with ring C atoms. The R4 groups are not fused to form a ring. In particular, the R4 groups are not fused into a spirocyclopropyl group. Preferably, each R5 group (R5A, R5B, R5C) is independently absent or selected from: H, deuterium, a halogen (such as -F, -Cl, -Br, and -I; preferably F or Cl), a nitrile group, a Ci-Ce alkyl group, a Ci-Ce halogenated alkyl group (preferably CF3, CHF2, or CH2CF3), a cyclopropyl group, an -OH group, a Ci-Ce alcohol group, a C1-C7 amino carbonyl group (such as -NH-CO-Me), an -NH2 group, a Ci-Ce amino group, and a Ci-Ce alkoxy group. When a pair of R5 groups forms a ring, the pair of R5 groups may together represent a group selected from -CH2-, -CH2CH2-, -CH=CH-CH=CH-, or -NH-CO-NH-. In particular, it is contemplated that two R5A groups may together represent an alkyl group bridging ring A. Various ones of the substituent groups may be bonded to a nitrogen atom. For example, when Q is: R8 is bonded to a nitrogen. In some instances, an R1, R4, or R5A or R5B group may be attached to a ring atom which is N. The preferred substituents for N atoms are: H; a substituted or unsubstituted linear or branched Ci-Ce alkyl group (such as Me, Et, Pr, i-Pr, n-Bu, i-Bu, t-Bu, pentyl and hexyl); a substituted or unsubstituted linear or branched Ci-Ce alkyl-aryl group (such as -CH2Ph, -CH2(2,3 or 4)F-Ph, -CH2(2,3 or 4)CI-Ph, -CH2(2,3 or 4)Br-Ph, -CH2(2,3 or4)l-Ph, -CH2CH2Ph, -CH2CH2CH2Ph, -CH2CH2CH2CH2Ph, -C^OhOhC^C^Ph, and -CH2CH2CH2CH2CH2CH2Ph); a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (such as -CH2F, -CF3, -CH2CH2F and -CH2CF3); a substituted or unsubstituted cyclic amine or amido group (such as pyrrolidin-3-yl, piperidin-3-yl, piperidin-4-yl, 2-keto-pyrrolidinyl, 3-keto-pyrrolidinyl, 2-keto-piperidinyl, 3-keto-piperidinyl, and 4-keto-piperidinyl); a substituted or unsubstituted cyclic C3-Cs alkyl group (such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl and cyclooctyl); a substituted or unsubstituted linear or branched C2-Ce alcohol group (such as -CH2CH2OH, -CH(CH3)CH2OH, -C(CH3)2OH, -CH2CH2CH2OH, -CH2CH2CH2CH2OH, -CH(CH3)CH2CH2OH, -CH(CH3)CH(CH3)OH, -CH(CH2CH3)CH2OH, -C(CH3)2CH2OH, -ch2ch2ch2ch2ch2oh, and -CH2CH2CH2CH2CH2CH2OH); a substituted or unsubstituted linear or branched C2-Ce carboxylic acid group (such as -CH2COOH, -CH2CH2COOH, -CH2CH2CH2COOH, -CH2CH2CH2CH2COOH, and -CH2CH2CH2CH2CH2COOH); a substituted or unsubstituted linear or branched carbonyl group (such as -(CO)Me, -(CO)Et, -(CO)Pr, -(CO)-i_Pr, -(CO)-n-Bu, -(CO)-i-Bu, -(CO)-t-Bu, -(CO)Ph, -(CO)CH2Ph, -(CO)CH2OH, -(CO)CH2OCH3, -(CO)CH2NH2, -(CO)CH2NHMe, -(CO)CH2NMe2, -(CO)-cyclopropyl, -(CO)-l,3-epoxypropan-2-y I; -(CO)NH2, -(CO)NHMe, -(CO)NMe2, -(CO)NHEt, -(CO)NEt2, -(CO)-pyrollidine-N-yl, -(CO)-morpholine-N-yl, -(CO)-piperazine-N-yl, -(CO)-N-methyl-piperazine -N-yl, -(CO)NHCH2CH2OH, -(CO)NHCH2CH2OMe, -(CO)NHCH2CH2NH2, -(CO)NHCH2CH2NHMe, and -(CO)NHCH2CH2NMe2); a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid ester group (such as -COOMe, -COOEt, -COOPr, -COO-i-Pr, -COO-n-Bu, -COO-i-Bu, -COO-t-Bu, -CH2COOMe, -CH2CH2COOMe, -CH2CH2CH2COOMe, and -CH2CH2CH2CH2COOMe); a substituted or unsubstituted linear or branched Ci-Ce amide group (such as -CO-NH2, -CO-NMeH, -CO-NMe2, -CO-NEtH, -CO-NEtMe, -CO-NEt2, -CO-NPrH, -CO-NPrMe, and -CO-NPrEt); a substituted or unsubstituted sulfonyl group (such as -SO2Me, -SO2Et, -SO2Pr, -SO2iPr, -SO2Ph, -SO2-(2,3 or 4)-F-Ph, -SO2-cyclopropyl, -SO2CH2CH2OCH3), -SO2NH2, -SO2NHMe, -SO2NMe2, -SO2NHEt, -SO2NEt2, -SO2-pyrrolidine-N-yl, -SO2-morpholine-N-yl, -SO2NHCH2OMe, and -SO2NHCH2CH2OMe); a substituted or unsubstituted aromatic group (such as Ph-, 2-F-Ph-, 3-F-Ph-, 4-F-Ph-, 2-CI-Ph-, 3-CI-Ph-, 4-CI-Ph-, 2-Br-Ph-, 3-Br-Ph-, 4-Br-Ph-, 2-l-Ph-, 3-l-Ph, 4-l-Ph-, 2,(3,4,5 or 6)-F2-Ph-, 2,(3,4,5 or 6)-CI2-Ph-, 2,(3,4,5 or 6)-Br2-Ph-, 2,(3,4,5 or 6)-l2-Ph-, 2,(3,4,5 or 6)-Me2-Ph-, 2,(3,4,5 or 6)-Et2-Ph-, 2,(3,4,5 or 6)-Pr2-Ph-, 2,(3,4,5 or 6)-Bu2-Ph-, 2,(3,4,5 or 6)-(CN)2-Ph-, 2,(3,4,5 or 6)-(NO2)2-Ph-, 2,(3,4,5 or 6)-(NH2)2-Ph-, 2,(3,4,5 or 6)-(MeO)2-Ph-, 2,(3,4,5 or 6)-(CF3)2-Ph-, 3,(4 or 5)-F2-Ph-, 3,(4 or 5)-CI2-Ph-, 3,(4 or 5)-Br2-Ph-, 3,(4 or 5)-12-Ph-, 3,(4 or 5)-Me2-Ph-, 3,(4 or 5)-Et2-Ph-, 3,(4 or 5)-Pr2-Ph-, 3,(4 or 5)-Bu2-Ph-, 3,(4 or 5)-(CN)2-Ph-, 3,(4 or 5)-(NO2)2-Ph-, 3,(4 or 5)-(NH2)2-Ph-, 3,(4 or 5)-(MeO)2-Ph-, 3,(4 or 5)-(CF3)2-Ph-, 2-Me-Ph-, 3-Me-Ph-, 4-Me-Ph-, 2-Et-Ph-, 3-Et-Ph-, 4-Et-Ph-, 2-Pr-Ph-, 3-Pr-Ph-, 4-Pr-Ph-, 2-Bu-Ph-, 3-Bu-Ph-, 4-Bu-Ph-, 2-(CN)-Ph-, 3-(CN)-Ph-, 4-(CN)-Ph-, 2-(NO2)-Ph-, 3-(NO2)-Ph-, 4-(NO2)-Ph-, 2-(NH2)-Ph-, 3-(NH2)-Ph-, 4-(NH2)-Ph-, 2-MeO-Ph-, 3-MeO-Ph-, 4-MeO-Ph-, 2-(NH2-CO)-Ph-, 3-(NH2-CO)-Ph-, 4-(NH2-CO)-Ph-, 2-CF3-Ph-, 3-CF3-Ph-, 4-CF3-Ph-, 2-CF3O-Ph-, 3-CF3O-Ph-, and 4-CF3O-Ph-); and a substituted or unsubstituted heterocyclic group (such as pyrrole-2-yl, pyrrole-3-yl, pyrazole-3-yl, pyrazole-4-yl, pyrazole-5-yl, imidazole-2-yl, imidazole-4-yl, imidazole-5-yl, l,2,3-triazole-4-yl, l,2,3-triazole-5-yl, l,2,4-triazole-3-yl, l,2,4-triazole-5-yl, pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, pyridazine-3-yl, pyridazine-4-yl, pyrimidin-2-yl, pyrimidin-4-yl, pyrimidin-5-yl, pyrimidin-6-yl, pyrazine-2-yl, pyrrolidine-2-yl, pyrrolidine-3-yl, piperidine-2-yl, piperidine-3-yl, piperidine-4-yl, 2-azapiperidine-3-yl, 2-azapiperidine-4-yl, 3-azapiperidine-2-yl, 3-azapiperidine-4-yl, 3-azapiperidine-5-yl, piperazine-2-yl, furan-2-yl, furan-3-yl, pyran-2-yl, pyran-3-yl, pyran-4-yl, 2-azapyran-3-yl, 2-azapyran-4-yl, 2-azapyran-5-yl, 2-azapyran-6-yl, 3-azapyran-2-yl, 3-azapyran-4-yl, 3-azapyran-5-yl, 3-azapyran-6-yl, 4-azapyran-2-yl, 4-azapyran-3-yl, 4-azapyran-5-yl, 4-azapyran-6-yl, tetrahydrofuran-2-yl, tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-4-yl, 2-aza-tetrahydrofuran-5-yl, 3-aza-tetrahydrofuran-2-yl, 3-aza-tetrahydrofuran-4-yl, 3-aza-tetrahydrofuran-5-yl, tetrahydropyran-2-yl, oxetan-3-yl, tetrahydropyran-3-yl, tetrahydropyran-4-yl, 2-aza-tetrahydropyran-3-yl, 2-aza-tetrahydropyran-4-yl, 2-aza-tetrahydropyran-5-yl, 2-aza-tetrahydropyran-6-yl, 3-aza-tetrahydropyran-2-yl, 3-aza-tetrahydropyran-4-yl, 3-aza-tetrahydropyran-5-yl, 3-aza-tetrahydropyran-6-yl, morpholine-2-yl, morpholine-3-yl, thiophen-2-yl, thiophen-3-yl, isothiazole-3-yl, isothiazole-4-yl, isothiazole-5-yl, thiazole-2-yl, thiazole-4-yl, thiazole-5-yl, thiopyran-2-yl, thiopyran-3-yl, thiopyran-4-yl, 2-azathiopyran-3-yl, 2-azathiopyran-4-yl, 2-azathiopyran-5-yl, 2-azathiopyran-6-yl, 3-azathiopyran-2-yl, 3-azathiopyran-4-yl, 3-azathiopyran-5-yl, 3-azathiopyran-6-yl, 4-azathiopyran-2-yl, 4-azathiopyran-3-yl, 4-azathiopyran-5-yl, 4-azathiopyran-6-yl, thiolane-2-yl, thiolane-3-yl, thiane-2-yl, thiane-3-yl, thiane-4-yl, oxazol-2-yl, oxazol-4-yl, oxazol-5-yl, isoxazol-3-yl, isoxazol-4-yl, isoxazol-5-yl, furazan-3-yl, (l,3,4-oxadiazol)-2-yl, (l,3,4-oxadiazol)-5-yl, (l,2,4-oxadiazol)-3-yl, (l,2,4-oxadiazol)-5-yl; and tetrazole-5-yl). Optionally, R8, or any R1, R4, or R5A or R5B that is attached to a ring nitrogen, may preferably be selected from H, a substituted or unsubstituted linear or branched Ci-Ce alkyl group, and a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group. An R1 or R4 attached to a N is preferably selected from H, a Cl to C3 alkyl group, and a Cl to C3 fluoroalkyl group, such as -CH2CF3. Head group - general The head group of the PARP1 inhibitor compound comprises rings D and E, as shown in the general formula below: A dotted line represents a bond selected from a single bond and a double bond. Ring D may be a saturated ring, an unsaturated non-aromatic ring, or an aromatic ring. y is 0,1, or 2. In other words, ring D may be a 5-, 6-, or 7-membered ring. In particular, ring D may be a 5-membered ring (y=0) or a 6-membered ring (y=l). Compounds having 6-membered D-rings are particularly preferred. Each XD represents an atom independently selected from C, N, O, and S. The XD atoms are typically selected such that ring D is free of any 0-0 bonds. Usually, at least one XD is C. Optionally, each XD is independently selected from C and N. Further optionally, each XD is C. Rings D and E are connected via atoms XET and XEB. These atoms may be referred to herein as the "bridgehead atoms". XET and XEB are each individually selected from C and N. Typically, at least one of XET and XEB is C. Preferably, XET is C and XEB is either C or N, and most preferably XET and XEB are each C. Ring D may bear optional substituents R1 and R4. In the above general formula, each R1 is independently absent or selected from H and a substituted or unsubstituted organic group; and each R4 is independently absent or selected from H and a substituted or unsubstituted organic group, with the proviso that the R4 groups are not fused to form a ring. For any given ring D atom XD, the number of substituents (R1 or R4 groups), and the nature of the bonds to adjacent atoms of ring D are selected as appropriate depending upon the identity of the XD atom, to satisfy the normal valency of that atom. When an XD atom is O: the atom lacks any substituent (R1 or R4); the atom is bonded to adjacent ring atoms via single bonds; and neither adjacent ring atom is O. When an XD atom is N: the atom bears up to one substituent (R1 or R4); if the atom bears a substituent, then the atom is bonded to adjacent ring atoms via single bonds; or if the atom does not bear a substituent, then the atom forms a double bond with one adjacent ring atom, and a single bond with the other adjacent ring atom. When an XD atom is C: the atom bears one or two substituents (R1 or R4); if the atom bears two substituents, then the atom is bonded to adjacent ring atoms via single bonds; or if the atom bears one substituent, then the atom forms a double bond with one adjacent ring atom, and a single bond with the other adjacent ring atom. Each R1 and each R4 may be independently absent or selected from H and a substituted or unsubstituted organic group. The organic group may be selected from any of the various groups already discussed, subject to the proviso that the R4 groups are not fused to form a ring. In particular, the R4 groups do not represent a spirocyclopropyl group. For example, each R1 and each R4 may independently be absent or selected from: H; a halogen; a nitrile group; a Cl to C6 acyclic alkyl group; a Cl to C6 acyclic alkoxy group; a Cl to C6 acyclic haloalkyl group; a Cl to C6 acyclic haloalkoxy group, such as -OCF3 or OCHF2; a Cl to C6 acyclic aminoalkyl group; and R22 being selected from H, a halogen, a Cl to C6 alkyl group, a C3 to C6 cycloalkyl group, a Cl to C6 alkoxy group, a Cl to C6 haloalkyl group, and each R23 being independently selected from H; a halogen; a Cl to C6 alkyl group; a Cl to C6 aminoalkyl group; a Cl to C6 alkoxy group; a Cl to C6 haloalkoxy group; such as -OCF3 or OCHF2; and a Cl to C6 haloalkyl group. Optionally, each R1 and each R4 is independently absent or selected from H; a halogen, optionally Cl or F; a Cl to C3 acyclic alkyl group, optionally a methyl group; a Cl to C3 haloalkyl group, optionally a halomethyl group such as -CH2F, -CHF2, or -CF3; a haloethyl group, such as -CH2CF3; and a nitrile group. Preferably, each R1 and each R4 is independently absent or selected from: H; Cl; F; a halomethyl group, such as CF3; and a nitrile group. Most preferably, each R1 and each R4 is independently absent or selected from H and F. For instance, exactly one R1 may be F, or alternatively exactly one R4 may be F. Alternatively, each R1 and each R4 is absent or H. 31 Typically, ring D bears no more than two organic groups in total, with all other R1 and R4 groups being either absent or H. 5 As shown in the general formula, ring E bears a substituent R3, which may be H or a substituted or unsubstituted organic group. R3 is preferably selected from H, a Cl to C3 alkyl group, and a Cl to C3 haloalkyl group. Most preferably, R3 is H. 10 Example head groups - N-bridged variants When XEB is N, the PARP1 inhibitor compound may have a structure selected from: with R1, R4, and R3 each being as defined above. 15 The preferred head group in this class is: Head group - general structural formulae for C-bridged variants In examples where XEB and XET are each C, the PARP1 inhibitor compound may have a structure selected from: with R1, R3 and R4 each being as previously discussed. Head groups - aromatic examples 5 Ring D of the PARP1 inhibitor compound may be an aromatic ring. For instance, ring D may be a 6-membered carbocyclic ring: R4 and each R1 being present. In such examples, the head group of the PARP1 inhibitor compound may have a substitution pattern as shown below: Preferred PARP1 inhibitor compounds in this class include: Other preferred examples of PARP1 inhibitor compounds with aromatic D rings include: R4 and each R1 being present. Particularly preferred PARP1 inhibitors in this class may be selected from: 5 Additional examples of PARP1 inhibitor compounds having aromatic D rings include those R4 and each R1 being present. Preferred structures for PARP1 inhibitor compounds with aromatic D rings include: Additional examples of PARP1 inhibitor compounds include those having a structure selected from: Alternatively, ring D may be a non-aromatic ring. 5 Ring D may be a non-aromatic carbocyclic ring. For example, the PARP1 inhibitor compound may have a structure selected from: As will be appreciated, in these examples, each R1 and each R4 is present. Preferred PARP1 inhibitor compounds in the above class have a structure of: O Ring D may alternatively be a cyclic ether, having a structure selected from: each R1 and each R4 being present. In accordance with a still further possibility, ring D may be a cyclic amine. Examples of such each R1 and each R4 is present. An R1 or R4 which is bonded to an N is preferably selected from H, a Cl to C3 alkyl group, and a Cl to C3 fluoroalkyl group. Preferred structures for PARP1 inhibitor compounds with non-aromatic D rings include: Additional examples of structures for PARP1 inhibitor compounds include: L group - general Group L of the PARP1 inhibitor compounds provided herein has a structure according to 5 general formula: where: ring C is an aromatic ring; XA1 is C or N; each XA2 is independently selected from C, N, O and S; each XB2 is independently selected from C, N, O and S; XB3 is selected from C and N; each Xc is independently selected from C, N, O, and S, with the proviso that ring C is a heterocycle; each R5A, R5B, and R5C is independently absent or selected from H and a substituted or unsubstituted organic group; R6 is selected from H and a substituted or unsubstituted organic group; n is 0,1, 2, 3, 4, or 5; m is 0,1, 2, 3, 4, or 5, with the proviso that n + m is in the range 2 to 5; p is 1, 2 or 3; q is 1, 2 or 3, with the proviso that p + q is in the range 2 to 5; r is 0,1, 2, 3, or 4; and s is 0,1, 2, 3, or 4, with the proviso that r + s is 3 or 4; and Q is a bond ora linking group having a structure selected from: where: t is 0, 1, 2, 3, 4 or 5; u is 0,1, 2, 3, 4 and 5, with the proviso that t + u is in the range 0 to 6; and each R7 and R8 is independently selected from H and a substituted or unsubstituted organic group. Each XA2, each XB2, and each Xc is independently selected from C, N, O and S, with the proviso that at least one Xc is O, N or S (preferably N) such that ring C is a heterocycle. One or more, and most preferably all, of the following provisos may apply: i) At least one X atom per ring is C. When ring A or ring B is 4-membered, that ring typically includes at most one heteroatom. When ring A or ring B is 5- or 6-membered, that ring typically includes at most three heteroatoms, optionally at most two heteroatoms. ii) Each of rings A, B, and C individually may comprise at most three heteroatoms. iii) The compound is not a quaternary ammonium compound. iv) The compound is free of 0-0, S-S, and S-0 bonds. Each portion of group L is discussed in more detail below. Ring A Ring A of the PARP1 inhibitor compound has the general structure: 5A2 n is 0,1, 2, 3, 4, or 5; and m is 0, 1, 2, 3, 4, or 5, with the proviso that n + m is in the range 2 to 5. In other words, ring A may be a 4, 5, 6, or 7-membered ring. Preferably, ring A is a 5- or 6-membered ring (n + m = 3 or 4), with 5-membered rings (n + m = 3) being particularly preferred. Preferably, both n and m are at least 1. In other words, the atoms which connect ring A to rings E and B are preferably non-adjacent. XA1 is bonded to ring E, and is selected from C and N. When XA1 is N, R5A1 is absent. When XA1 is C, R5A1 may be present or absent, and is preferably present. Each XA2 is independently selected from C, N, O, and S. Preferably, each XA2 is independently selected from C and N. Most preferably, each XA2 is C. Each R5A group (i.e., R5A1, R5A2, R5A3) is independently absent or selected from H and a substituted or unsubstituted organic group. The number of R5A groups may be selected such that ring A is saturated, unsaturated and non-aromatic, or aromatic. Preferably, ring A is saturated. In most implementations, no more than two R5A groups are substituted or unsubstituted organic groups. Most typically, no more than one R5A group is a substituted or unsubstituted organic group. Generally, when an R5A group is present, that R5A group is preferably H. Ring A may be a bicyclic ring, in which two R5A groups are fused together. The bicyclic ring may be a bridged bicyclic ring. r5A3 js most typically H. It is preferable that, when present, each R5A is independently selected from H; a halogen, optionally F; a hydroxyl group; a carbonyl group; and a Cl to C3 alkyl group, optionally wherein a pair of R5A groups form a ring, further optionally wherein the ring bridges ring A. Particularly preferably: i) one pair of R5A groups forms -CH2- group bridging ring A, with each other R5A being H; or ii) each R5A is H. Ring A may be a 7-membered ring. For example, ring A may be a cycloheptane having a structure selected from: each R5A being present. Alternatively, ring A may be a 6-membered non-aromatic ring, such as a cyclohexane, cyclohexene, or tetrahydropyran. Ring A may for example have a structure selected from: (to Ring E) R5\R“r5a r5A _5A __o5A3 R / \ (to Ring B) p5A \ 5a R R _5A (to Ring E). R r5^V\—R5A 5A __.r5A3 R -7\ K R5A / \ / sa\ 5A (to Ring B) R R r5A (to Ring Ek 1 r5A r5a — 5A__ __r5A3 R — 5A / R (to Ring B) 6a\ 5a R R (to Ring E). r~- \ / „5A _5A X R \ R \ \ / _ 5A R5A\^^^ R -7 (to Ring B) p5A\sa R R each R5A being present. In accordance with another possibility, ring A may be a 5-membered non-aromatic ring, such as a cyclopentane, cyclopentene, or a tetra hydrofuran. Ring A may for example have a 5 structure selected from: 50 each R5A being present. In other examples, ring A may be a 4-membered ring having a structure of: In accordance with still another possibility, ring A may be a bridged ring. Examples of suitable bridged ring structures include: each R5A being present. Ring A typically includes no more than one bridging group. In the three examples immediately above, no R5A groups are fused to form a further ring, and each 10 R5A group is preferably H. Examples of suitable structures for ring A include: where Qa represents a bond to ring E and Qb represents a bond to ring B. Ring A may have a structure of: wherein: Qa represents a bond to ring E and Q.b represents a bond to ring B; 5 mis lor 2; n is 1 or 2; each R5A2 and R5A3 independently is absent or selected from H and a substituted or unsubstituted organic group, preferably wherein R5A3 is H; and wherein: 10 i) XA1 is C and R5A1 is selected from H and a substituted or unsubstituted organic group; or ii) XA1 is N and R5A1 is absent. Each R5A1, R5A2 and R5A3 may independently be absent or selected from H; a halogen, 15 optionally F; a hydroxyl group; a carbonyl group; and a Cl to C3 alkyl group, optionally wherein a pair of R5A groups form a Cl to C3 alkyl group bridging ring A. Preferably, each R5A1, R5A2 and R5A3 is absent or H. Preferred A ring structures include: (to ring E) / \ (to ring B) (to ring E) p _(to ring B) (to ring E) p 'l ..........