PARP1 Inhibitor Compounds

Abstract

A PARPI inhibitor compound having a structure of Formula (I): (I) [Refer to original abstract doc for image] Wherein y is 0 or 1; each XD is C, O, N, or S; XET and XEB are selected from C and N ring

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. etal. 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. et al. 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. et al. 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, several PARPl-selective inhibitors have entered clinical development, the most advanced being AZD5305 (Saruparib). 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. Chem. 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 (111 uzzi, G. et al. Clin. Cancer Res. 2022; 28:4724-736). An additional highly selective PARP1 inhibitor, AZD9574, which demonstrated significant CNS penetrance and efficacy in preclinical intracranial animal models, is also under clinical development (Staniszewska, A. et al. Clin. Cancer Res. 2024; 30:1338-1351). 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 compounds and pharmaceutical compositionsfortreating a cancer. It is also an aim to provide methods of synthesis of the compounds. Summary In one aspect, there is provided a PARP1 inhibitor compound having a structure of: where: y is 0 or 1; each XD is independently selected from C, O, N, and S, and XET and XEB are each independently selected from C and N, with the proviso that ring D is a heteroaromatic ring; each R1 is independently absent or selected from Handa substituted or unsubstituted organic group; R2 and R3 are each independently selected from H and a substituted or unsubstituted organic group; R4 is absent or selected from H and a substituted or unsubstituted organic group; and L is a group having a structure of: 5B r5B R \' 7 B R f JX'JP I I / \ 1 (C)j---N B ZX— I7   X R JX )q where: a dashed line represents a bond selected from a single bond and a double bond; X1 and X2 are each independently selected from C and N; each XA, XB, and Xc is independently selected from C, N, O, and S; m is 0,1, or 2, and n is 1 or 2, with the proviso that m + n is 1, 2, or 3; up to one pair of R5A groups together represent a group bridging ring A, and each other R5A group is independently absent, H, or selected from a substituted or unsubstituted organic group; j is 1 or 2; each R7 is independently selected from H and a substituted or unsubstituted organic group; p is 1, 2 or 3; q is 1, 2, or 3; up to one pair of R5B groups together represent a bond or group bridging ring B, and each other R5B group is independently absent, H, or selected from a substituted or unsubstituted organic group; r is 1, 2, 3, or 4, and s is 1, 2, 3, or 4, with the proviso that r + s is 3 or 4; each R5C is independently absent or selected from H and a substituted or unsubstituted organic group; R6 is H or a substituted or unsubstituted organic group; and Q is a bond or a linking group having a structure selected from: R7 R7 R 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 R8 is independently selected from H and a substituted or unsubstituted organic group. The PARP1 inhibitor compound may be for use in medicine, for example for use in treating a cancer. Another aspect provides a pharmaceutical composition comprising a PARP1 inhibitor compound as defined herein. Still another aspect provides a pharmaceutical kit for treating a cancer. The pharmaceutical kit comprises: a) a PARP1 inhibitor compound as defined herein; and b) a further agent for treating cancer. The PARP1 inhibitor compound and the further agent are suitable for administration simultaneously, sequentially or separately. A further provides a method of treating a disease and / or a condition and / or a disorder. The method comprises administering to a patient a PARP1 inhibitor compound, a composition or a kit as defined herein. Also provided is 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. Where it is said that an organic group is "substituted or unsubstituted", the group is most typically unsubstituted. 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. 5 Where a general formula depicts an element in the format (X)j, 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)2 encompasses C-C, C-N, and N-N. Where stereochemistry is depicted, the stereochemistry shown is relative stereochemistry 10 rather than absolute stereochemistry. Discussion Provided herein are PARP1 inhibitor compounds having a structure of: where: y is 0 or 1; each XD is independently selected from C, O, N, and S, and XET and XEB are each independently selected from C and N, with the proviso that ring D is a heteroaromatic ring; each R1 is independently absent or selected from Handa substituted or unsubstituted organic group; R2 and R3 are each independently selected from H and a substituted or unsubstituted organic group; R4 is absent or selected from H and a substituted or unsubstituted organic group; and a dashed line represents a bond selected from a single bond and a double bond; X1 and X2 are each independently selected from C and N; each XA, XB, and Xc is independently selected from C, N, O, and S; m is 0,1, or 2, and n is 1 or 2, with the proviso that m + n is 1, 2, or 3; upto one pair of R5A groups together represent a group bridging ring A, and each other R5A group is independently absent, H, or selected from a substituted or unsubstituted organic group; j is 1 or 2; each R7 is independently selected from H and a substituted or unsubstituted organic group; p is 1, 2 or 3; q is 1, 2, or 3; up to one pair of R5B groups together represent a bond or group bridging ring B, and each other R5B group is independently absent, H, or selected from a substituted or unsubstituted organic group; r is 1, 2, 3, or 4, and s is 1, 2, 3, or 4, with the proviso that r + s is 3 or 4; each R5C is independently absent or selected from H and a substituted or unsubstituted organic group; R6 is H or a substituted or unsubstituted organic group; and Q is a bond or a 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 R8 is independently selected from H and a substituted or unsubstituted organic group. Rings D and E are referred to collectively as the "head group". Rings A to C and the linkers therebetween are referred to collectively as the "L group". Various aspects of this general structure are discussed in detail below. Stereochemistry Some of the PARP1 inhibitor compounds provided herein include one or more chiral centres. 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, and / or epimers, or as a racemic mixture. Some PARP1 inhibitor compounds provided herein may be capable of tautomerism. Such compounds may be provided in the form of any possible tautomer. Substituents The expression "R5 group" refers generally 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. The expression "X atom" refers generally to atoms XA, XB, Xc, XD, XET, XEB, X1, and X2. 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 non-zero order. As will be appreciated, the number of ring bonds and the number of substituents are selected such that the XA, XB, Xc, XD, XET, XEB, X1, and X2 atoms 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 in which an X atom is tetravalent N are also contemplated. Tetravalent N is positively charged, and such compounds may have a counterion. Preferably, the PARP1 inhibitor compound includes at most one tetravalent N, and more preferably no tetravalent N. Each R5 group may be absent or present, and may be the same or different. Forthe avoidance of doubt, where the number of R5 groups may vary according to the choice of corresponding X group, the following provisos typically apply: i) When X1 or X2 is N, its corresponding R5 is absent. ii) When X1 or X2 is C and is double bonded to an adjacent ring atom, its corresponding R5B is absent. iii) When X1 or X2 is C and is not double bonded to an adjacent ring atom, its corresponding R5B is present. iv) When an XA, XB, or Xc is O, its corresponding R5 / R6 groups are both absent. v) When an XA, XB, or Xc is S, its corresponding R5 / R6 groups are both absent or are both selected from =0 and =NR10, where R10is H or a substituted or unsubstituted organic group, preferably a Cl to C3 alkyl group. vi) When an XA, XB, Xc, or XD is N and is double bonded to an adjacent ring atom, the or each corresponding R1 / R4 / R5 / R6 is absent. vii) When an XA, XB, Xc, or XD is N and not double bonded to an adjacent ring atom, exactly one corresponding R1 / R4 / R5 / R6 is present. viii) When an XA, XB, or Xc is C and is double bonded to an adjacent ring atom, exactly one corresponding / R5 / R6 is present. ix) When an XA, XB, or Xc 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. x) When an XD is C, the corresponding R1 or R4 is present; and when an XD is O or S, the corresponding R1 or R4 is absent. The substituents (i.e. R groups; R1, R2, 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 R5 or R6 group on an atom, or two R5 / R6 