(to r'n8 B) (to ring E) „ _(to ring B) (to ring B) (to ring E) (to ring B) (to ring E) (to ring E) (to ring B) Particularly preferred A ring structures are: (to ring E) (to ring B) (to ring E) (to ring E) (to ring E) The most preferred ring A structure is: (to ring E) (to ring B) Ring B Ring B of group L has a general structure of: Each XB2 is independently selected from C, N, O and S. XB3 is selected from C and N. p is 1, 2 or 3; and q is 1, 2 or 3, with the proviso that p + q is in the range 2 to 5. In other words, ring B may be a 4-, 5-, 6- or 7-membered ring. Preferably, ring B is a 6-membered ring, and most preferably p and q are both equal to 2. Each R5B is independently absent or selected from H and a substituted or unsubstituted organic group. Preferably, each R5B is independently absent or H. Depending upon the number of R5B groups present, ring B may be saturated or unsaturated. Preferably, ring B is a saturated ring. Preferably, each XB2 is C, and ring B has a structure of: XB3 is preferably N. In such examples, Ring B may have a structure of: 5B R (C)p Ring B may have a general structure selected from: More specific examples of suitable ring B structures include: Most preferably, ring B has a structure of: Linker - Q group Ring B is coupled to ring C via a linker Q: Q may be a bond. In other words, atom XB3 may be directly connected to ring C. 10 Alternatively, Qmay be a group selected from: where: t is a number selected from 0, 1, 2, 3, 4 and 5; and u is independently a number selected from 0,1, 2, 3, 4 and 5; with the proviso that t + u is a number selected from 0,1, 2, 3, 4, 5 and 6; and 5 each R7 and R8 is independently selected from H and a substituted or unsubstituted organic group. Preferably, each R7 is independently selected from H; a halogen, optionally F; a Cl to C6 alkyl group; and a Cl to C6 haloalkyl group. When XB3 of ring B is N, and Q is R , t is typically at least one. When Qis: 7 7 7 7 R R R R R8 may be selected from: H; a substituted or unsubstituted linear or branched Ci-Ce alkyl group (such as Me, Et, Pr, i-Pr, n-Bu, i-Bu, t-Bu, pentyl and hexyl); a substituted or unsubstituted linear or branched Ci-Ce alkyl-aryl group (such as -CH2Ph, -CH2(2,3 or 4)F-Ph, -CH2(2,3 or 4)CI-Ph, -CH2(2,3 or 4)Br-Ph, -CH2(2,3 or4)l-Ph, -CH2CH2Ph, -CH2CH2CH2Ph, -CH2CH2CH2CH2Ph, -CH2CH2CH2CH2CH2Ph, and -CH2CH2CH2CH2CH2CH2Ph); a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (such as -CH2F, -CF3, -CH2CH2F and -CH2CF3); a substituted or unsubstituted cyclic amine or amido group (such as pyrrolidin-3-yl, piperidin-3-yl, piperidin-4-yl, 2-keto-pyrrolidinyl, 3-keto-pyrrolidinyl, 2-keto-piperidinyl, 3-keto-piperidinyl, and 4-keto-piperidinyl); a substituted or unsubstituted cyclic C3-C8 alkyl group (such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl and cyclooctyl); a substituted or unsubstituted linear or branched C2-Ce alcohol group (such as -CH2CH2OH, -CH(CH3)CH2OH, -C(CH3)2OH, -CH2CH2CH2OH, -CH2CH2CH2CH2OH, -CH(CH3)CH2CH2OH, -CH(CH3)CH(CH3)OH, -CH(CH2CH3)CH2OH, -C(CH3)2CH2OH, -ch2ch2ch2ch2ch2oh, and -CH2CH2CH2CH2CH2CH2OH); a substituted or unsubstituted linear or branched C2-Ce carboxylic acid group (such as -CH2COOH, -CH2CH2COOH, -CH2CH2CH2COOH, -CH2CH2CH2CH2COOH, and -CH2CH2CH2CH2CH2COOH); a substituted or unsubstituted linear or branched carbonyl group (such as -(CO)Me, -(CO)Et, -(CO)Pr, -(CO)-i_Pr, -(CO)-n-Bu, -(CO)-i-Bu, -(CO)-t-Bu, -(CO)Ph, -(CO)CH2Ph, -(CO)CH2OH, -(CO)CH2OCH3, -(CO)CH2NH2,-(CO)CH2NHMe, -(CO)CH2NMe2, -(CO)-cyclopropyl, -(CO)-l,3-epoxypropan-2-yl; -(CO)NH2, -(CO)NHMe , -(CO)NMe2, -(CO)NHEt, -(CO)NEt2, -(CO)-pyrollidine-N-yl, -(CO)-morpholine-N-yl, -(CO)-piperazine-N-yl, -(CO)-N-methyl-piperazine-N-yl, -(CO)NHCH2CH2OH, -(CO)NHCH2CH2OMe, -(CO)NHCH2CH2NH2, -(CO)NHCH2CH2NHMe, and -(CO)NHCH2CH2NMe2); a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid ester group (such as -COOMe, -COOEt, -COOPr, -COO-i-Pr, -COO-n-Bu, -COO-i-Bu, -COO-t-Bu, -CH2COOMe, -CH2CH2COOMe, -CH2CH2CH2COOMe, and -CH2CH2CH2CH2COOMe); a substituted or unsubstituted linear or branched Ci-Ce amide group (such as -CO-NH2, -CO-NMeH, -CO-NMe2, -CO-NEtH, -CO-NEtMe, -CO-NEt2, -CO-NPrH, -CO-NPrMe, and -CO-NPrEt); a substituted or unsubstituted sulfonyl group (such as -SO2Me, -SO2Et, -SO2Pr, -SO2iPr, -SO2Ph, -SO2-(2,3 or 4)-F-Ph, -SO2-cyclopropyl, -SO2CH2CH2OCH3), -SO2NH2, -SO2NHMe, -SO2NMe2, -SO2NHEt, -SO2NEt2, -SO2-pyrrolidine-N-yl, -SO2-morpholine-N-yl, -SO2NHCH2OMe, and -SO2NHCH2CH2OMe); a substituted or unsubstituted aromatic group (such as Ph-, 2-F-Ph-, 3-F-Ph-, 4-F-Ph-, 2-CI-Ph-, 3-CI-Ph-, 4-CI-Ph-, 2-Br-Ph-, 3-Br-Ph-, 4-Br-Ph-, 2-l-Ph-, 3-l-Ph, 4-l-Ph-, 2,(3,4,5 or 6)-F2-Ph-, 2,(3,4,5 or 6)-CI2-Ph-, 2,(3,4,5 or 6)-Br2-Ph-, 2,(3,4,5 or 6)-l2-Ph-, 2,(3,4,5 or 6)-Me2-Ph-, 2,(3,4,5 or 6)-Et2-Ph-, 2,(3,4,5 or 6)-Pr2-Ph-, 2,(3,4,5 or 6)-Bu2-Ph-, 2,(3,4,5 or 6)-(CN)2-Ph-, 2,(3,4,5 or 6)-(NO2)2-Ph-, 2,(3,4,5 or 6)-(NH2)2-Ph-, 2,(3,4,5 or 6)-(MeO)2-Ph-, 2,(3,4,5 or 6)-(CF3)2-Ph-, 3,(4 or 5)-F2-Ph-, 3,(4 or 5)-CI2-Ph-, 3,(4 or 5)-Br2-Ph-, 3,(4 or 5)-12-Ph-, 3,(4 or 5)-Me2-Ph-, 3,(4 or 5)-Et2-Ph-, 3,(4 or 5)-Pr2-Ph-, 3,(4 or 5)-Bu2-Ph-, 3,(4 or 5)-(CN)2-Ph-, 3,(4 or 5)-(NO2)2-Ph-, 3,(4 or 5)-(NH2)2-Ph-, 3,(4 or 5)-(MeO)2-Ph-, 3,(4 or 5)-(CF3)2-Ph-, 2-Me-Ph-, 3-Me-Ph-, 4-Me-Ph-, 2-Et-Ph-, 3-Et-Ph-, 4-Et-Ph-, 2-Pr-Ph-, 3-Pr-Ph-, 4-Pr-Ph-, 2-Bu-Ph-, 3-Bu-Ph-, 4-Bu-Ph-, 2-(CN)-Ph-, 3-(CN)-Ph-, 4-(CN)-Ph-, 2-(NO2)-Ph-, 3-(NO2)-Ph-, 4-(NO2)-Ph-, 2-(NH2)-Ph-, 3-(NH2)-Ph-, 4-(NH2)-Ph-, 2-MeO-Ph-, 3-MeO-Ph-, 4-MeO-Ph-, 2-(NH2-CO)-Ph-, 3-(NH2-CO)-Ph-, 4-(NH2-CO)-Ph-, 2-CF3-Ph-, 3-CF3-Ph-, 4-CF3-Ph-, 2-CF3O-Ph-, 3-CF3O-Ph-, and 4-CF3O-Ph-); and a substituted or unsubstituted heterocyclic group (such as pyrrole-2-yl, pyrrole-3-yl, pyrazole-3-yl, pyrazole-4-yl, pyrazole-5-yl, imidazole-2-yl, imidazole-4-yl, imidazole-5-yl, l,2,3-triazole-4-yl, l,2,3-triazole-5-yl, l,2,4-triazole-3-yl, l,2,4-triazole-5-yl, pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, pyridazine-3-yl, pyridazine-4-yl, pyrimidin-2-yl, pyrimidin-4-yl, pyrimidin-5-yl, pyrimidin-6-yl, pyrazine-2-yl, pyrrolidine-2-yl, pyrrolidine-3-yl, piperidine-2-yl, piperidine-3-yl, piperidine-4-yl, 2-azapiperidine-3-yl, 2-azapiperidine-4-yl, 3-azapiperidine-2-yl, 3-azapiperidine-4-yl, 3-azapiperidine-5-yl, piperazine-2-yl, furan-2-yl, furan-3-yl, pyran-2-yl, pyran-3-yl, pyran-4-yl, 2-azapyran-3-yl, 2-azapyran-4-yl, 2-azapyran-5-yl, 2-azapyran-6-yl, 3-azapyran-2-yl, 3-azapyran-4-yl, 3-azapyran-5-yl, 3-azapyran-6-yl, 4-azapyran-2-yl, 4-azapyran-3-yl, 4-azapyran-5-yl, 4-azapyran-6-yl, tetra hydrofuran-2-yl, tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-4-yl, 2-aza-tetrahydrofuran-5-yl, 3-aza-tetrahydrofuran-2-yl, 3-aza-tetrahydrofuran-4-yl, 3-aza-tetrahydrofuran-5-yl, tetrahydropyran-2-yl, oxetan-3-yl, tetrahydropyran-3-yl, tetrahydropyran-4-yl, 2-aza-tetrahydropyran-3-yl, 2-aza-tetrahydropyran-4-yl, 2-aza-tetrahydropyran-5-yl, 2-aza-tetrahydropyran-6-yl, 3-aza-tetrahydropyran-2-yl, 3-aza-tetrahydropyran-4-yl, 3-aza-tetrahydropyran-5-yl, 3-aza-tetrahydropyran-6-yl, morpholine-2-yl, morpholine-3-yl, thiophen-2-yl, thiophen-3-yl, isothiazole-3-yl, isothiazole-4-yl, isothiazole-5-yl, thiazole-2-yl, thiazole-4-yl, thiazole-5-yl, thiopyran-2-yl, thiopyran-3-yl, thiopyran-4-yl, 2-azathiopyran-3-yl, 2-azathiopyran-4-yl, 2-azathiopyran-5-yl, 2-azathiopyran-6-yl, 3-azathiopyran-2-yl, 3-azathiopyran-4-yl, 3-azathiopyran-5-yl, 3-azathiopyran-6-yl, 4-azathiopyran-2-yl, 4-azathiopyran-3-yl, 4-azathiopyran-5-yl, 4-azathiopyran-6-yl, thiolane-2-yl, thiolane-3-yl, thiane-2-yl, thiane-3-yl, thiane-4-yl, oxazol-2-yl, oxazol-4-yl, oxazol-5-yl, isoxazol-3-yl, isoxazol-4-yl, isoxazol-5-yl, furazan-3-yl, (l,3,4-oxadiazol)-2-yl, (l,3,4-oxadiazol)-5-yl, (l,2,4-oxadiazol)-3-yl, (l,2,4-oxadiazol)-5-yl; and tetrazole-5-yl). In particular, R8 may be selected from H, a substituted or unsubstituted Ci-Ce alkyl group or a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group. Preferably, Q is a bond or -CH2-. Most preferably, Q is a bond. Ring C Ring C of the PARP1 inhibitor compound is a heteroaromatic ring having a general structure of: r is 0,1, 2, 3, or 4; and s is 0,1, 2, 3, or 4, with the proviso that r + s is 3 or 4. In other words, ring C may be a 5-membered ring or a 6-membered ring. Each R5C is independently absent or selected from H and a substituted or unsubstituted organic group. Preferably, each R5C is absent, H or an organic group selected from a halogen, preferably F; a Cl to C3 alkyl group; a Cl to C3 haloalkyl group, optionally a fluoromethyl group such as CF2H or CF3; and a nitrile group. F is the preferred organic group. Optionally, exactly one R5C is an organic group. Further optionally, exactly one R5C is F, with each other R5C being either absent or H. Alternatively, each R5C may be absent or H. At least one Xc is a heteroatom. When ring C is a 5-membered ring, each Xc is independently selected from C, N, O, and S, with at least one Xc being C, N, or O. Optionally, each Xc is independently selected from C and N. When ring C is a 6-membered ring, each Xc is independently selected from C and N, with at least one Xc being N. Preferably, the carbon atom which is connected to linker Q and the carbon atom which bears terminal substituent R6 are non-adjacent. In other words, it is preferable that r is at least 1 and s is at least 1. Ring C may be a 6-membered ring (r + s = 4). Preferably, in such examples, terminal substituent Q is para to terminal substituent R6 (r = 2, s = 2). Ring C preferably has a general structure of: Co wherein: XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N; when XCo is C, RCo is H or a halogen, F being the preferred halogen; when XCo is N, RCo is absent; when XCm is C, RCm is H or a halogen, F being the preferred halogen; when XCm is N, RCm is absent. Optionally, exactly one of XCo and XCm is N. Ring C may be a pyridine group, optionally having a structure selected from: Preferably, ring C is a pyridine group having a structure of: More preferably, ring C has a structure of: R5C Most preferably, ring C has a structure of: 10 Alternatively, ring C may be a diazine group, optionally having a structure selected from: In accordance with another possibility, ring C may be a 5-membered ring (r+s=3). For example, ring C may be an imidazole group, optionally 10 Alternatively, ring C may be a thiophene group, optionally having a structure selected from: In accordance with another possibility, ring C may be a thiazole group. For instance, ring C may have a structure selected from: 5 Alternatively, ring C may be a triazole, optionally having a structure selected from: More specific examples of suitable ring C structures include: CN N=N Terminal substituent R6 Ring C bears a substituent R6, which is selected from H and a substituted or unsubstituted 5 organic group. R6 may in particular be selected from H, -F, -Cl, -Br, -I, -CN, -CONR51R51, -NR51COR52, -SO2NR51R51, -NR51SO2R52, -O-CR52R52R52, -CR52R52NR51R51, and any of the following structures: R51 and R52 are each independently selected from H and a substituted or unsubstituted organic group. Optionally, R51 and R52 are each independently selected from H, a halogen, optionally-deuterated Cl to C3 alkyl, and Cl to C3 haloaIkyI. Optionally, R6 is selected from -F, -Cl, -CN, -CONH2, -CONHMe (optionally -CONHCD3), - CONHEt, -CONMe2, -CONHCOMe, -CONHCH2-CH2OMe, -CONH-CH2-CH2F, -CONH-CH2-CF3, - CONH-CH2-CHF2, -OCHF2, -NHCOMe, -NHSO2Me, -SO2NHMe, -CONHSO2Me, Particularly preferably, R6 is selected from: i) CONHMe; ia) CONHCD3; iii) F; iv) Cl; and v) CN. Where a compound is depicted with an R6 group selected from i) to v) as defined immediately above, replacement of the R6 group with any other one of groups i) to v) is explicitly contemplated. 5 Example L groups Group L of the PARP1 inhibitor compound may in particular be selected from: Group L may have a cis configuration with respect to ring A. For example, group L may have a structure selected from: Alternatively, group L may have a trans configuration with respect to ring A. For example, 5 group L may have a structure selected from: Example Compounds Provided are PARP1 inhibitor compounds having a structure of: O wherein: XD is selected from C and N; when XD is N: RD1 is selected from H, a Cl to C3 alkyl group, and a Cl to C3 haloalkyl group; 10 preferably a methyl group; and RD2 is absent; when XD is C: RD1 and RD2 are each H; 15 n is 1 or 2; RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ring A, with the proviso that when n is 1, RA1 and RA3 are each H; XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N; when XCo is C, RCo is H or a halogen, preferably F; when XCo is N, RCo is absent; when XCm is C, RCm is H or a halogen, preferably F; when XCm is N, RCm is absent; R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl. XD is preferably C. n is preferably 2. RA1 and RA3 are preferably each H XCm is preferably N, and RCo is preferably H or F. R6 is preferably-C(O)NHMe, e.g. C(O)NHCD3. When RA1 and RA3 are each H, the compound may have a cis configuration across ring A: or a trans configuration across ring A: Specific examples of compounds in this class are: Itrans Also provided are PARP1 inhibitor compounds having a general structure of: wherein: 10 XD isCorN; when XD is C, RD4 is selected from H and a halogen, and is preferably H; when XD is N, RD4 is absent; RD1 and RD2 are each independently selected from H and a halogen; n is 1 or 2; XA is C or N; when XA is C: RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ring A, with the proviso that when n is 1, RA1 and RA3 are each H; 15 whenXAisN: RA1 is absent, and RA3 is H; XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N; when XCo is C, RCo is H or a halogen, preferably H or F; when XCo is N, RCo is absent; when XCm is C, RCm is H or a halogen, preferably H or F; when XCm is N, RCm is absent; R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl. Preferably, XD is C and RD4 is H. RD1 and RD2 are preferably selected from H and F. In such examples, exactly one of RD1 and RD2 may be F. n is preferably 2. When R6 is C(O)NHMe, XCm is preferably N. When XA is C and RA1 and RA3 are each H, the compound may have a cis configuration across or a trans configuration across ring A: 78 4 Seis lOtrans Further provided are PARP1 inhibitor compounds having a general structure of: C wherein: a dotted line represents a single bond or a double bond; XEB isCorN; XD1 and XD2 are each independently selected from C and N, with the proviso that when XEB is N, XD1 is C; RD1 and RD2 are each independently absent or present and selected from H, a halogen, a methyl group, and a halomethyl group, such as CF3; RD3 is selected from H, a halogen, a methyl group, and a halomethyl group, such as CF3; n is 1 or 2; RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ring A, with the proviso that when n is 1, RA1 and RA3 are each H; XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N; when XCo is C RCo is H or a halogen, and is optionally H or F; when XCo is N, RCo is absent; when XCm is C, RCm is H or a halogen, and is optionally H or F; when XCm is N, RCm is absent; R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl. In particular: a) XEB may be C, XD1 may be N, and XD2 may be C, with RD1 and RD2 each being present; b) XEB may be C, XD1 may be N, and XD2 may be N, with RD1 being present and RD2 being 5 absent; or c) XEB may be N, XD1 and XD2 may each be C, with RD1 and RD2 each being present RD3 is preferably CF3. 