groups on the same atom, may form a group which is double bonded to that atom. Accordingly, an R5 or R6 group, or two R5 / R6 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 straight 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 or a C=C(R')2 group. Thus in some cases an X2 group 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 ora 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, tetrahydropyran, 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 3 / 7-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. Typically, when one or more of R1, R2, R3, R4, R5A, R5B, R5C, R6, R7, 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 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 -CH2CCI3); NH2; 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 or 4)F-Ph, -NH-(2,3 or 4)CI-Ph, -NH-(2,3 or 4)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 or 4)Pr-Ph, -NH-(2,3 or 4)Bu-Ph, NH-(2,3 or 4)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, -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)-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-); 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). The above-listed organic groups are most preferably unsubstituted. 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. An R5C group and an R6 group attached to different atoms may together form a ring with ring C atoms. Each R5A, R5B, and R5Cmay in particular be absent or selected from: H; deuterium; a halogen (such as -F, -Cl, -Br, and -I; preferably F or Cl); a nitrile group; a substituted or unsubstituted Ci-Ce alkyl group; a substituted or unsubstituted linear or branched Ci-Ce halogenated alkyl group (preferably CF3 or CHF2); a cyclopropyl group; an -OH group; a substituted or unsubstituted linear or branched Ci-Ce alcohol group; a substituted or unsubstituted linear or branched C1-C7 amino carbonyl group (such as -NH-CO-Me); an -NH2 group; a substituted or unsubstituted Ci-Ce amino group; and a substituted or unsubstituted Ci-Ce alkoxy group. 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, each of the pair of R5A, R5B or R5C groups independently comprises -CH2- or -CH2CH2-, or the pair of groups together comprise -CH=CH-CH=CH- or -NH-CO-NH-. Head groups: general Rings D and E of the PARP1 inhibitor compound are referred to collectively as the 'head group': Each R1 is independently absent or selected from H and a substituted or unsubstituted organic group. R2 and R3 are each independently selected from H and a substituted or unsubstituted organic group. R4 is absent or selected from H and a substituted or unsubstituted organic group. Ring D may be 5-membered (y=0) or 6-membered (y=l). Each XD is independently selected from C, O, N, and S, and XET and XEB are each independently selected from C and N. Optionally, each XD atom is independently selected from C and N. Ring D is a heteroaromatic ring, with at least one XD, XET, and / or XEB being a heteroatom. Each R1 and R4 is independently absent or selected from H and a substituted or unsubstituted organic group. When an XD atom is C, the corresponding R1 or R4 group is H or a substituted or unsubstituted organic group. When an XD atom is O, or S, the corresponding R1 or R4 group is absent. When an XD atom is N, the corresponding RI or R4 group is absent if ring D is 6-membered, or may be absent or present if ring D is 5-membered. A "corresponding" R1 or R4 group is the R1 or R4 group that is directly attached to the XD atom in question in the general formula. By way of illustration, in the formula below atom XD1's corresponding R1 group is Rla; XD2's corresponding R1 group is Rlb, and XD3's corresponding R group is R4: When present, R4 and each R1 may each be independently selected from: H; a halogen; a nitrile group; a Cl to C6 acyclic alkyl group; a C3 to C6 cycloalkyl 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 23 r23,r R22^^^ R22 is 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 is 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, R4 and each R1 are 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. Further optionally, each R1 and each R4 is independently absent or selected from: H; Cl; F; a halomethyl group, such as CF3; and a nitrile group. Each R1 independently may be absent or H. R4 may be absent or H. However, R4 is more typically a substituted or unsubstituted organic group. For example, R4 may be selected from Cl; F; and a halomethyl group, such as CF3. R2 is H or a substituted or unsubstituted organic group. In particular, R2 may be selected from H; halogen, optionally F or Cl; Cl to C3 alkyl, optionally isopropyl or cyclopropyl; Cl to C3 haloalkyl, optionally -CH2F, -CHF2, -CF3, -CH2CF3, or -CH2CH2F; Cl to C3 alcohol, optionally -CH2CH2OH; Cl to C3 alkoxy, optionally methoxy, methoxymethyl, or methoxyethyl; or Cl to C3 aminoalkyl. For example, R2 may be H. R3 is H or a substituted or unsubstituted organic group. For example, R3 may be selected from H, Cl to C3 alkyl, and Cl to C3 haloalkyl. Optionally, R3 is H. Head groups: N-bridqed examples Typically, at least one of atoms XET and XEB is C. Optionally, exactly one of XET and XEB is C, and 5 the other of XETand XEB is N. The head group of the PARP1 inhibitor compound may have a structure of: i.e. ring D may be 5-membered (y=0), XET may be C, and XEB may be N. 10 For example, the head group of the PARP1 inhibitor compound may have a structure selected from: Structures G1 and G2 are the preferred members of this class. More specific examples of head group structures include: H5 H6 H17 Of these, Hl, H2, H3, H4, H5, and H6 are preferred. In accordance with another possibility, ring D may be 5-membered (y=0), XET may be N, and 5 XEB may be C: For example, the head group of the PARP1 inhibitor compound may have a structure selected from: 5 Specific examples of head group structures in which XET is N include: Head groups: C-bridqed examples Alternatively, XET may be C and XEB may be C: 5 In such implementations, each XD is independently selected from C, O, N, and S with the proviso that at least one XD is a heteroatom selected from N, 0, or S. For example, exactly one XD atom may be a heteroatom, or exactly two XD atoms may be heteroatoms. The PARP1 inhibitor compound may for example have a head group selected from: 0 More specific examples of such head groups include: Group L of the PARP1 inhibitor compounds provided herein has a structure according to general formula: 5B r5B R\' 7 B R f JX'JP I I Z \ 1 (C);---N B ZX— l7   \ R JX )q Each XA, XB, and Xc is independently selected from C, N, O and S. Optionally, each XA is independently selected from C and O; each XB is C; and each Xc is independently selected from C and N. X1 and X2 are each independently selected from C and N. For example, X1 may be N and X2 may be C. m is 0,1, or 2, and n is 1 or 2, with the proviso that m + n is 1, 2, or 3. Optionally, m is 1 and n is 1. j is 1 or 2, and optionally j is 1. p is 1, 2 or 3, and q is 1, 2, or 3. Optionally, p is 2 and q is 2. Q is a bond or a linking group as defined further below. Optionally, Q is a bond. Ring A and / or ring B may be bridged, with a pair of R5A groups or a pair of R5B groups together representing a group bridging the respective ring. Ring B may be a fused ring system, in which a pair of R5B groups together represent a bond. Each R5A, R5B, or R5C may be independently absent, H, or a substituted or unsubstituted organic group. Optionally, ring A is a 3- or 4- membered ring; j is 1; ring B is a 6-membered saturated ring; Q is a bond; and ring C is a 5- or 6-membered aromatic ring. 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 is a 3-membered ring, ring A is typically a carbocycle. When ring A or ring B is 4-membered, that ring typically includes at most one heteroatom. When ring A, ring B, or ring C is 5- or 6-membered, that ring typically includes at most three heteroatoms, optionally at most two heteroatoms. ii) The compound is not a quaternary ammonium compound. iii) The compound is free of O-O, S-S, and S-0 bonds. Each portion of group L is discussed in more detail below. Rina A Ring A of group L has a structure of: 5A2 d5A2 R \ / A dashed line indicates a covalent bond selected from a single bond and a double bond. m is 0, 1, or 2; and n is 1 or 2. In other words, ring A may be a 3-, 4-, or 5-membered ring. Optionally, ring A is a 3-membered ring (m=0, n=l) or a 4-membered ring (m+n=2, e.g. m=l, n=l). Each XA is independently selected from C, N, O, and S. Optionally, each XA is independently selected from C and O. For example, exactly one XA may be O. Alternatively, each XA may be C. The XA atoms are typically selected such that ring A is free of 0-0 bonds. Each R5A group (i.e., R5A1, R5A2, R5A3) may independently be 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. As will be appreciated, the number of R5A groups attached to any given XA group (referred to herein as "corresponding R5A groups") is selected depending upon the identity of the XA atom and the nature of the ring bonds. When an XA atom is 0, that atom is unsubstituted, in other words the corresponding R5A groups are both absent. When an XA atom is C, there may be either one or two corresponding R5A substituents, depending upon whether or not that XA atom has a double bond to another ring atom. 