10 n is preferably 2. RA1 and RA3 are preferably each H. R6 is preferably C(O)NHMe (e.g., C(O)NHCD3). XCm is preferably N. RCo is preferably H. Examples of compounds in this class include: 14 14trans Medical Uses The compounds described herein may be for use in medicine. In the context of the present invention, the medicinal use is not especially limited, provided that it is a use which is facilitated by the PARP1 inhibitory effect of the compound. Thus, the compounds of the invention may be for use in any disease, condition or disorder that may be prevented, ameliorated or treated using a PARP1 inhibitor. The PARP1 inhibitor compounds provided herein may be selective for PARP1 over PARP2. As such, the PARP1 inhibitor compounds may have reduced toxicity. PARP2 inhibition is believed to be a major driver of haematological toxicities such as anaemia, neutropenia and thrombocytopenia. The PARP1 inhibitor compound may be for use in treating a cancer. The nature of the cancer is not especially limited, provided that the cancer is one which may be treated, prevented or ameliorated by using a PARP1 inhibitor. The cancer may comprise a solid or liquid tumour. For example, the cancer may be selected from: a cancer of the eye, brain (such as gliomas, glioblastomas, medulloblastomas, craniopharyngioma, ependymoma, and astrocytoma), spinal cord, kidney, mouth, lip, throat, oral cavity, nasal cavity, small intestine, colon, parathyroid gland, gall bladder, head and neck, breast, bone, bile duct, cervix, heart, hypopharyngeal gland, lung, bronchus, liver, skin, ureter, urethra, testicles, vagina, anus, laryngeal gland, ovary, thyroid, oesophagus, nasopharyngeal gland, pituitary gland, salivary gland, prostate, pancreas, adrenal glands; an endometrial cancer, oral cancer, melanoma, neuroblastoma, gastric cancer, an angiomatosis, a hemangioblastoma, a pheochromocytoma, a pancreatic cyst, a renal cell carcinoma, Wilms' tumour, squamous cell carcinoma, sarcoma, osteosarcoma, Kaposi sarcoma, rhabdomyosarcoma, hepatocellular carcinoma, PTEN Hamartoma-Tumor Syndromes (PHTS) (such as Lhermitte-Duclos disease, Cowden syndrome, Proteus syndrome, and Proteus-like syndrome), leukaemias and lymphomas (such as acute lymphoblastic leukaemia, chronic lymphocytic leukaemia, acute myelogenous leukaemia, chronic myelogenous leukaemia, hairy cell leukaemia, T-cell prolymphocytic leukaemia (T-PLL), large granular lymphocytic leukaemia, adult T-cell leukaemia, juvenile myelomonocytic leukaemia, Hodgkin lymphoma, non-Hodgkin lymphoma, mantle lymphoma, follicular lymphoma, primary effusion lymphoma, AIDS-related lymphoma, diffuse B cell lymphoma, Burkitt lymphoma, cutaneous T-cell lymphoma, nasopharyngeal and gastrointestinal cancers. For instance, the cancer may be a cancer of the brain or spinal cord. In addition, the compounds described herein may be of use in cancers where Epstein Barr Virus, EBV, plays a contributing role such as Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal and gastrointestinal cancers. The compounds described herein may be provided for use in for treating a cancer which is deficient in one or more DNA damage response repair pathways, in particular in Homologous Recombination ("HR") dependent DNA Double Strand Break ("DSB") DNA repair activity. Components of HR dependent DNA DSB repair pathways and other DNA damage response pathways include but are not limited to the following proteins: ATM, ATR, ERCC1, XRCC1, XRCC2, XRCC3, RAD51, RAD51L1, RAD51C, RAD51D, RAD51L3, DMC1, RAD52, RAD54L, RAD54B, RAD50, MRE11A, NBS1, BRCA1, BRCA2, FANCP (SLX4), FEN1, PALB2, PBRM1, SMARCA4, ARID1A, ARID1B, FANCD2, BLM. Other components involved in HR dependent DNA DSB repair include regulatory factors such as ESMY (Hughes-Davies, L. et al. Cell. 2003; 115: 523-535). A cancer which is deficient in HR-dependent DNA DSB repair typically becomes dependent on alternative DSB pathway repair mechanisms. Such cancers include but are not limited to cancers of the ovary, prostate, breast, lung, gastrointestine, blood and pancreas. The cancer cells may have a BRCA1 and / or BRCA2 deficient phenotype, i.e. the cancer cells may be deficient in BRCA1 and / or 2 function. The deficiency may arise by means of mutation, polymorphism or epigenetic silencing in the encoding nucleic acids or by means of mutation, polymorphism, amplification in a gene encoding a regulatory factor, e.g. the ESMY gene which encodes a BRCA2 regulatory factor (Hughes-Davies, L. et al. Cell. 2003; 115: 523-535). Amplification of the ESMY gene is associated with breast and ovarian cancer. Carriers of mutations in the tumour suppressor BRCA1 and / or BRCA2 genes are known to have an elevated risk of developing certain cancers including ovarian, prostate and breast. Wild-type alleles of BRCA1 and / or BRCA2 are frequently lost in tumours of heterozygous carriers (Jasin, M. et al. Oncogene. 2002; 21: 8981-93) and their detection, as a means of patient selection, is well known in the art (Radice, PJ. et al. Exp. Clin. Cancer. Res. 2002; 21: 9-12; Chappnis, PO and Foulkes WO. Cancer Treat Res. 2002; 107: 29-59). The compounds provided herein may be administered to a patient who is undergoing radiotherapy and / or chemotherapy using a further agent for treating cancer. For example, the PARP1 inhibitor compound may be administered in conjunction with a further agent for treating cancer. The further agent for treating cancer may be selected from: anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, immunotherapeutic agents, hormone deprivation therapy, proapoptotic agents, radioligand therapies, cell cycle signalling inhibitors, and anti-angiogenic agents. In particular, the further agent may comprise an immunotherapeutic agent selected from: an anti-tumour vaccine; an oncolytic virus; an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR; a pattern recognition receptor agonist such as a STING, TLR-9 or RIG-1 Helicase agonist; an IDO orTDO inhibitor; a novel adjuvant; a peptide; a cytokine; a chimeric antigen receptor T cell therapy (CAR-T); a small molecule immune modulator; and a tumour microenvironment modulator. Pharmaceutical Compositions Another aspect provides a pharmaceutical composition comprising a PARP1 inhibitor compound as defined herein. Typically, the composition includes a pharmaceutically acceptable additive and / or excipient. In the pharmaceutical composition, the PARP1 inhibitor compound as defined above may be present in the form described above, but may alternatively be in a form suitable for improving bioavailability, solubility, and / or activity, and / or may be in a form suitable for improving formulation. Thus, the compound may be in the form of a pharmaceutically acceptable salt, hydrate, acid, ester, or other alternative suitable form. Typically, the composition is for use in medicine, e.g. for use in treating a disease, condition or disorder as defined above. For example, the pharmaceutical composition may be for use in treating a cancer. The composition may further comprise a further agent for treating cancer. The further agent for treating cancer is not especially limited, provided that it affords some utility for cancer treatment. The further agent for treating cancer may comprise one or more chemotherapeutic agents such as anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, immunotherapeutic agents, hormone-deprivation therapies, proapoptotic agents, radioligand therapies, anti-angiogenic agents, and cell cycle signalling inhibitors. In particular, the further agent for treating cancer may comprise an immunotherapeutic agent selected from: an anti-tumour vaccine; an oncolytic virus; an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR; a pattern recognition receptor agonist such as a STING, TLR-9 or RIG-1 Helicase agonist; an IDO or TDO inhibitor; a novel adjuvant; a peptide; a cytokine; a chimeric antigen receptor T cell therapy (CAR-T); a small molecule immune modulator; and a tumour microenvironment modulator. Kits Another aspect provides a pharmaceutical kit for treating a cancer. The pharmaceutical kit comprises a PARP1 inhibitor compound as defined herein, and a further agent for treating cancer. The compound and the further agent are suitable for administration simultaneously, sequentially or separately. The further agent for treating cancer may be any of the further agents for treating cancer identified above in the discussion of the pharmaceutical composition. In particular, the further agent for treating cancer may comprise one or more chemotherapeutic agents selected from: anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, hormone-deprivation therapies, radioligand therapies, antiangiogenic agents, immunotherapeutic agents (such as selected from an anti-tumour vaccine, an oncolytic virus, an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR, a pattern recognition receptor agonist such as a STING, TLR- 9 or RIG-1 Helicase agonist, an IDO orTDO inhibitor, a novel adjuvant, a peptide, a cytokine, a chimeric antigen receptor T cell therapy (CAR-T), a small molecule immune modulator, tumour microenvironment modulators), proapoptotic agents and cell cycle signalling inhibitors. Methods of Treatment Another aspect of the invention provides a method of treating a disease and / or a condition and / or a disorder, which method comprises administering to a patient (or subject) a PARP1 inhibitor compound, or a composition, or a kit as defined herein. The method is typically a method for treating any disease condition or disorder mentioned herein. In typical embodiments, the method is a method for treating a cancer. The patient may be any animal, preferably a mammal. For example, the patient may be a human, canine, equine or feline; and is preferably a human. The method may comprise administering to the patient (or subject) a compound or a composition as defined above and a further agent for treating cancer as defined above. The compound or composition and the further agent may be administered simultaneously, sequentially or separately, depending upon the agents and patients involved, and the disease to be treated (e.g., the type of cancer to be treated). The patient may be undergoing treatment using ionising radiation. Methods of synthesising PARP1 inhibitor compounds Also provided are methods for synthesising the PARP1 inhibitor compounds as defined herein. In general, the method comprises conducting a reaction between: (i) a first reactant comprising ring E bearing a first portion of group L, and (ii) a second reactant comprising a remainder of group L, to form the PARP1 inhibitor compound. The skilled person may select reaction conditions with reference to known synthesis techniques depending on the appropriate starting materials. The method may comprise one or more additional steps. Exemplary synthesis methodology is shown in the Examples hereinbelow. In one example method, the first reactant comprises rings D, E and ring A, and the second reactant comprises a ring B precursor bearing a reactive group, which method comprises joining ring A to the ring B precursor. In this method, the reactive group of the ring B precursor may comprise a carbonyl group, an alkyl halide, or an alkyl sulfonate. The reaction may comprise alkylation, reductive amination, or amide formation so as to form group L. In another example method, the first reactant comprises rings D, E, ring A, and ring B, and the second reactant comprises a ring C derivative bearing a leaving group such as a halide or sulfonate. In this method, the reaction may comprise a nucleophilic substitution reaction, such as a nucleophilic aromatic substitution reaction, so as to form group L. The PARP1 inhibitor compound may be obtained in the form of a mixture of two or more structural isomers. The method may further comprise separating the structural isomers. For example, the method may further comprise comprising separating structural isomers of the PARP1 inhibitor compound using chiral supercritical fluid chromatography ("SFC") and / or chiral high-performance liquid chromatography ("HPLC"). When the PARP1 inhibitor compound is diastereomeric, separation may proceed in two stages. In a first stage, two pairs of stereoisomers may be isolated by HPLC. In a second stage, individual stereoisomers may be isolated from the pairs of stereoisomers by SFC. Examples Example 1: synthesis of 4a and 4b Preparation of tert-butyl 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)pyrrolidine-1-carboxylate (1003) To a solution of tert-butyl 3-oxopyrrolidine-l-carboxylate 1001 (170 mg, 0.92 mmol) in MeOH 10 (5 mL) was added N-methyl-5-(piperazin-l-yl)picolinamide 1002 (202 mg, 0.92 mmol). Then acetic acid (2 drops) and NaBHsCN (115 mg, 1.84 mmol) were added. The mixture was stirred for 2 h at 50 °C. The reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 93 : 7) to give tert-butyl 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)pyrrolidine-l-carboxylate 1003 (195 mg, 49 % yield) as a white solid. LCMS (ESI) calcd for C20H31N5O3 [M + H] + m / z 390.24, found 390.10. Preparation of N-methyl-5-(4-(pyrrolidin-3-yl)piperazin-l-yl)picolinamide (1004) Tert-butyl 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)pyrrolidine-l-carboxylate 1003 (195 mg, 0.50 mmol) was added to HCI in dioxane (4 M, 10 mL), stirred for lh at room temperature, concentrated to give N-methyl-5-(4-(pyrrolidin-3-yl)piperazin-l-yl)picolinamide 1004 (160 mg, 99 % yield) as a yellow solid. LCMS (ESI) calcd for C15H17N3O [M + H] + m / z 290.19, found 290.20. Preparation of 5-(4-(l-(4-methoxyquinazolin-2-yl)pyrrolidin-3-yl)piperazin-l-yl)-N-methylpicolinamide (1006) To a solution of N-methyl-5-(4-(pyrrolidin-3-yl)piperazin-l-yl)picolinamide 1004 (160 mg, 0.56 mmol) and 2-chloro-4-methoxyquinazoline 1005 (215 mg, 1.11 mmol) in dioxane (10 mL) was added DIEA (143 mg, 1.1 mmol). The reaction mixture was irradiated in a microwave reactor at 100 °C for 1 h. The reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 95 : 5) to give 5-(4-(l-(4-methoxyquinazolin-2-yl)pyrrolidin-3-yl)piperazin-l-yl)-N-methylpicolinamide 1006 (120 mg, 44 % yield) as a white solid. LCMS (ESI) calcd for C24H29N7O2 [M + H]+ m / z 448.24, found 448.15. Preparation of tert-butyl N-methyl-5-(4-(l-(4-oxo-3,4-dihydroquinazolin-2-yl)pyrrolidin-3-yl)piperazin-l-yl)picolinamide (4a and4b) 5-(4-(l-(4-methoxyquinazolin-2-yl)pyrrolidin-3-yl)piperazin-l-yl)-N-methylpicolinamide 1006 (120 mg, 0.27 mmol) was added to pyridine chlorhydrate (62 mg, 0.54 mmol), heated to 130 °C stirred for lh, then cooled to room temperature, separated with EtOAc (30 mL*3) and brine, the organic phase concentrated and purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 90 :10) to give crude product, which was separated by SFC (Column: Daicel Chiralpak OJ-H 250 mm x 20 mm I.D., 5 pmm; Mobile phase: CO2 / MeOH[0.1 %(NHs)] = 65 / 35) and concentrated under reduced pressure to afford the first fraction as 4a (28.05 mg, 100 % purity, ee%: 100, white solid) and the second fraction as 4b (37.9 mg, 100 % purity, ee%: 100, white solid). 4a 2H NMR (400 MHz, DMSO) 6 11.04 (s, 1H), 8.40 (dd, J = 4.0 Hz, 1H), 8.29 (d, J = 2.4 Hz, 1H), 7.93-7.81 (m, 2H), 7.60-7.51 (m, 1H), 7.44-7.39 (m, 1H), 7.24 (d, J = 8.4 Hz, 1H), 7.14-6.98 (m, 1H), 3.90-3.83 (m, 1H), 3.78-3.71 (m, 1H), 3.49-3.43 (m, 1H), 3.39-3.34 (m, 4H), 3.28 (s, 1H), 3.00-2.89 (m, 1H), 2.78 (d, J = 4.8 Hz, 3H), 2.69-2.56 (m, 4H), 2.24-2.15 (m, 1H), 1.90-1.77 (m, 1H). LCMS (ESI) calcd for C23H27N7O2 [M + H] + m / z 434.22, found 434.40. 4b TH NMR (400 MHz, DMSO) 6 10.88 (s, 1H), 8.40 (q, J = 4.4 Hz, 1H), 8.29 (d, J = 2.8 Hz, 1H), 7.91-7.81 (m, 2H), 7.59-7.51 (m, 1H), 7.41 (dd, J = 8.8, 2.8 Hz, 1H), 7.30-7.16 (m, 1H), 7.15-7.00 (m, 1H), 3.91-3.82 (m, 1H), 3.79-3.70 (m, 1H), 3.49-3.42 (m, 1H), 3.38-3.34 (m, 4H), 3.28 (s, 1H), 3.01-2.89 (m, 1H), 2.78 (d, J = 4.8 Hz, 3H), 2.71-2.63 (m, 2H), 2.61-2.55 (m, 2H), 2.25-2.15 (m, 1H), 1.90-1.77 (m, 1H). LCMS (ESI) calcd for C23H27N7O2 [M + H] + m / z 434.22, found 434.35. Example 2: synthesis of 5cis and 5trans Preparation of methyl 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylate (1102} To a solution of methyl 3-oxocyclobutane-l-carboxylate 1101 (230 mg, 1.80 mmol) in MeOH (50 mL) was added N-methyl-5-(piperazin-l-yl) picolinamide 1002 (395 mg, 1.80 mmol), then two drops of acetic acid and NaBH(OAc)3 (950 mg, 4.49 mmol) were added at room temperature. After 1 h, NaBHsCN (135 mg, 2.15 mmol) was added. The reaction mixture was stirred at 50 °C for 5 h. After cooling to room temperature, the reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 90 : 10) to give 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylate 1102 (600 mg, 90 % yield) as a white solid. LCMS (ESI) calcd for C17H24N4O3 [M + H] + m / z 333.18, found 333.00. Preparation of 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylic acid (1103) To a solution of methyl 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylate 1102 (400 mg, 1.20 mmol) in MeOH:H2O=l:l (20 mL) was added LiOH (43 mg, 1.80 mmol). The reaction mixture stirred at room temperature for 1 h. The reaction mixture was concentrated under reduced pressure to give 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylic acid 1103 (260 mg, 61 % yield ) as a white solid. LCMS (ESI) calcd for C16H22N4O3 [M + H] + m / z 319.17, found 319.00. Preparation of   5-(4-(3-((2-carbamoylphenyl)carbamoyl)cyclobutyl)piperazin-l-yl)-N- methylpicolinamide (1105) To a solution of 3-(4-(6-(methylcarbamoyl)pyridin-3-yl)piperazin-l-yl)cyclobutane-l-carboxylic acid 1103 (260 mg, 0.86 mmol) in DMF (10 mL) was added 2-aminobenzamide 1104 (222 mg, 1.63 mmol), HATU (621 mg, 1.63 mmol) and DIEA (528 mg, 4.08 mmol), stirred for lh at room temperature. The reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100: 0 to 97: 3) to give 5-(4-(3-((2-carbamoylphenyl)carbamoyl)cyclobutyl)piperazin-l-yl)-N-methylpicolinamide 1105 (150 mg, 53 % yield) as a white solid. LCMS (ESI) calcd for C23H28N6O3 [M + H] + m / z 437.22, found 437.10. Preparation of N-methyl-5-(4-(3-(4-oxo-3,4-dihydroquinazolin-2-yl)cyclobutyl)piperazin-l-yl)picolinamide (5) To a solution of 5-(4-(3-((2-carbamoylphenyl)carbamoyl)cyclobutyl)piperazin-l-yl)-N-methylpicolinamide 1105 (150 mg, 0.34 mmol) in DME (15 mL) was added KOH (81 mg, 1.03 mmol). The reaction mixture stirred at 60 °C for 2 h. After cooling to room temperature, the reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100: 0 to 95: 5) to give N-methyl-5-(4-(3-(4-oxo-3,4-dihydroquinazolin-2-yl)cyclobutyl)piperazin-l-yl)picolinamide 5 (30 mg, 19 % yield) as a white solid. LCMS (ESI) calcd for C23H26N6O2 [M + H] + m / z 419.21, found 419.00. Preparation of N-methyl-5-(4-(3-(4-oxo-3,4-dihydroquinazolin-2-yl)cyclobutyl)piperazin-l-yl)picolinamide (5cis and 5trans) N-methyl-5-(4-(3-(4-oxo-3,4-dihydroquinazolin-2-yl)cyclobutyl)piperazin-l-yl)picolinamide cis / trans mixture 5 was separated by prep-HPLC (Column Gemini 5um C18 150*21.2mm; Mobile phase: ACN—H2O(0.1 %FA) and concentrated under reduced pressure to afford the first fraction as 5cis (14 mg, 97 % purity, white solid) and the second fraction as 5trans (1.8 mg, 97 % purity, white solid). 5cis XH NMR (400 MHz, DMSO) 6 12.21 (s, 1 H), 8.41 (d, J = 4.8 Hz, 1 H), 8.27 (s, 1 H), 8.07 (d, J = 8.0 Hz, 1 H), 7.87-7.74 (m, 2 H), 7.65 (d, J = 8.0 Hz, 1 H), 7.50-7.36 (m, 2 H), 3.20-3.13 (m, 1 H), 2.78 (d, J = 4.8 Hz, 4 H), 2.50-2.49 (m, 4 H), 2.44 (s, 6 H), 2.23 (d, J = 9.6 Hz, 2 H). NOE experiments suggested cis stereochemistry for this compound. LCMS (ESI) calcd for C23H26N6O2 [M + H]+ m / z 419.21, found 419.00. 