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. Optionally each R5A is, when present, independently selected from H; a halogen, optionally F; a hydroxyl group; an oxo group (in other words, a carbonyl group: =0); and a Cl to C3 alkyl group. Alternatively or additionally, a pair of R5A groups (e.g., R5A1 and R5A3) may together represent a Cl to C3 alkylene group (e.g., a methylene group, -CH2-) bridging ring A. For example: 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 4-membered (n + m = 2). For example, ring A may have a structure of: (to ring E) r5A2 R5A2 R 5A2 where: each XA is independently selected from C and O; when an XA is O: both corresponding R5A2 groups are absent; when an XA is C: each corresponding R5A2 group is independently selected from H and a substituted or unsubstituted organic group, and optionally each corresponding R5A2 group is H; R5A1 and R5A3 are each independently selected from H and a substituted or unsubstituted organic group; or wherein R5A1 and R5A3 together represent a group bridging ring A. In some example A rings according to the above formula, R5A1 is H and R5A3 is H. Ring A may for example be selected from: A2cis A2trans Alternatively, ring A may be a bridged 4-membered ring, for example having a structure of: In the above formula, each R5A2 is independently absent, H, or a substituted or unsubstituted 5 organic group. In other words, ring A does not include two bridging groups. Examples of bridged 4-membered A ring structures include: In accordance with another possibility, ring A may be a 3-membered ring (n + m = 1). In such 10 examples, the XA atom is typically C, with each R5A being present and independently selected from Hora substituted or unsubstituted organic group: Examples of 3-membered ring A structures include: A5trans Ring A may alternatively be a 5-membered ring (n + m = 3). For example, ring A may have a 5 structure of: (to ring E) where each XA is independently selected from C and O, with the proviso that ring A is free of 0-0 bonds. 10 Ring A may be a bridged 5-membered ring. For example, ring A may have a structure of: Examples of 5-membered ring A structures include: A7cis A7trans A8 A8cis A9trans A12 A13 Ring B Ring B of group L has a general structure of: 5B2 R5B2 R \ I \ B (Xjp N 'X \ B'' (X )q / 5B3 R 5B2 R 5B2 R Each XB is independently selected from C, N, O and S; and X1 is selected from C and N. p is 1, 2 or 3; and q is 1, 2 or 3. Typically, p + q is in the range 2 to 5: in other words, ring B is typically a 4-, 5-, 6- or 7-membered ring. Optionally, ring B may be a 6-membered ring. For example, p and q may both be equal to 2. Alternatively, p + q may be 6. Each R5B group (R5B2, R5B3) may be independently absent or selected from H and a substituted or unsubstituted organic group. When present, each R5B is typically H. In certain examples, particularly those in which p + q is 6, two R5B groups may together represent a bond bridging ring B. In other words, ring B may be a fused ring system comprising two rings. Depending upon the number of R5B groups present, ring B may be saturated or unsaturated. Preferably, ring B is a saturated ring. Each XB may be C, with ring B having a structure of: X1 may be N, and R5B3 may be absent. For example, ring B may have a structure of: Ring B may be a 7-membered ring, for example: each R5B being independently selected from H and a substituted or unsubstituted organic 10 group. Optionally, each R5B may be H. Alternatively, ring B may be a 6-membered ring, such as: each R5B being independently selected from H and a substituted or unsubstituted organic group. Each R5B may be H. In accordance with another possibility, ring B may be a 5-membered ring, optionally having a structure of: each R5B being independently selected from H and a substituted or unsubstituted organic 10 group. Each R5B may be H. In still further examples, ring B is a 4-membered ring, optionally having a structure of: each R5B being independently selected from H and a substituted or unsubstituted organic 15 group. Each R5B may be H. Alternatively, X1 may be C. When X1 is C, ring B may be a 7-membered ring, optionally having a structure of: each R5B being independently selected from H and a substituted or unsubstituted 5 organic group. Optionally, each R5B is H. Alternatively, ring B may be a 6-membered ring such as: each R5B being independently selected from H and a substituted or unsubstituted organic 10 group. Each R5B may be H. In accordance with another possibility, ring B may be a 5-membered ring, optionally having a structure of: 15 each R5B being independently selected from H and a substituted or unsubstituted organic group. Each R5B may be H. In still further examples, ring B may be a 4-membered ring, optionally having a structure of: each R5B being independently selected from H and a substituted or unsubstituted organic 5 group. Each R5B may be H. More specific examples of ring B structures include: Ring B may have a structure of: 10 Alternatively, ring B may have a structure of: 5 In accordance with another possibility, ring B has a structure of: and Q may be -O-. In accordance with still a further possibility, p + q may be 6 and ring B may comprise two fused 10 rings. For example, ring B may have a structure of: For example, ring B may have a structure of: or Specific examples of ring B structures comprising two fused rings are: H Linkers Ring A is coupled to ring B via an optionally-substituted methylene or ethylene group Cj(R7)2j, and ring B is coupled to ring C via a linker Q: SB r5B R\' 7 B R f (X'JP / I X \ 1 (c)j--N B ZX— j is 1 or 2. Typically, j is 1 and group L has a structure of: SB r5B R \ ? \ D 5B \ B R (Xjp / / \ 1 N B ZX---- \ BZ 5B R 5B R 10 Each R7 is independently selected from H and a substituted or unsubstituted organic group. For example, each R7 may be independently selected from H; a halogen, such as -F, -Cl, -6r, 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. Optionally, each R7 is independently selected from: H; a halogen, optionally 15 F; a methyl group; and a halomethyl group. In particular, each R7 may be H. The linker Q between rings B and C is a bond, or a linking group selected from: where t is 0, 1, 2, 3, 4 or 5; and u is 0, 1, 2, 3, 4 and 5, with the proviso that t + u is in the range 0 to 6. R8 is independently selected from H and a substituted or unsubstituted organic group. When Q is: the values of t and u are selected such that the bond between atom X1 of ring B and Q and the bond between Q and atom X2 of ring C are not N-N bonds. In other words, t is at least 1 when X1 is N; and u is at least 1 when X2 is N. R8 may be H or an organic group selected from: 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-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, -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)-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). When R8 is an organic group, that organic group is preferably unsubstituted. R8 may in particular be selected from H, a Ci-Ce alkyl group, or a Ci-Ce halogenated alkyl group. Q may be selected from a bond, -O-, or -CH2-. Q is most typically a bond, and in such examples group L has a structure according to general formula: 5C Typically, when Q is a bond, at least one of X1 and X2 is C. For example, when Q is a bond, X1 may be N and X2 may be C, with group L having a structure of: In instances of the above formula where p> 2 and / or q >2, bonds between adjacent XB atoms may be single bonds or double bonds. Ring C Ring C of group L has a structure of: Q X2 is selected from C and N. Each Xc is independently selected from C, N, O, and S. Optionally, each Xc is independently selected from C and N. r is 1, 2, 3 or 4, and s is 1, 2, 3, or 4, with the proviso that r + s is 3 or 4. In other words, ring C is a 5- or 6-membered ring. Typically, r is at least 1 and s is at least 1. In other words, the Xc atom which bears substituent R6 is typically not adjacent to atom X2. Ring C may be a 6-membered ring (r + s = 4). When ring C is 6-membered, linker Q and substituent R6 may be in a para relationship (r = 2, s = 2). Each R5C is independently absent or selected from H and a substituted or unsubstituted organic group. The number of R5C groups may be selected such that ring C is saturated; unsaturated and non-aromatic; or aromatic. Optionally, ring C is an aromatic ring. When present, each R5C may be independently selected from H or an organic group selected from a halogen, preferably F; a Cl to C3 alkyl group, optionally a cyclopropyl group; a Cl to C3 haloalkyl group, optionally a fluoromethyl group such as CF2H or CF3; a Cl to C3 alkoxy group; and a nitrile group. Optionally, the organic group may be selected from F, Cl, a nitrile group, a methyl group, and a fluoromethyl group, optionally CF2H. Exactly one R5C may be an organic group, such as F, with each other R5C being absent or H. Alternatively, each R5C may be absent or H. Ring C may be a heterocycle, optionally an aromatic heterocycle. Optionally, exactly one Xc atom is N, or exactly two Xc atoms are N. In such examples, each other Xc atom may be C. Ring C may for example have a structure of: Co where: 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 present; when XCo is N, RCo is absent; when XCm is C, RCm is present; and when XCm is N, RCm is absent. 