5trans XH NMR (400 MHz, DMSO) 6 12.11 (s, 1 H), 8.41 (d, J = 4.8 Hz, 1 H), 8.28 (s, 1 H), 8.08 (d, J = 7.6 Hz, 1 H), 7.89-7.73 (m, 2 H), 7.66 (d, J = 8.0 Hz, 1 H), 7.43 (dd, J = 23.3, 8.0 Hz, 2 H), 3.04-2.89 (m, 2 H), 2.78 (d, J = 3.6 Hz, 3 H), 2.49-2.48 (m, 3 H), 2.45 (s, 7 H), 2.28 (d, J = 7.6 Hz, 2 H). NOE experiments suggested trans stereochemistry for this compound. LCMS (ESI) calcd for C23H26N6O2 [M + H] + m / z 419.21, found 419.00. Example 3: synthesis of 6 o 0 ^NH2 r 1104 H |V-^—NHBoc EDCI, pyridine, rt, 12 h 1201 0 "Vy N-yj 0 -^>NH2 T 2 KOH NH X^NHBoc DME’ 60°C 1202 0 rAz;N _ 0 F 1208 y )—\ Cs,CO,, DMF, 150°C ' HN— microwave, 5h 1206 Preparation of tert-butyl (4-((2-carbamoylphenyl)carbamoyl)bicyclo[2.1.1]hexan-l-yl)carbamate (1202) To a solution of 4-((tert-butoxycarbonyl)amino)bicyclo[2.1.1]hexane-l-carboxylic acid 1201 (350 mg, 1.45 mmol) and 2-aminobenzamide 1104 (217 mg, 1.59 mmol) in pyridine (20 mL) was added EDCI (305 mg, 1.59 mmol), then the mixture was stirred for 12 h at room temperature. The reaction mixture was quenched with water, the aqueous layer was extracted with EtOAc (150 mL x 3). The combined organic layers were washed by IM HCI solution and brine, dried over Na2SO4, concentrated under reduced pressure to give product of tert-butyl (4-((2-carbamoylphenyl)carbamoyl)bicyclo[2.1.1]hexan-l-yl)carbamate 1202 (500 mg, 86 % yield) as a white solid. LCMS (ESI) calcd for C19H25N3O4 [M + H] + m / z 360.18, found 360.10. Preparation of tert-butyl (4-(4-oxo-3,4-dihydroquinazolin-2-yl)bicyclo[2.1.1]hexan-l-yl)carbamate (1203) To the solution of tert-butyl (4-((2-carbamoylphenyl)carbamoyl)bicyclo[2.1.1]hexan-l-yl)carbamate 1202 (500 mg, 1.39 mmol) in DME (50 mL) was added KOH (234 mg, 4.17 mmol), stirred at 60 °C for 2 h, cooled to room temperature, the reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 90 : 10) to give tert-butyl (4-(4-oxo-3,4-dihydroquinazolin-2-yl)bicyclo[2.1.1]hexan-l-yl)carbamate 1203 (400 mg, 76 % yield) as a white solid. LCMS (ESI) calcd for C19H23N3O3 [M + H] + m / z 342.17, found 342.15. Preparation of 2-(4-aminobicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one (1204) To a solution of tert-butyl (4-(4-oxo-3,4-dihydroquinazolin-2-yl)bicyclo[2.1.1]hexan-l-yl)carbamate 1203 (400 mg, 1.17 mmol) in DCM (20 mL) was added HCI in dioxane (4M, 10 mL). The mixture was stirred for lh at room temperature. The reaction mixture was concentrated under reduced pressure to give product of 2-(4-aminobicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one 1204 (250 mg, 80 % yield) as a white solid. LCMS (ESI) calcd for C14H15N3O [M + H] + m / z 242.12, found 242.10. Preparation of 2-(4-(4-benzylpiperazin-l-yl)bicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one (1206) To the solution of 2-(4-aminobicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one 1204 (250 mg, 1.04 mmol) in DIPEA (40 mL) was added N-benzyl-2-chloro-N-(2-chloroethyl)ethan-l-amine 1205 (483 mg, 2.07 mmol).The reaction mixture was stirred at 120 °C for 5 h, the reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 90 : 10) to give N-benzyl-2-chloro-N-(2-chloroethyl)ethan-l-amine 1206 (150 mg, 29 % yield ) as a brown solid. LCMS (ESI) calcd for C25H28N4O [M + H] + m / z 401.23, found 401.15. Preparation of2-(4-(piperazin-l-yl)bicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one (1207) To a solution of N-benzyl-2-chloro-N-(2-chloroethyl)ethan-l-amine 1206 (150 mg, 0.37 mmol) in IPA (30 mL) was added Pd / C (39 mg). The mixture was evacuated and backfilled with hydrogen three times and then charged with hydrogen. The resulting mixture was stirred at 70 °C for 5 h. Then, the mixture was filtered through celite and concentrated under vacuum to give 2-(4-(piperazin-l-yl)bicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one 1207 (90 mg, 62 % yield) as a white solid. LCMS (ESI) calcd for C18H22N4O [M + H]+ m / z 311.18, found 311.10. Preparation of N-methyl-5-(4-(4-(4-oxo-3,4-dihydroquinazolin-2-yl)bicyclo[2.1.1]hexan-l-yl)piperazin-l-yl)picolinamide (6) To a solution 2-(4-(piperazin-l-yl)bicyclo[2.1.1]hexan-l-yl)quinazolin-4(3H)-one 1207 (30 mg, 0.09 mmol) in DMF (5 mL) was added CS2CO3 (63 mg, 0.19 mmol) and 5-fluoro-N-methylpicolinamide 1208 (22 mg, 0.14 mmol). The mixture was stirred for 5 h at 150 °C using a microwave. The reaction mixture was concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 : 0 to 92 : 8) to give crude N-methyl-5-(4-(4-(4-oxo-3,4-dihydroquinazolin-2-yl)bicyclo[2.1.1]hexan-l- yl)piperazin-l-yl)picolinamide (10 mg, 70 % purity) as a yellow solid. The crude product was purified by prep-HPLC (Gemini 5um Cis 150 x 21.2 mm, mobile phase: ACN - H2O (0.1 %TFA), gradient: 20 - 80) to give N-methyl-5-(4-(4-(4-oxo-3,4-dihydroquinazolin-2- yl)bicyclo[2.1.1]hexan-l-yl)piperazin-l-yl)picolinamide 6 (1.8 mg, 91 % purity, 4 % yield) as a yellow solid. XH NMR (400 MHz, DMSO-d6, ppm) 6: 12.28 (s, 1 H), 11.79-11.33 (m, 1 H), 8.46 (d, J = 4.6 Hz, 1 H), 8.37-8.44 (m, 1 H), 8.11 (dd, J = 6.8 Hz, 1.6 Hz, 1 H), 7.91 (d, J = 8.8 Hz, 1 H), 7.83-7.79 (m, 1 H), 7.63 (d, J = 8.0 Hz, 1 H), 7.56-7.49 (m, 2 H), 4.16-4.13 (m, 2 H), 3.92 (s, 2 H), 3.27 (s, 4 H), 2.80 (d, J = 4.8 Hz, 3 H), 2.43 (s, 2 H), 2.13-2.12 (m, 4 H), 2.04 (s, 2 H). LCMS (ESI) calcd for C25H28N6O2 [M + H]+m / z 445.23, found 445.20. Example 4: synthesis of3cis-a, 3cis-b, 3trans-a, 3trans-b 3cis-a / 3cis-b I 3trans-a I 3trans-b Preparation of 2-fluoro-6-(3-oxocyclopentane-l-carboxamido)benzamide (1303) To a solution of 3-oxocyclopentane-l-carboxylic acid 1302 (2.08 g, 16.2 mmol) in pyridine (30 mL) were added 2-amino-6-fluorobenzamide 1301 (2.5 g, 16.2 mmol) and EDCI (6.2 g, 32.4 mmol) at room temperature successively. The mixture was kept stirring at room temperature for 2 h. The resulting mixture was diluted with water (200 mL) and extracted with EtOAc (50 mL x 3). The combined organic phases were washed with brine, dried over sodium sulfate, concentrated, and purified by silica gel column chromatography (eluting with MeOH / DCM, 2 % to 5 %) to give 2-fluoro-6-(3-oxocyclopentane-l-carboxamido)benzamide 1303 (3 g, 90 % purity, 62 % yield) as a yellow solid. LCMS (ESI) calcd for Ci3Hi3FN2O3 [M + H] + m / z 265.09, found 265.05. Preparation of 5-fluoro-2-(3-oxocyclopentyl)quinazolin-4(3H)-one (1304) To a solution of 2-fluoro-6-(3-oxocyclopentane-l-carboxamido)benzamide 1303 (3 g, 11-4 mmol) in DME (200 mL) was added KOH (1.92 g, 34.2 mmol). The mixture was heated at 50 °C for 2 hours. The final mixture was quenched with saturated aqueous NH4CI solution and extracted with EtOAc. The combined organic phases were washed with brine, dried over sodium sulfate and concentrated to give 5-fluoro-2-(3-oxocyclopentyl)quinazolin-4(3H)-one 1304 (2 g, 90 % purity, 64 % yield) as a yellow solid. LCMS (ESI) calcd for Ci3HnFN2O2 [M + H]+ m / z 247.08, found 247.05. Preparation of 6-fluoro-5-(4-(3-(5-fluoro-4-oxo-3,4-dihydroquinazolin-2- yl)cyclopentyl)piperazin-l-yl)-N-methylpicolinamide (3cis-a / 3cis-b racemic mixture and 3trans-a / 3trans-b racemic mixture) To a solution of 5-fluoro-2-(3-oxocyclopentyl)quinazolin-4(3H)-one 1304 (300 mg, 1.22 mmol) in MeOH (30 mL) were added 6-fluoro-N-methyl-5-(piperazin-l-yl)picolinamide 1305 (435 mg, 1.83 mmol), NaBH3CN (77 mg, 1.22 mmol) and NaBH(OAc)3 (516 mg, 2.44 mmol) at room temperature. The reaction mixture was stirred at 50 °C for 1 h. The resulting solution was quenched with water and concentrated under reduced pressure. The residue was purified by flash chromatography (eluting with DCM / MeOH = 100 :0 to 90 :10) to afford the first fraction as 6-fluoro-5-(4-(3-(5-fluoro-4-oxo-3,4-dihydroquinazolin-2-yl)cyclopentyl)piperazin-l-yl)-N-methylpicolinamide 3cis-a / 3cis-b racemic mixture (50 mg, 90 % purity, 8 % yield, racemic mixture of cis enantiomers) and the second fraction as 6-fluoro-5-(4-(3-(5-fluoro-4-oxo-3,4-dihydroquinazolin-2-yl)cyclopentyl)piperazin-l-yl)-N-methylpicolinamide 3trans-a / 3trans-b racemic mixture (25 mg, 90 % purity, 4 % yield, racemic mixture of trans enantiomers) as a white solid. Preparation          of         6-fluoro-5-(4-(3-(5-fluoro-4-oxo-3,4-dihydroquinazolin-2- yl)cyclopentyl)piperazin-l-yl)-N-methylpicolinamide (3cis-a and 3cis-b) 3cis-a / 3cis-b racemic mixture was separated by SFC (Column: Daicel Chiralpak-AD-H 20 mm I.D. x 250 mm, 5 pm; Mobile phase: CO2 / MeOH [0.1 % (NH3)] = 60 / 40) and concentrated under reduced pressure to afford the first fraction as 3cis-a (13.6 mg, 99.94 % purity, 100% ee, white solid) and the second fraction as 3cis-b (16.6 mg, 99.37 % purity, 100% ee, white solid). 3cis-a XH NMR (400 MHz, DMSO-d6, ppm) 6: 12.49 (s, 1 H), 8.44-8.37 (m, 1.4 H), 7.86 (d, J = 8.0 Hz, 1 H), 7.78-7.68 (m, 1 H), 7.60-7.51 (m, 1 H), 7.42 (d, J = 8.0 Hz, 1 H), 7.26-7.10 (m, 1 H), 3.24-3.19 (m, 4 H), 3.15-3.08 (m, 1 H), 2.78-2.70 (m, 4 H), 2.68-2.63 (m, 4 H), 2.23-2.16 (m, 1 H), 2.09-2.00 (m, 1 H), 1.98-1.86 (m, 2 H), 1.86-1.72 (m, 2 H). NOE experiments suggested cis stereochemistry. LCMS (ESI) calcd for C24H26F2N6O2 [M + H] + m / z 469.21, found 469.25. 3cis-b XH NMR (400 MHz, DMSO-de, ppm) 6: 12.50 (s, 1 H), 8.45-8.34 (m, 1.5 H), 7.86 (d, J = 8.0 Hz, 1 H), 7.79-7.68 (m, 1 H), 7.62-7.53 (m, 1 H), 7.42 (d, J = 8.0 Hz, 1 H), 7.24-7.13 (m, 1 H), 3.24-3.18 (m, 4 H), 3.15-3.09 (m, 1 H), 2.80-2.70 (m, 4 H), 2.69-2.63 (m, 4 H), 2.27-2.16 (m, 1 H), 2.12-2.01 (m, 1 H), 1.97-1.87 (m, 2 H), 1.85-1.65 (m, 2 H). NOE experiments suggested cis stereochemistry. LCMS (ESI) calcd for C24H26F2N6O2 [M + H] + m / z 469.21, found 469.20. Preparation          of         6-fluoro-5-(4-(3-(5-fluoro-4-oxo-3,4-dihydroquinazolin-2- yl)cyclopentyl)piperazin-l-yl)-N-methylpicolinamide (3trans-a and 3trans-b) 3trans-a / 3trans-b racemic mixture was separated by SFC (Column: Daicel IJ 20 mml.D. x 250 mmL, 5 pmm; Mobile phase: CO2 / MeOH[0.1 %(NHs)] = 75 / 25) and concentrated under reduced pressure to afford the first fraction as 3trans-a (9.3 mg, 99.54 % purity, 100% ee, white solid) and the second fraction as 3trans-b (7.0 mg, 99.79 % purity, 100% ee, white solid). 3trans-a XH NMR (400 MHz, DMSO-d6, ppm) 6: 12.56-11.47 (m, 1 H), 8.42-8.35 (m, 2 H), 7.90-7.82 (m, 1 H), 7.76-7.69 (m, 1 H), 7.61-7.51 (m, 1 H), 7.42 (d, J = 8.4 Hz, 1 H), 7.25-7.13 (m, 1 H), 3.19-3.14 (m, 5 H), 2.86-2.80 (m, 1 H), 2.77 (d, J = 4.8 Hz, 3 H), 2.62-2.56 (m, 4 H), 2.22-2.06 (m, 2 H), 2.01-1.88 (m, 3 H), 1.57-1.47 (m, 1 H). NOE experiments suggested trans stereochemistry. LCMS (ESI) calcd for C24H26F2N6O2 [M + H] + m / z 469.21, found 469.10. 3trans-b XH NMR (400 MHz, DMSO-de, ppm) 6: 12.17 (s, 1 H), 8.43-8.36 (m, 1.6 H), 7.85 (d, J = 8.0 Hz, 1 H), 7.76-7.66 (m, 1 H), 7.61-7.51 (m, 1 H), 7.41 (d, J = 8.4 Hz, 1 H), 7.22-7.14 (m, 1 H), 3.20-3.11 (m, 5 H), 2.87-2.80 (m, 1 H), 2.77 (d, J = 4.8 Hz, 3 H), 2.64-2.56 (m, 4 H), 2.21-2.02 (m, 2 H), 2.03-1.85 (m, 3 H), 1.59-1.47 (m, 1 H). NOE experiments suggested trans stereochemistry. LCMS (ESI) calcd for C24H26F2N6O2 [M + H] + m / z 469.21, found 469.10. Example 5: Assays Exemplary compounds of the invention were prepared and tested to determine their effect as PARP1 and PARP2 inhibitors. Typical assays are described below. Example 5A. PARP1 biochemical dissociation-enhanced lanthanide fluorescence immunoassay (DELFIA assay) Optiplate HB 384-well plates were coated with anti-FLAG antibody, supplied as a 4 mg / ml solution, using a NazCOs / HCOs coating buffer at pH 9.6, overnight at 4 °C, in order to achieve a final immobilisation per well of 0.3 pg. Wells were then washed 3x5 min in coating wash buffer (PBS / 0.05 % Tween (v / v)), and blocked with 2 % BSA (w / v) in coating wash buffer overnight at 4 °C. Prior to assay, wells were washed 3x5 min in coating wash buffer. For the assay 20 pl of 2.5 nM recombinant full length human N-terminally FLAG-tagged PARP1 was added to each well of the 384-well plate for 30 min at room temperature followed by addition of 50 nL of compound solution in DMSO using pintool technology. Following incubation for 30 min at room temperature, 5 pl of 10 pM biotin-NAD+ and 10 nM activation DNA (sequence shown below) in solution in 20 mM HEPES (pH 7.5), 100 mM NaCI, 2 mM DTT, 0.1 % BSA (w / v), 0.02 % Tween (v / v) assay buffer. Auto-PARylation proceeded for 2 h at room temperature prior to the addition of 5 pl of 12 mM NAD+ quenching solution. After 30 min at room temperature, assay solution was removed and following washing 5 times for 3 min, 100 pl of a 1:1000 dilution of DELFIA Eu-Nl Streptavidin reagent was added. Plates were then incubated for 30 min at room temperature. The reaction mixture was removed and the plates washed 5 times for 3 min prior to the addition of 25 pl DELFIA enhancement solution. Following incubation for 30 min at room temperature, fluorescence was measured on a Pherastar FS (Ex337 nm, Em620 nm; integration start 60 ps; integration time 400 ps). Typically compounds were tested from 20 pM at 3-fold dilution intervals in 12-point concentration-response curves to determine IC50 values. Data was analysed using ActivityBase software and replicate values for the low (without enzyme, 0.2 % DMSO) and high (0.2 % DMSO) % controls were averaged and the data obtained from the test compounds expressed as a % of 100 % using the below formulae: % value = 100-(100*((high control - unknown) / (high control - low control)) % data was fitted to a non-linear regression equation (log inhibitor vs response-variable slope 4-parameters) to obtain IC50 values. The IC50 values for a variety of test compounds are shown in Table 1. Activation DNA sequence: 5'AG(XTGCr§WK^^ (SEQ ID NO:1) 5\ATCACCnGTTCWCAHGCCCACAGCAGGGT~3' (SEQ ID NO:2) 5’~ ~3*(SEQIDNO:3) i ii i h h n h 111 m i Example 5B. PARP1 probe displacement homogeneous time-resolved fluorescence assay (HTRF assay) 10 nM full length N-terminally FLAG-tagged PARP1 was incubated with 2 nM Anti-FLAG Tb-cryptate antibody and PARP1 / 2 Cy5 fluorescent dye-labelled binding probe (10-fold probe Kd = 270 nM) in 20 mM HEPES (pH 7.5), 100 mM NaCI, 2 mM DTT, 0.1 % BSA (w / v), 0.02 % Tween (v / v) assay buffer for 40 min at room temperature. A Cy5-labelled binding probe is shown below and described in Papeo, G. et al. J. Biomol. Screen. 2014; 19:1212-1219. 6 pl of this reaction mixture was then transferred to each well of a black non-binding surface 384-well plate and 35 nl of compound solution in DMSO was then added using pintool technology. Following incubation for 1 h at room temperature, fluorescence was measured on a Pherastar FS (Ex 337 nm, Em620 nm, em665 nm; integration start 60 ps; integration time 400 ps) using the HTRF module. Typically compounds were tested from 58.5 pM at factor 3 dilution intervals in 12-point concentration-response curves to determine IC50 values. Data was analysed using ActivityBase software and replicate values for the low (without enzyme but with probe and Tb-cryptate antibody, 0.6 % DMSO) and high (0.6 % DMSO) % controls were averaged and the data obtained from the test compounds expressed as a % of 100 % using the below formulae: %activity = 100*(value - low control) / (high control - low control) %activity data was fitted to a non-linear regression equation to obtain IC50 values Kd values were calculated using Cheng-Prussoff formula: IC5o = (1+ ([probe concentration] / [KmProbe]))*Kd Therefore Kd = IC50 / (l+[[probe concentration] / [Kmprobe])); using probe at 10 x Km, this equated to Kd = IC50 / H Example 10C. PARP2 probe displacement homogeneous time-resolved fluorescence assay (HTRF assay) This assay was performed under identical conditions as for PARP1, except that N-terminally FLAG-tagged PARP2 (amino acids 1-583) was used instead of PARP1, and PARP1 / 2 binding probe was used at 10-fold probe Kd = 540 nM. Data analysis was performed identical as for PARP1. Cy5 probe structure: NanoBRET cellular target occupancy assay NanoBRET assays were employed to demonstrate cellular target engagement and selectivity at PARP1 and PARP2. These assays are based on bioluminescence resonance energy transfer (BRET) between a Nano-luc-tagged protein (eg PARP1 or PARP2) and a fluorescent group on a high affinity NAD+ competitive binding probe. Such cellular probe displacement assays can be utilised to measure inhibitor affinities and selectivity ratios at PARP1 and 2. Frozen HEK293 cells transiently transfected with either PARPl-NanoLuc® fusion or PARP2-NanoLuc® fusion constructs (Promega) were thawed and dispensed as a suspension in 384-well microplates each at a density of 1750 cells per well. NanoBRET™ TE PARP Tracer-01 was then added to final concentrations of 11 and 2 nM for PARP1 and PARP2 assays, respectively. Compounds were added from 25 pM at factor 3 dilution intervals in 12-point concentrationresponse curves and plates were incubated for 2 hours at 37 °C. BRET ratios were then measured using a NanoBRET module (LUM 610-LP 450-80) and PHERAstar FS or FSX reader following addition of NanoBRET™ Nano-Gio® Substrate and Extracellular NanoLuc® Inhibitor 5 according to manufacturer's instructions. Kd values were calculated using Cheng-Prussoff formula: IC50 = (1+ ([tracer concentration] / [Kmtracer])) * Kd Binned potency, affinity and selectivity data for a variety of test compounds are shown in 10 Table 1 where DELFIA and Probe Displacement HTRF assays were used. Binned potency, affinity and selectivity data for a subset of test compounds where the NanoBRET assay was used are shown in Table 1. TABLE 1 15 Results ofParp 1 / 2 assays for selected compounds (DELFIA and Probe Displacement HTRF) Compound PARP1 DELFIA PARP1 HTRF PARP2 HTRF Selectivity 2cis-rac ++++ ++++ +++ +++ 2trans-a ++++ ++++ ++ +++ 2trans-b ++++ ++++ +++ +4- 3cis-a ++++ ++++ +++ +++ 3cis-b ++++ ++++ + +++ 3trans-a ++++ ++++ - +++ 3trans-b ++++ ++++ +++ +4- 4a +++ ++++ - +++ 4b ++++ ++++ - +++ 5cis ++++ ++++ - +++ 5trans +++ +++ - 4-4- 6 +++ +++ - +++ 7cis-rac ++++ ++++ ++ +++ 7trans-a ++++ ++++ - +++ 7trans-b ++++ ++++ +++ ++ 8cis-rac ++++ ++++ +++ +++ 8trans-a ++++ ++++ ++ +++ 8trans-b ++++ ++++ +++ +++ 9cis-a ++++ ++++ ++ +++ 9cis-b ++++ ++++ + +++ 9trans-a ++++ ++++ ++ +++ 9trans-b +++ +++ - +++ 18cis-a ++++ ++++ ++ +++ 18cis-b ++++ ++++ ++ +++ 18trans-a ++++ ++++ + +++ 18trans-b ++++ ++++ +++ ++ TABLE 2 Results ofParp 1 / 2 assays for selected compounds (NanoBRET) Compound PARP1 NanoBRET PARP2 NanoBRET Selectivity 2trans-b ++++ +++ +++ 3cis-a ++++ ++ +++ 3cis-b ++++ - +++ 3trans-b ++++ ++ +++ 7cis-rac ++++ ++ +++ 7trans-b ++++ ++ +++ 8trans-b ++++ ++ +++ Key DELFIA, Probe Displacement HTRF and NanoBRET assay categories: - indicates ICso or Ka value above 10 pM 10 + indicates IC50 or Ka value above 1 pM up to 10 pM ++ indicates IC50 or Ka value above 100 nM up to 1 pM +++ indicates IC50 or Ka value above 10 nM up to 100 nM ++++ indicates IC50 or Ka value of 10 nM or less 15 Selectivity categories: - indicates a value of less than 10 + indicates a value of 10 to less than 50 ++ indicates a value of 50 to less than 100 +++ indicate a value of at least 100 5 The selectivity values relate to the selectivity preference of PARP1 over PARP2. They are calculated from the ratio of Kd values for PARP1 and PARP2 inhibition as Kd (PARP2) / Kd (PARP1). 10 It will be appreciated that the above embodiments have been described by way of example only. Other variants or use cases of the disclosed techniques may become apparent to the person 15 skilled in the art once given the disclosure herein. The scope of the disclosure is not limited by the described embodiments but only by the accompanying claims.

Claims

1. A PARP1 inhibitor compound having a structure of:wherein:a dotted line represents a bond selected from a single bond and a double bond;y is 0,1, or 2;each XD is independently selected from C, N, O and S;Xr and XEB are each independently selected from C and N;each R1 is independently absent or selected from H and a substituted or unsubstituted organic group;each R4 is independently absent or selected from H and a substituted or unsubstituted organic group, with the proviso that the R4 groups are not fused to form a ring;R3 is H ora substituted or unsubstituted organic group;L is a group having a structure of:wherein:ring C is an aromatic ring;XA1 is C or N;each XA2 is independently selected from C, N, O and S;each XB2 is independently selected from C, N, O and S;XB3 is selected from C and N;each Xc is independently selected from C, N, O, and S, with the proviso that ring C is a heterocycle;each R5A, R5B, and R5C is independently absent or selected from H and a substituted or unsubstituted organic group;R6 is selected from H and a substituted or unsubstituted organic group;n is 0,1, 2, 3, 4, or 5;m is 0,1, 2, 3, 4, or 5, with the proviso that n + m is in the range 2 to 5;p is 1, 2 or 3;q is 1, 2 or 3, with the proviso that p + q is in the range 2 to 5;r is 0,1, 2, 3, or 4; ands is 0,1, 2, 3, or 4, with the proviso that r + s is 3 or 4;Q is a bond ora linking group having a structure selected from:wherein:t is 0, 1, 2, 3, 4 or 5;u is 0,1, 2, 3, 4 and 5, with the proviso that t + u is in the range 0 to 6;andeach R7 and R8 is independently selected from H and a substituted orunsubstituted organic group.

2. The PARP1 inhibitor compound according to any preceding claim, wherein each R1 and each R4 is independently absent or selected from:H;a halogen;a nitrile group;a Cl to C6 acyclic alkyl group;a Cl to C6 acyclic alkoxy group;a Cl to C6 acyclic haloalkyl group;a Cl to C6 acyclic haloalkoxy group, such as -OCF3 or OCHF2;a Cl to C6 acyclic aminoalkyl group; and22RR22 being selected from H, a halogen, a Cl to C6 alkyl group, a C3 to C6 cycloalkyl group, a Cl to C6 alkoxy group, a Cl to C6 haloalkyl group, and each R23 being independently selected from H; a halogen; a Cl to C6 alkyl group; a Cl to C6 aminoalkyl group; a Cl to C6 alkoxy group; a Cl to C6 haloalkoxy group; such as -OCF3 or OCHF2; and a Cl to C6 haloalkyl group.

3. The PARP1 inhibitor compound according to claim 2, wherein each R1 and each R4 is independently absent or selected from H; a halogen, optionally Cl or F; a Cl to C3 acyclic alkyl group, optionally a methyl group; a Cl to C3 haloalkyl group, optionally a halomethyl group such as -CH2F, -CHF2, or -CF3; a haloethyl group, such as -CH2CF3; and a nitrile group.

4. The PARP1 inhibitor compound according to claim 3, wherein each R1 and each R4 is independently absent or selected from: H; Cl; F; a halomethyl group, such as CF3; and a nitrile group.

5. The PARP1 inhibitor compound according to claim 4, wherein each R1 and each R4 is independently absent or selected from H and F.

6. The PARP1 inhibitor compound according to claim 5, wherein exactly one R1 or exactly one R4 is F;or wherein each R1 and each R4 is absent or H.

7. The PARP1 inhibitor compound according to any preceding claim, wherein at least one of XETand XEBisC.

8. The PARP1 inhibitor compound according to claim 7, wherein XEB is N.

9. The PARP1 inhibitor compound according to claim 8, having a structure selected from:

10. The PARP1 inhibitor compound according to claim 7, wherein XET is C and XEB is C.

11. The PARP1 inhibitor compound according to claim 10, having a structure selectedfrom:

12. The PARP1 inhibitor compound according to any preceding claim, wherein each XD is independently selected from C and N.

13. The PARP1 inhibitor compound according to claim 12, wherein each XD is C.

14. The PARP1 inhibitor compound according to any preceding claim, wherein y is 1.

15. The PARP1 inhibitor compound according to any of claims 1 to 13, wherein y is 0.

16. The PARP1 inhibitor compound according to any preceding claim, wherein ring D is anaromatic ring.

17. The PARP1 inhibitor compound according to claim 16, having a structure of:

18. The PARP1 inhibitor compound according to claim 17, having a structure selectedfrom:19.The PARP1 inhibitor compound according to claim16, having a structure selectedfrom:

20. The PARP1 inhibitor compound according to claim 19, having a structure selectedfrom:21.The PARP1 inhibitor compound according to claim19, having a structure selectedfrom:

22. The PARP1 inhibitor compound according to any of claims 1 to 15, wherein ring D is anon-aromatic ring.

23. The PARP1 inhibitor compound according to claim 22, having a structure selectedfrom:

24. The PARP1 inhibitor compound according to claim 23, having a structure of:O25. The PARP1 inhibitor compound according to claim 22, having a structure selected from:26.ThePARP1 inhibitor compound according to claim22, having a structure selectedfrom:

27. The PARP1 inhibitor compound according to claim 22, having a structure selectedfrom:

028. The PARP1 inhibitor compound according to any preceding claim, wherein R3 is selected from H, a Cl to C3 alkyl group, and a Cl to C3 haloalkyl group.

29. The PARP1 inhibitor compound according to claim 28, wherein R3 is H.

30. The PARP1 inhibitor compound according to claim 1, having a structure selected from:

31. The PARP1 inhibitor compound according to any preceding claim, wherein both n andm are at least 1.

32. The PARP1 inhibitor compound according to any preceding claim, wherein XA1 is C.

33. The PARP1 inhibitor compound according to claim 32, wherein:i) ring A is a 7-membered ring, optionally a cycloheptane having a structure selected from:each R5A and R5A3 being independently selected from H and a substituted or unsubstituted organic group, wherein R5A3 is most preferably H; orii) ring A is a 6-membered non-aromatic ring, optionally a cyclohexane, cyclohexene, or tetrahydropyran and further optionally having a structure selected from:each R5A and R5A3 being independently selected from H and a substituted or unsubstituted organic group, wherein R5A3 is most preferably H; oriii) ring A is a 5-membered non-aromatic ring, optionally a cyclopentane, cyclopentene, or atetrahydrofuran, and further optionally having a structure selected from:each R5A and R5A3 being independently selected from H and a substituted or unsubstituted organic group, wherein R5A3 is most preferably H; oriv) ring A is a 4-membered ring having a structure of:each R5A and R5A3 being independently selected from H and a substituted or unsubstituted organic group, wherein R5A3 is most preferably H; orv) ring A is a bridged ring, optionally having a structure selected from:each R5A and R5A3 being independently selected from H and a substituted orunsubstituted organic group, wherein R5A3 is most preferably H.

34. The PARP1 inhibitor compound according to any preceding claim, wherein whenpresent each R5A is independently selected from H; a halogen, optionally F; a hydroxyl group;a carbonyl group; and a Cl to C3 alkyl group, optionally wherein a pair of R5A groups form a ring, further optionally wherein the ring bridges ring A;preferably wherein each R5A is H.

35. The PARP1 inhibitor compound according to claim 33, wherein ring A has a structureselected from:where Qa represents a bond to ring E and Qb represents a bond to ring B.

36. The PARP1 inhibitor compound according to claim 31, wherein ring A has a structure of:wherein:Qa represents a bond to ring E and Qb represents a bond to ring B;m is 1 or 2;n is 1 or 2;each R5A2 and R5A3 independently is absent or selected from H and a substituted or unsubstituted organic group, preferably wherein R5A3 is H;and wherein:i) XA1 is C and R5A1 is selected from H and a substituted or unsubstituted organic group; orii) XA1 is N and R5A1 is absent.

37. The PARP1 inhibitor compound according to claim 36, wherein each R5A1, R5A2 and R5A3 is independently is absent or selected from H; a halogen, optionally F; a hydroxyl group; a carbonyl group; and a Cl to C3 alkyl group, optionally wherein a pair of R5A groups form a Cl to C3 alkyl group bridging ring A;preferably wherein each R5A1, R5A2 and R5A3 is absent or H.

38. The PARP1 inhibitor compound according to claim 36, wherein ring A has a structureselected from:(to ring E)(to ring B)(to ring E)(to ring B)(to ring E)(to ring E)(to ring E)(to ring E)(to ring B)(to ring E)preferably wherein ring A has a structure selected from:(to ring B)(to ring E)and most preferably wherein ring A has a structure of:(to ring E)(to ring B)39. The PARP1 inhibitor compound according to any preceding claim, wherein ring A is a5-membered ring.

40. The PARP1 inhibitor compound according to any preceding claim, wherein ring B hasa structure of:

41. The PARP1 inhibitor compound according to any preceding claim, wherein XB3 is N.

42. The PARP1 inhibitor compound according to claim 40, wherein ring B has a structureselected from:5B R43. The PARP1 inhibitor compound according to any preceding claim, wherein each R5B is independently absent or H.

44. The PARP1 inhibitor compound according to claim 42, wherein ring B has a structureselected from:

45. The PARP1 inhibitor compound according to claim 44, wherein ring B has a structureof:

46. The PARP1 inhibitor compound according to claim 44, wherein ring B has a structureof:

47. The PARP1 inhibitor compound according to any preceding claim, wherein Q isselected from:and R7 tR7 R7 R7 ;wherein t + u is at least 1; andwherein R7 is selected from H; a halogen, such as -F, -Cl, -Br, and -I, and preferably -F; an -OH group; a Cl to C6 alkyl group; a Cl to C6 haloalkyl group, preferably CF3; an -NH2 group; a Cl to C6 amino group; a Cl to C6 alcohol group; and a Cl to C6 alkoxy group.

48. The PARP1 inhibitor compound according to claim 47, wherein R7 is selected from: H; a halogen, optionally F; a Cl to C6 alkyl group; and a Cl to C6 haloalkyl group.

49. The PARP1 inhibitor compound according to any preceding claim, wherein Q has a structure of:and wherein R8 is selected from:H;a substituted or unsubstituted linear or branched Ci-Ce alkyl group(such as Me, Et, Pr, i-Pr, n-Bu, i-Bu, t-Bu, pentyl and hexyl);a substituted or unsubstituted linear or branched Ci-Ce alkyl-aryl group(such as -CH2Ph, -CH2(2,3 or 4)F-Ph, -CH2(2,3 or 4)CI-Ph, -CH2(2,3 or 4)Br-Ph,-CH2(2,3 or4)l-Ph, -CH2CH2Ph, -CH2CH2CH2Ph,-CH2CH2CH2CH2Ph, -CH2CH2CH2CH2CH2Ph, and -CH2CH2CH2CH2CH2CH2Ph);a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (such as -CH2F, -CF3, -CH2CH2F and -CH2CF3);a substituted or unsubstituted cyclic amine or amido group(such as pyrrolidin-3-yl, piperidin-3-yl, piperidin-4-yl, 2-keto-pyrrolidinyl, 3-keto-pyrrolidinyl, 2-keto-piperidinyl, 3-keto-piperidinyl, and 4-keto-piperidinyl);a substituted or unsubstituted cyclic C3-Cs alkyl group(such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl and cyclooctyl);a substituted or unsubstituted linear or branched C2-C6 alcohol group(such as -CH2CH2OH, -CH(CH3)CH2OH, -C(CH3)2OH, -CH2CH2CH2OH, -CH2CH2CH2CH2OH, -CH(CH3)CH2CH2OH, -CH(CH3)CH(CH3)OH, -CH(CH2CH3)CH2OH, -C(CH3)2CH2OH, -CH2CH2CH2CH2CH2OH,and -CH2CH2CH2CH2CH2CH2OH);a substituted or unsubstituted linear or branched C2-C6 carboxylic acid group (such as -CH2COOH, -CH2CH2COOH, -CH2CH2CH2COOH, -CH2CH2CH2CH2COOH, and -CH2CH2CH2CH2CH2COOH);a substituted or unsubstituted linear or branched carbonyl group(such as -(CO)Me, -(CO)Et, -(CO)Pr, -(CO)-i_Pr, -(CO)-n-Bu, -(CO)-i-Bu, -(CO)-t-Bu, -(CO)Ph, -(CO)CH2Ph, -(CO)CH2OH, -(CO)CH2OCH3, -(CO)CH2NH2, -(CO)CH2NHMe, -(CO)CH2NMe2, -(CO)-cyclopropyl, -(CO)-l,3-epoxypropan-2-y I; -(CO)NH2, -(CO)NHMe, -(CO)NMe2, -(CO)NHEt, -(CO)NEt2, -(CO)-pyrollidine-N-yl, -(CO)-morpholine-N-yl, -(CO)-piperazine-N-yl, -(CO)-N-methyl-piperazine -N-yl, -(CO)NHCH2CH2OH, -(CO)NHCH2CH2OMe, -(CO)NHCH2CH2NH2, -(CO)NHCH2CH2NHMe, and -(CO)NHCH2CH2NMe2);a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid ester group (such as -COOMe, -COOEt, -COOPr, -COO-i-Pr, -COO-n-Bu, -COO-i-Bu, -COO-t-Bu, -CH2COOMe, -CH2CH2COOMe, -CH2CH2CH2COOMe, and -CH2CH2CH2CH2COOMe);a substituted or unsubstituted linear or branched Ci-Ce amide group(such as -CO-NH2, -CO-NMeH, -CO-NMe2, -CO-NEtH, -CO-NEtMe, -CO-NEt2, -CO-NPrH, -CO-NPrMe, and -CO-NPrEt);a substituted or unsubstituted sulfonyl group(such as -SO2Me, -SO2Et, -SO2Pr, -SO2iPr, -SO2Ph, -SO2-(2,3 or 4)-F-Ph,-SO2-cyclopropyl, -SO2CH2CH2OCH3), -SO2NH2, -SO2NHMe, -SO2NMe2, -S02NHEt, -SO2NEt2, -SO2-pyrrolidine-N-yl,-SO2-morpholine-N-yl, -SO2NHCH2OMe, and -SO2NHCH2CH2OMe);a substituted or unsubstituted aromatic group(such as Ph-, 2-F-Ph-, 3-F-Ph-, 4-F-Ph-, 2-CI-Ph-, 3-CI-Ph-, 4-CI-Ph-, 2-Br-Ph-, 3-Br-Ph-, 4-Br-Ph-, 2-l-Ph-, 3-l-Ph, 4-l-Ph-, 2,(3,4,5 or 6)-F2-Ph-,2,(3,4,5 or 6)-CI2-Ph-, 2,(3,4,5 or 6)-Br2-Ph-, 2,(3,4,5 or 6)-l2-Ph-, 2,(3,4,5 or 6)-Me2-Ph-, 2,(3,4,5 or 6)-Et2-Ph-, 2,(3,4,5 or 6)-Pr2-Ph-, 2,(3,4,5 or 6)-Bu2-Ph-, 2,(3,4,5 or 6)-(CN)2-Ph-, 2,(3,4,5 or 6)-(NO2)2-Ph-, 2,(3,4,5 or 6)-(NH2)2-Ph-, 2,(3,4,5 or 6)-(MeO)2-Ph-, 2,(3,4,5 or 6)-(CF3)2-Ph-, 3,(4 or 5)-F2-Ph-, 3,(4 or 5)-CI2-Ph-, 3,(4 or 5)-Br2-Ph-, 3,(4 or 5)-l2-Ph-, 3,(4 or 5)-Me2-Ph-, 3,(4 or 5)-Et2-Ph-, 3,(4 or 5)-Pr2-Ph-, 3,(4 or 5)-Bu2-Ph-, 3,(4 or 5)-(CN)2-Ph-, 3,(4 or 5)-(NO2)2-Ph-, 3,(4 or 5)-(NH2)2-Ph-,3,(4 or 5)-(MeO)2-Ph-, 3,(4 or 5)-(CF3)2-Ph-, 2-Me-Ph-, 3-Me-Ph-, 4-Me-Ph-, 2-Et-Ph-, 3-Et-Ph-, 4-Et-Ph-, 2-Pr-Ph-, 3-Pr-Ph-, 4-Pr-Ph-, 2-Bu-Ph-, 3-Bu-Ph-, 4-Bu-Ph-, 2-(CN)-Ph-, 3-(CN)-Ph-, 4-(CN)-Ph-, 2-(NO2)-Ph-, 3-(NO2)-Ph-, 4-(NO2)-Ph-, 2-(NH2)-Ph-, 3-(NH2)-Ph-, 4-(NH2)-Ph-, 2-MeO-Ph-, 3-MeO-Ph-, 4-MeO-Ph-, 2-(NH2-CO)-Ph-, 3-(NH2-CO)-Ph-, 4-(NH2-CO)-Ph-, 2-CF3-Ph-, 3-CF3-Ph-, 4-CF3-Ph-, 2-CF3O-Ph-, 3-CF3O-Ph-, and 4-CF3O-Ph-); and a substituted or unsubstituted heterocyclic group(such as pyrrole-2-yl, pyrrole-3-yl, pyrazole-3-yl, pyrazole-4-yl, pyrazole-5-yl, imidazole-2-yl, imidazole-4-yl, imidazole-5-yl, l,2,3-triazole-4-yl, l,2,3-triazole-5-yl, l,2,4-triazole-3-yl, l,2,4-triazole-5-yl, pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, pyridazine-3-yl, pyridazine-4-yl, pyrimidin-2-yl, pyrimidin-4-yl, pyrimidin-5-yl, pyrimidin-6-yl, pyrazine-2-yl, pyrrolidine-2-yl, pyrrolidine-3-yl, piperidine-2-yl, piperidine-3-yl, piperidine-4-yl, 2-azapiperidine-3-yl, 2-azapiperidine-4-yl, 3-azapiperidine-2-yl, 3-azapiperidine-4-yl, 3-azapiperidine-5-yl, piperazine-2-yl, furan-2-yl, furan-3-yl, pyran-2-yl, pyran-3-yl, pyran-4-yl, 2-azapyran-3-yl, 2-azapyran-4-yl, 2-azapyran-5-yl, 2-azapyran-6-yl, 3-azapyran-2-yl, 3-azapyran-4-yl, 3-azapyran-5-yl, 3-azapyran-6-yl, 4-azapyran-2-yl, 4-azapyran-3-yl,4-azapyran-5-yl, 4-azapyran-6-yl, tetrahydrofuran-2-yl, tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-4-yl, 2-aza-tetrahydrofuran-5-yl, 3-aza-tetrahydrofuran-2-yl, 3-aza-tetrahydrofuran-4-yl, 3-aza-tetrahydrofuran-5-yl, tetrahydropyran-2-yl, oxetan-3-yl, tetrahydropyran-3-yl, tetrahydropyran-4-yl, 2-aza-tetrahydropyran-3-yl, 2-aza-tetrahydropyran-4-yl, 2-aza-tetrahydropyran-5-yl, 2-aza-tetrahydropyran-6-yl, 3-aza-tetrahydropyran-2-yl, 3-aza-tetrahydropyran-4-yl, 3-aza-tetrahydropyran-5-yl, 3-aza-tetrahydropyran-6-yl, morpholine-2-yl, morpholine-3-yl, thiophen-2-yl, thiophen-3-yl, isothiazole-3-yl, isothiazole-4-yl, isothiazole-5-yl, thiazole-2-yl, thiazole-4-yl, thiazole-5-yl, thiopyran-2-yl, thiopyran-3-yl, thiopyran-4-yl, 2-azathiopyran-3-yl, 2-azathiopyran-4-yl, 2-azathiopyran-5-yl, 2-azathiopyran-6-yl, 3-azathiopyran-2-yl, 3-azathiopyran-4-yl, 3-azathiopyran-5-yl, 3-azathiopyran-6-yl, 4-azathiopyran-2-yl, 4-azathiopyran-3-yl, 4-azathiopyran-5-yl, 4-azathiopyran-6-yl, thiolane-2-yl, thiolane-3-yl, thiane-2-yl, thiane-3-yl, thiane-4-yl, oxazol-2-yl, oxazol-4-yl, oxazol-5-yl, isoxazol-3-yl, isoxazol-4-yl, isoxazol-5-yl, furazan-3-yl, (l,3,4-oxadiazol)-2-yl, (l,3,4-oxadiazol)-5-yl, (l,2,4-oxadiazol)-3-yl, (l,2,4-oxadiazol)-5-yl; and tetrazole-5-yl).

50. The PARP1 inhibitor compound according to claim 49, wherein R8 is selected from H, a substituted or unsubstituted linear or branched Ci-Ce alkyl group, and a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group.

51. The PARP1 inhibitor compound according to any of claims 1 to 46, wherein Q is a bond or -CH2-,preferably wherein Q is a bond.

52. The PARP1 inhibitor compound according to any preceding claim, wherein r is at least 1 and s is at least 1.

53. The PARP1 inhibitor compound according to any preceding claim, wherein each Xc is independently selected from C and N.

54. The PARP1 inhibitor compound according to claim 53, wherein r+s is 4; optionally wherein r is 2 and s is 2.

55. The PARP1 inhibitor compound according to claim 53, wherein ring C has a structure of:wherein:XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N;when XCo is C, RCo is H or a halogen, F being the preferred halogen;when XCo is N, RCo is absent;when XCm is C, RCm is H or a halogen, F being the preferred halogen; and when XCm is N, RCm is absent;optionally wherein exactly one of XCo and XCm is N.

56. The PARP1 inhibitor compound according to claim 54, wherein ring C is a pyridine group, optionally having a structure selected fromr5G r5Ceach R5C being independently selected from H and a substituted orunsubstituted organic group.

57. The PARP1 inhibitor compound according to claim 56, wherein ring C is a pyridinegroup having a structure of:and more preferablyF58. The PARP1 inhibitor compound according to claim 54, wherein ring C is a diazinegroup, optionally having a structure selected from:each R5C being independently selected from H and a substituted orunsubstituted organic group.

59. The PARP1 inhibitor compound according to any of claims 1 to 53, wherein r+s is 3 andeach Xc is independently selected from C, N, O and S.

60. The PARP1 inhibitor compound according to claim 58, wherein ring C is selected from:i) an imidazole group, optionally an imidazole group having a structure selected from:each R5C being independently selected from H and a substituted or unsubstituted organic group;ii) a thiophene group, optionally having a structure selected from:each R5C being independently selected from H and a substituted orunsubstituted organic group, optionally wherein each R5C is H;iii) a thiazole group, optionally having a structure selected from:each R5C being independently selected from H and a substituted orunsubstituted organic group, optionally wherein each R5C is H;iv) a triazole, optionally a triazole having a structure of:R5C being selected from H and a substituted or unsubstituted organic group,optionally wherein R5C is H.

61. The PARP1 inhibitor compound according to any preceding claim, wherein when present each R5C is H or an organic group selected from a halogen, preferably F; a Cl to C3 alkyl group; a Cl to C3 haloalkyl group, optionally a fluoromethyl group such as CF2H or CF3; and a nitrile group.

62. The PARP1 inhibitor compound according to claim 61, wherein exactly one R5C is an organic group.

63. The PARP1 inhibitor compound according to claim 62, wherein exactly one R5C is F.

64. The PARP1 inhibitor compound according to claim 61, wherein when present each R5Cis H.

65. The PARP1 inhibitor compound according to any preceding claim, wherein ring C hasa structure selected from:

66. The PARP1 inhibitor compound according to any preceding claim, wherein R6 isselected from H, -F, -Cl, -Br, -I, -CN, -CONR51R51, -NR51COR52, -SO2NR51R51, -NR51SO2R52,-O-CR52R52R52, -CR52R52NR51R51, and any of the following structures:wherein R51 and R52 are each independently selected fromH and a substituted orunsubstituted organic group, optionally wherein R51 and R52 are each independentlyselected from H, a halogen, optionally-deuterated Cl to C3 alkyl, and Cl to C3haloalkyl.

67. The PARP1 inhibitor compound according to claim 66, wherein R6 is selected from -F,-Cl, -CN, -CONH2, -CONHMe (optionally -CONHCD3), -CONHEt, -CONMe2,-CONHCOMe, -CONHCH2-CH2OMe, -CONH-CH2-CH2F, -CONH-CH2-CF3, -CONH-CH2-CHF2,-OCHF2, -NHCOMe, -NHSO2Me, -SO2NHMe, -CONHSO2Me, O , O68. The PARP1 inhibitor compound for use according to claim 67, wherein R6 is CONHMe.69.The PARP1 inhibitor compound according to claim 68, wherein R6 is70. The PARP1 inhibitor compound according to claim 68, wherein R6 is 071. The PARP1 inhibitor compound according to claim 68, wherein R6 is F.

72. The PARP1 inhibitor compound according to claim 68, wherein R6 is Cl.

73. The PARP1 inhibitor compound according to claim 68, wherein R6 is CN.

74. The PARP1 inhibitor compound according to any preceding claim, wherein L has a structure selected from:

75. The PARP1 inhibitor compound according to any preceding claim, wherein rings E andB are in a cis configuration with respect to ring A, optionally wherein group L is selected from:

76. The PARP1 inhibitor compound according to any of claims 1 to 72, wherein rings E and B are in a trans configuration with respect to ring A, optionally wherein group L is selected from:

77. The PARP1 inhibitor compound according to any preceding claim, having a structureof:wherein:XD is selected from C and N;when XD is N:RD1 is selected from H, a Cl to C3 alkyl group, and a Cl to C3 haloalkyl group; preferably a methyl group; andRD2 is absent;when XD is C:RD1 and RD2 are each H;n is 1 or 2;RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ringA, with the proviso that when n is 1, RA1 and RA3 are each H;XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N;when XCo is C, RCo is H or a halogen, and is optionally H or F;when XCo is N, RCo is absent;when XCm is C, RCm is H or a halogen, and is optionally H or F;when XCm is N, RCm is absent;R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl.

78. The PARP1 inhibitor compound according to any of claims 1 to 76, having a structureof:wherein:XD is C or N;when XD is C, RD4 is selected from H and a halogen, and is preferably H;when XD is N, RD4 is absent;RD1 and RD2 are each independently selected from H and a halogen;n is 1 or 2;XA is C or N;when XA is C:RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ring A, with the proviso that when n is 1, RA1 and RA3 are each H;when XA is N:RA1 is absent, and RA3 is H;XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N;when XCo is C, RCo is H or a halogen, and is optionally H or F;when XCo is N, RCo is absent;when XCm is C, RCm is H or a halogen, and is optionally H or F;when XCm is N, RCm is absent;R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl.

79. The PARP1 inhibitor compound according to any of claims 1 to 76, having a structure of:wherein:a dotted line represents a single bond or a double bond;XEB is C or N;XD1 and XD2 are each independently selected from C and N, with the proviso that whenXEB isN,XD1 is C;RD1, and RD2 are each independently absent or present and selected from H, a halogen, a methyl group, and a halomethyl group, such as CF3;RD3 is selected from H, a halogen, a methyl group, and a halomethyl group, such asCF3;n is 1 or 2;RA1 and RA3 are each H, or RA1 and RA3 together represent a -CH2- group bridging ringA, with the proviso that when n is 1, RA1 and RA3 are each H;XCo and XCm are each selected from C and N, with the proviso that at least one of XCo and XCm is N;when XCo is C, RCo is H or a halogen, and is optionally H or F;when XCo is N, RCo is absent;when XCm is C, RCm is H or a halogen, and is optionally H or F;when XCm is N, RCm is absent;R6 is selected from -C(O)NHMe; -CN; and a halogen, optionally F or Cl.

80. The PARP1 inhibitor compound according to claim 1, having a structure selected from:18trans81. The PARP1 inhibitor compound according to any of claims 1 to 76, wherein when one or more of R1, R3, R4, R5A(e.g. R5A1, R5A2, R5A3), R5B, R5C, R6, R7, R8, R51, and R52 is a substituted or unsubstituted organic group, the or each substituted or unsubstituted organic group is independently selected from:deuterium;a halogen (such as -F, -Cl, -Br and -I);a substituted or unsubstituted linear or branched Ci-Ce alkyl group(such as Me, Et, Pr, i-Pr, n-Bu, i-Bu, t-Bu, pentyl and hexyl);a substituted or unsubstituted linear or branched Ci-Ce alkyl-aryl group(such as -CH2Ph, -CH2(2,3 or 4)F-Ph, -CH2(2,3 or 4)CI-Ph, -CH2(2,3 or 4)Br-Ph,-CH2(2,3 or4)l-Ph, -CH2CH2Ph, -CH2CH2CH2Ph,-CH2CH2CH2CH2Ph, -CH2CH2CH2CH2CH2Ph, and -CH2CH2CH2CH2CH2CH2Ph);a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (such as -CH2F, -CH2CI, -CH2Br, -CH2I, -CHF2, -CF3, -CCI3 -CBr3, -Cl3, -CH2CH2F, -CH2CF3, -CH2CCI3, -CH2CBr3, and -CH2CI3);NH2 or a substituted or unsubstituted linear or branched primary secondary or tertiary Ci-Ce amine group(such as -NMeH, -NMe2, -NEtH, -NEtMe, -NEt2, -NPrH, -NPrMe, -NPrEt, -NPr2, -NBuH, -NBuMe, -NBuEt, -CH2-NH2, -CH2-NMeH, -CH2-NMe2, -CH2-NEtH, -CH2-NEtMe,-CH2-NEt2, -CH2-NPrH, -CH2-NPrMe, and -CH2-NPrEt);a substituted or unsubstituted amino-aryl group(such as -NH-Ph, -NH-(2,3 or4)F-Ph, -NH-(2,3 or4)CI-Ph, -NH-(2,3 or4)Br-Ph,-NH-(2,3 or 4)I-Ph, -NH-(2,3 or 4)Me-Ph, -NH-(2,3 or 4)Et-Ph,-NH-(2,3 or4)Pr-Ph, -NH-(2,3 or4)Bu-Ph, NH-(2,3 or4)OMe-Ph,-NH-(2,3 or 4)OEt-Ph, -NH-(2,3 or 4)OPr-Ph, -NH-(2,3 or 4)OBu-Ph,-NH-2,(3,4,5 or 6)F2-Ph, -NH-2,(3,4,5 or 6)CI2-Ph, -NH-2,(3,4,5 or 6)Br2-Ph,-NH-2,(3,4,5 or 6)I2-Ph, -NH-2,(3,4,5 or 6)Me2-Ph, -NH-2,(3,4,5 or 6)Et2-Ph,-NH-2,(3,4,5, or 6)Pr2-Ph, -NH-2,(3,4,5 or 6)Bu2-Ph), a substituted or unsubstituted cyclic amine or amido group(such as pyrrolidin-l-yl, pyrrolidin-2-yl, pyrrolidin-3-yl, piperidin-l-yl, piperidin-2-yl, piperidin-3-yl, piperidin-4-yl, morpholin-2-yl, morpholin-3-yl, morpholin-4-yl, 2-keto-pyrrolidinyl, 3-keto-pyrrolidinyl, 2-keto-piperidinyl, 3-keto-piperidinyl, and 4-keto-piperidinyl);a substituted or unsubstituted cyclic C3-Cs alkyl group(such as cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl and cyclooctyl);a substituted or unsubstituted linear or branched Ci-Ce alcohol group(such as-CH2OH, -CH2CH2OH, -CH(CH3)CH2OH, -C(CH3)2OH, -CH2CH2CH2OH, -CH2CH2CH2CH2OH, -CH(CH3)CH2CH2OH, -CH(CH3)CH(CH3)OH, -CH(CH2CH3)CH2OH, -C(CH3)2CH2OH, -ch2ch2ch2ch2ch2oh, and -CH2CH2CH2CH2CH2CH2OH);a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid group(such as -COOH, -CH2COOH, -CH2CH2COOH, -CH2CH2CH2COOH, -CH2CH2CH2CH2COOH, and -CH2CH2CH2CH2CH2COOH);a substituted or unsubstituted linear or branched carbonyl group(such as -(CO)Me, -(CO)Et, -(CO)Pr, -(CO)iPr, -(CO)nBu, -(CO)iBu, -(CO)tBu, -(CO)Ph, -(CO)CH2Ph, -(CO)CH2OH, -(CO)CH2OCH3, -(CO)CH2NH2, -(CO)CH2NHMe, -(CO)CH2NMe2, -(CO)-cyclopropyl, -(CO)-l,3-epoxypropan-2-yl; -(CO)NH2, -(CO)NHMe, -(CO)NMe2,-(CO)NHEt, -(CO)NEt2,-(CO)-pyrollidine-N-yl, -(CO)-morpholine-N-yl, -(CO)-piperazine-N-yl, -(CO)-N-methyl-piperazine-N-yl, -(CO)NHCH2CH2OH, -(CO)NHCH2CH2OMe, -(CO)NHCH2CH2NH2, -(CO)NHCH2CH2NHMe, and -(CO)NHCH2CH2NMe2);a substituted or unsubstituted linear or branched Ci-Ce carboxylic acid ester group (such as -COOMe, -COOEt, -COOPr, -COO-i-Pr, -COO-n-Bu, -COO-i-Bu, -COO-t-Bu, -CH2COOMe, -CH2CH2COOMe, -CH2CH2CH2COOMe, and -CH2CH2CH2CH2COOMe);a substituted or unsubstituted linear or branched Ci-Ce amide group(such as -CO-NH2, -CO-NMeH, -CO-NMe2, -CO-NEtH, -CO-NEtMe, -CO-NEt2, -CO-NPrH, -CO-NPrMe, and -CO-NPrEt);a substituted or unsubstituted linear or branched C1-C7 amino carbonyl group (such as -NH-CO-Me, -NH-CO-Et, -NH-CO-Pr, -NH-CO-Bu, -NH-CO-pentyl, -NH-CO-hexyl, -NH-CO-Ph, -NMe-CO-Me, -NMe-CO-Et, -NMe-CO-Pr, -NMe-CO-Bu, -NMe-CO-pentyl, -NMe-CO-hexyl, -NMe-CO-Ph);a substituted or unsubstituted linear or branched C1-C7 alkoxy or aryloxy group (such as -OMe, -OEt, -OPr, -O-i-Pr, -O-n-Bu, -O-i-Bu, -O-t-Bu, -O-pentyl, -O-hexyl, -OCH2F, -OCHF2, -OCF3, -OCH2CI, -OCHCI2, -OCCI3, -O-Ph, -O-CH2-Ph,-O-CH2-(2,3 or 4)-F-Ph, -O-CH2-(2,3 or 4)-CI-Ph, -CH2OMe, -CH2OEt, -CH2OPr, -CH2OBu, -CH2CH2OMe, -CH2CH2CH2OMe, -CH2CH2CH2CH2OMe, and -CH2CH2CH2CH2CH2OMe);a substituted or unsubstituted linear or branched aminoalkoxy group(such as -OCH2NH2, -OCH2NHMe, -OCH2NMe2, -OCH2NHEt, -OCH2NEt2, -OCH2CH2NH2, -OCH2CH2NHMe, -OCH2CH2NMe2, -OCH2CH2NHEt, and -OCH2CH2NEt2);a substituted or unsubstituted sulfonyl group(such as -SO2Me, -SO2Et, -SO2Pr, -SO2iPr, -SO2Ph, -SO2-(2,3 or 4)-F-Ph,-SO2-cyclopropyl, -SO2CH2CH2OCH3, -SO2NH2, -SO2NHMe, -SO2NMe2,-SO2NHEt, -SO2NEt2, -SO2-pyrrolidine-N-yl,-SO2-morpholine-N-yl, -SO2NHCH2OMe,and -SO2NHCH2CH2OMe);a substituted or unsubstituted aminosulfonyl group(such as -NHSO2Me, -NHSO2Et, - NHSO2Pr, -NHSO2iPr, -NHSO2Ph, -NHSO2-(2,3 or4)-F-Ph, -NHSO2-cyclopropyl, -NHSO2CH2CH2OCH3);a substituted or unsubstituted aromatic group(such as Ph-, 2-F-Ph-, 3-F-Ph-, 4-F-Ph-, 2-CI-Ph-, 3-CI-Ph-, 4-CI-Ph-, 2-Br-Ph-, 3-Br-Ph-, 4-Br-Ph-, 2-l-Ph-, 3-l-Ph, 4-l-Ph-, 2,(3,4,5 or 6)-F2-Ph-, 2,(3,4,5 or 6)-CI2-Ph-, 2,(3,4,5 or 6)-Br2-Ph-, 2,(3,4,5 or 6)-l2-Ph-, 2,(3,4,5 or 6)-Me2-Ph-, 2,(3,4,5 or 6)-Et2-Ph-, 2,(3,4,5 or 6)-Pr2-Ph-,2,(3,4,5 or 6)-Bu2-Ph-, 2,(3,4,5 or 6)-(CN)2-Ph-, 2,(3,4,5 or 6)-(NO2)2-Ph-, 2,(3,4,5 or 6)-(NH2)2-Ph-, 2,(3,4,5 or 6)-(MeO)2-Ph-, 2,(3,4,5 or 6)-(CF3)2-Ph-, 3,(4 or 5)-F2-Ph-, 3,(4 or 5)-CI2-Ph-, 3,(4 or 5)-Br2-Ph-, 3,(4 or 5)-12-Ph-, 3,(4 or 5)-Me2-Ph-, 3,(4 or 5)-Et2-Ph-, 3,(4 or 5)-Pr2-Ph-, 3,(4 or 5)-Bu2-Ph-, 3,(4 or 5)-(CN)2-Ph-, 3,(4 or 5)-(NO2)2-Ph-, 3,(4 or 5)-(NH2)2-Ph-,3,(4 or 5)-(MeO)2-Ph-, 3,(4 or 5)-(CF3)2-Ph-, 2-Me-Ph-, 3-Me-Ph-, 4-Me-Ph-,2-Et-Ph-, 3-Et-Ph-, 4-Et-Ph-, 2-Pr-Ph-, 3-Pr-Ph-, 4-Pr-Ph-, 2-Bu-Ph-, 3-Bu-Ph-, 4-Bu-Ph-, 2-(CN)-Ph-, 3-(CN)-Ph-, 4-(CN)-Ph-, 2-(NO2)-Ph-, 3-(NO2)-Ph-, 4-(NO2)-Ph-, 2-(NH2)-Ph-, 3-(NH2)-Ph-, 4-(NH2)-Ph-, 2-MeO-Ph-, 3-MeO-Ph-, 4-MeO-Ph-, 2-(NH2-CO)-Ph-, 3-(NH2-CO)-Ph-, 4-(NH2-CO)-Ph-, 2-CF3-Ph-, 3-CF3-Ph-, 4-CF3-Ph-, 2-CF3O-Ph-, 3-CF3O-Ph-, and 4-CF3O-Ph-);a saturated or unsaturated, substituted or unsubstituted, heterocyclic group, optionally an aromatic heterocyclic group or a non-aromatic heterocyclic group(such as pyrrole-l-yl, pyrrole-2-yl, pyrrole-3-yl, pyrazole-l-yl, pyrazole-3-yl, pyrazole-4-yl, pyrazole-5-yl, imidazole-l-yl, imidazole-2-yl, imidazole-4-yl, imidazole-5-yl, 1,2,3-triazole-l-yl, l,2,3-triazole-4-yl, l,2,3-triazole-5-yl, 1,2,4-triazole-l-yl, l,2,4-triazole-3-yl, l,2,4-triazole-5-yl, pyridin-2-yl, pyridin-3-yl, pyridin-4-yl, pyridazine-3-yl, pyridazine-4-yl, pyrimidin-2-yl, pyrimidin-4-yl, pyrimidin-5-yl, pyrimidin-6-yl, pyrazine-2-yl, pyrrolidine-l-yl, pyrrolidine-2-yl, pyrrolidine-3-yl, piperidine-l-yl, piperidine-2-yl, piperidine-3-yl, piperidine-4-yl, 2-azapiperidine-l-yl, 2-azapiperidine-3-yl, 2-azapiperidine-4-yl, 3-azapiperidine-l-yl, 3-azapiperidine-2-yl, 3-azapiperidine-4-yl, 3-azapiperidine-5-yl, piperazine-l-yl, piperazine-2-yl, furan-2-yl, furan-3-yl, pyran-2-yl, pyran-3-yl, pyran-4-yl, 2-azapyran-2-yl, 2-azapyran-3-yl, 2-azapyran-4-yl, 2-azapyran-5-yl, 2-azapyran-6-yl, 3-azapyran-2-yl, 3-azapyran-4-yl, 3-azapyran-5-yl, 3-azapyran-6-yl, 4-azapyran-2-yl, 4-azapyran-3-yl, 4-azapyran-4-yl, 4-azapyran-5-yl, 4-azapyran-6-yl, oxetan-2-yl, oxetan-3-yl, tetrahydrofuran-2-yl, tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-2-yl, 2-aza-tetrahydrofuran-3-yl, 2-aza-tetrahydrofuran-4-yl, 2-aza-tetrahydrofuran-5-yl, 3-aza-tetrahydrofuran-2-yl, 3-aza-tetrahydrofuran-3-yl, 3-aza-tetrahydrofuran-4-yl, 3-aza-tetrahydrofuran-5-yl, tetrahydropyran-2-yl, tetrahydropyran-3-yl, tetrahydropyran-4-yl, 2-aza-tetrahydropyran-2-yl, 2-aza-tetrahydropyran-3-yl, 2-aza-tetrahydropyran-4-yl, 2-aza-tetrahydropyran-5-yl, 2-aza-tetrahydropyran-6-yl, 3-aza-tetrahydropyran-2-yl, 3-aza-tetrahydropyran-3-yl, 3-aza-tetrahydropyran-4-yl, 3-aza-tetrahydropyran-5-yl, 3-aza-tetrahydropyran-6-yl, morpholine-2-yl, morpholine-3-yl, morpholine-4-yl, thiophen-2-yl, thiophen-3-yl, isothiazole-3-yl, isothiazole-4-yl, isothiazole-5-yl, thiazole-2-yl, thiazole-4-yl, thiazole-5-yl, thiopyran-2-yl, thiopyran-3-yl, thiopyran-4-yl, 2-azathiopyran-2-yl, 2-azathiopyran-3-yl, 2-azathiopyran-4-yl, 2-azathiopyran-5-yl, 2-azathiopyran-6-yl, 3-azathiopyran-2-yl, 3-azathiopyran-4-yl,3-azathiopyran-5-yl, 3-azathiopyran-6-yl, 4-azathiopyran-2-yl, 4-azathiopyran-3-yl, 4-azathiopyran-4-yl, 4-azathiopyran-5-yl, 4-azathiopyran-6-yl, thiolane-2-yl, thiolane-3-yl, thiane-2-yl, thiane-3-yl, thiane-4-yl, oxazol-2-yl, oxazol-4-yl, oxazol-5-yl, isoxazol-3-yl, isoxazol-4-yl, isoxazol-5-yl, furazan-3-yl, (l,3,4-oxadiazol)-2-yl, (l,3,4-oxadiazol)-5-yl, (l,2,4-oxadiazol)-3-yl, (l,2,4-oxadiazol)-5-yl; and tetrazole-l-yl, tetrazole-2-yl, tetrazole-5-yl);wherein:a pair of R5A groups attached to different atoms may together form a ring with ring A atoms; and / ora pair of R5B groups attached to different atoms may together form a ring with ring B atoms, and / ora pair of R5C groups attached to different atoms may together form a ring with ring C atoms; and / oran R5C group and an R6 group attached to different atoms may together form a ring with ring C atoms.

82. The PARP1 inhibitor compound for use according to claim 81, wherein each of R5A(e.g., rsa1, r5A2, r5A3), rsb, and r5c js independently absent or selected from:H,deuterium,a halogen (such as -F, -Cl, -Br, and -I; preferably F or Cl),a nitrile group,a Ci-Ce alkyl group,a Ci-C6 halogenated alkyl group (preferably CF3 or CHFz),a cyclopropyl group,an -OH group,a Ci-Ce alcohol group,a C1-C7 amino carbonyl group (such as -NH-CO-Me),an -NH2 group,a Ci-Ce amino group, andmwherein, when a pair of R5A groups attached to different atoms together forms a ring with ring A atoms and / or a pair of R5B groups attached to different atoms together forms a ring with ring B atoms and / or a pair R5C groups attached to different atoms together forms a ring with ring C atoms, the pair of R5A, R5B or R5C groups represents an alkyl group such as -CH2- or -CH2CH2-; or -CH=CH-CH=CH-; or -NH-CO-NH-.

83. The PARP1 inhibitor compound according to any preceding claim, which is in the form of:an isolated enantiomer, ora mixture of two or more enantiomers, ora mixture of two or more diastereomers, and / or epimers, ora racemic mixture, ora tautomer of the compound.

84. The PARP1 inhibitor compound according to any preceding claim, which is selective for PARP1 over PARP2.

85. The PARP1 inhibitor compound of any preceding claim, for use in medicine.

86. The PARP1 inhibitor compound for use according to claim 85, which is for use intreating a cancer.

87. The PARP1 inhibitor compound for use according to claim 86, wherein the cancer is selected from: a cancer of the eye; brain, such as gliomas, glioblastomas, medulloblastomas, craniopharyngioma, ependymoma, and astrocytoma; spinal cord; kidney; mouth; lip; throat; oral cavity; nasal cavity; small intestine; colon; parathyroid gland; gall bladder; head and neck; breast; bone; bile duct; cervix; heart; hypopharyngeal gland; lung; bronchus; liver; skin; ureter; urethra; testicles; vagina; anus; laryngeal gland; ovary; thyroid; oesophagus; nasopharyngeal gland; pituitary gland; salivary gland; prostate; pancreas; adrenal glands; an endometrial cancer; oral cancer; melanoma; neuroblastoma; gastric cancer; an angiomatosis; a hemangioblastoma; a pheochromocytoma; a pancreatic cyst; a renal cell carcinoma; Wilms' tumour; squamous cell carcinoma; sarcoma; osteosarcoma; Kaposi sarcoma;rhabdomyosarcoma; hepatocellular carcinoma; PTEN Hamartoma-Tumor Syndromes, such as Lhermitte-Duclos disease, Cowden syndrome, Proteus syndrome, and Proteus-like syndrome; leukaemias and lymphomas, such as acute lymphoblastic leukaemia, chronic lymphocytic leukaemia, acute myelogenous leukaemia, chronic myelogenous leukaemia, hairy cell leukaemia, T-cell prolymphocytic leukaemia, large granular lymphocytic leukaemia, adult T-cell leukaemia, juvenile myelomonocytic leukaemia, Hodgkin lymphoma, non-Hodgkin lymphoma, mantle lymphoma, follicular lymphoma, primary effusion lymphoma, AIDS-related lymphoma, diffuse B cell lymphoma, Burkitt lymphoma, cutaneous T-cell lymphoma, nasopharyngeal and gastrointestinal cancers;optionally wherein the cancer is a cancer of the brain or spinal cord.

88. The PARP1 inhibitor compound for use according to claim 86 or claim 87, wherein the cancer is deficient in a DNA damage response repair pathway, such as Homologous Recombination dependent DNA Double Strand Break DNA repair activity.

89. The PARP1 inhibitor compound for use according to any of claims 86 to 88, wherein the cancer is deficient in BRCA1 and / or BRCA2 function.

90. The PARP1 inhibitor compound for use according to any of claims 86 to 89, which is to be administered in conjunction with a further agent for treating cancer; optionally wherein the further agent for treating cancer is selected from anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, immunotherapeutic agents, hormone deprivation therapy, proapoptotic agents, radioligand therapies, cell cycle signalling inhibitors, and anti-angiogenic agents.

91. The PARP1 inhibitor compound for use according to claim 90, wherein the further agent is an immunotherapeutic agent selected from: an anti-tumour vaccine; an oncolytic virus; an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR; a pattern recognitionreceptor agonist such as a STING, TLR-9 or RIG-1 Helicase agonist; an IDO or TDO inhibitor; a novel adjuvant; a peptide; a cytokine; a chimeric antigen receptor T cell therapy; a small molecule immune modulator; and a tumour microenvironment modulator.

92. A pharmaceutical composition comprising a PARP1 inhibitor compound as defined in any of claims 1 to 84.

93. A pharmaceutical composition according to claim 92, further comprising a pharmaceutically acceptable additive and / or excipient, and / or wherein the compound is in the form of a pharmaceutically acceptable salt, hydrate, acid, ester, or other alternative form of the compound.

94. The pharmaceutical composition according to claim 92 or claim 93, further comprising a further agent for treating cancer; optionally wherein the further agent for treating cancer is selected from anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, immunotherapeutic agents, hormone deprivation therapy, proapoptotic agents, radioligand therapies, anti-angiogenic agents, and cell cycle signalling inhibitors.

95. The pharmaceutical composition according to claim 94, wherein the further agent comprises an immunotherapeutic agent selected from: an anti-tumour vaccine; an oncolytic virus; an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR; a pattern recognition receptor agonist such as a STING, TLR-9 or RIG-1 Helicase agonist; an IDO or TDO inhibitor; a novel adjuvant; a peptide; a cytokine; a chimeric antigen receptor T cell therapy; a small molecule immune modulator; and a tumour microenvironment modulator.

96. The pharmaceutical composition according to any of claims 92 to 95, for use in treatinga cancer.

97. A pharmaceutical kit for treating a cancer, which pharmaceutical kit comprises:a) a PARP1 inhibitor compound as defined in any of claims 1 to 84; and b) a further agent for treating cancer;wherein the PARP1 inhibitor compound and the further agent are suitable for administration simultaneously, sequentially or separately; andoptionally wherein the further agent for treating cancer is selected from anti-microtubule agents, platinum coordination complexes, alkylating agents, antibiotic agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, senolytic agents, hormones and hormone analogues, signal transduction pathway inhibitors, other DNA damage repair pathway inhibitors, non-receptor tyrosine kinase angiogenesis inhibitors, antibody-drug conjugates, hormone-deprivation therapy, immunotherapeutic agents (such as selected from an anti-tumour vaccine; an oncolytic virus; an immune stimulatory antibody such as anti-CTLA4, anti-PDl, anti-PDL-1, anti-OX40, anti-41BB, anti-CD27, anti-CD40, anti-LAG3, anti-TIM3, and anti-GITR; a pattern recognition receptor agonist such as a STING, TLR-9 or RIG-1 Helicase agonist; an IDO orTDO inhibitor; a novel adjuvant; a peptide; a cytokine; a chimeric antigen receptor T cell therapy; a small molecule immune modulator; a tumour microenvironment modulator), proapoptotic agents, radioligand therapies, anti-angiogenic agents, and cell cycle signalling inhibitors.

98. A method of treating a disease and / or a condition and / or a disorder, which method comprises administering to a patient a PARP1 inhibitor compound, a composition or a kit as defined in any preceding claim.

99. The method according to claim 98, wherein the patient is an animal, preferably a mammal, optionally a human, canine, equine or feline; and preferably a human.

100. A method of synthesising a PARP1 inhibitor compound as defined in any of claims 1 to 84, which method comprises conducting a reaction between:i) a first reactant comprising rings D and E and bearing a first portion of group Land ii) a second reactant comprising a remainder of group L,to form the PARP1 inhibitor compound.

101. A method according to claim 100, wherein the first reactant comprises rings D, E and ring A, and the second reactant comprises a ring B precursor bearing a reactive group, which method comprises joining ring A to the ring B precursor.

102. A method according to claim 101, wherein the reactive group precursor comprises a carbonyl group, an alkyl halide, or an alkyl sulfonate.

103. A method according to any of claims 100 to 102, wherein the reaction comprises alkylation, reductive amination or amide formation so as to form group L.

104. A method according to claim 100, wherein the first reactant comprises rings D, E, ring A, and ring B, and the second reactant comprises a ring C derivative bearing a leaving group such as a halide or sulfonate.

105. A method according to claim 104, wherein the reaction comprises a nucleophilic substitution reaction, such as a nucleophilic aromatic substitution reaction, so as to form group L.

106. The method according to any of claims 100 to 105, further comprising separating structural isomers of the PARP1 inhibitor compound using chiral supercritical fluid chromatography and / or chiral high-performance liquid chromatography.

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