10 RCo and RCm may, when present, each be independently selected from H; a halogen, optionally F; -CN; a methyl group; and a halomethyl group, optionally a fluoromethyl group such as -CF3. Optionally, XCo is C and XCm is N. 15 Ring C may be a pyridine group having a structure selected from: For example, C is a pyridine group having a structure of: Preferred ring C structures include: Alternatively, ring C may be a diazine group such as: In accordance with still further possibilities, ring C may be a 5-membered ring (r + s = 3), and 10 optionally a 5-membered heteroaromatic ring. For example, ring C may be an imidazole group, such as: Alternatively, ring C may be a thiophene group, such as: Ring C may alternatively be a thiazole group, such as: 10 In accordance with still another possibility, ring C may be a triazole such as: Examples of suitable C structures include: Cl C2 C3 F C4 C29 Of these, C4 is preferred. Ring C may have a structure selected from: =N O F 'NH-- T1 N=\ r jC / Cl J T4 / =N O J ' HN—y F J\_ / F H T7 2=N O 1C D / “ J \— / hn—(-d _c / D J V_ T10 F \ \=N 0 (- / = / hn— T13 F _ r?"N\ / ° j\ / \ / \ n- HN—( O T16 / NH Cl' - N=\ N ? / NH T3 T2 N=\ N / F \ ,- \=N O T5 yC )—( HN— T6 O N y~- y. T8 T9 j- / =N O N 0 ^^-^HN^ \ / '—F HN^| T12 Til o / 'N Jf H—\ F _y^NH / =\ P T14 HN— T15 N I Z^nh ^VV-A-'N T17 T18 N=\ r / =N P <Z>~f -vG*-^ / N—9 J HN—< T2° T21 T31 Of these, T2 is preferred. Terminal substituent R6 Ring C bears a substituent R6, which is selected from H and a substituted or unsubstituted 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 5 organic group. Optionally, R51 and R52 may each be independently selected from H, a halogen, optionally-deuterated Cl to C3 alkyl, and Cl to C3 haloalkyl. R6 may be selected from -F, -Cl, -CN, -CONH2, -CONMe2, -CONHCOMe, -CONHCH2-CH2OMe, - OCHF2, -NHCOMe, -NHSO2Me, -SO2NHMe, -CONHSO2Me, O , O Alternatively, R6 may have a structure of: 0 II 51 SA nh wherein R51 is selected from: a Cl to C6 alkyl group, optionally a C3 to C6 cycloalkyl group, a Cl to C3 alkyl 5 group, or a Cl to C3 deuterated alkyl group; a Cl to C3 haloalkyl group, optionally a Cl to C3 fluoroalkyl group; and a 4-, 5-, 6-, or 7-membered saturated heterocyclic group, optionally a 4-, 5- or 6-membered cyclic ether group. 10 Examples of R6 groups according to the above formula include: In particular, R6 may be -CONHMe, optionally In accordance with another possibility, R6 may be a heterocyclic group having a structure of: wherein: each X6 is independently selected from C, N, and O; 5 R61 is absent or H; each R62 is independently absent or selected from H; a halo group, such as F; an oxo group (in other words, a carbonyl group; =0); a Cl to C3 alkyl group; a Cl to C3 haloalkyl group, optionally a Cl to C3 fluoroalkyl group; and -NHR63, wherein R63 is H or a Cl to C3 alkyl group. 10 Examples of heterocyclic R6 groups include: Example L groups Group L may have a structure of: where: R5A1 is H and R5A3 is H, or R5A1 and R5A3 together represent a -CH2- group bridging ring A; each XA is independently selected from C and O; when an XA is O, each corresponding R5A is absent; when an XA is C, each corresponding R5A is H; XB is a carbon atom; X1 is selected from C and N; when X1 is C, R5B is absent and the bond between XB and X1 is a double bond; when X1 is N, R5B is H and the bond between XB and X1 is a single bond; each Xc is independently selected from C and N; when an Xc is N, the corresponding R5C is absent; when an Xc is C, each R5C is H or a substituted or unsubstituted organic group, optionally any of the R5C groups defined in the discussion of ring C; and R6 is as discussed hereinabove. Ring C is optionally a pyridine ring, with group L having a structure of: More specifically, ring C may be a pyridine ring that is substituted at the 2-position: X1 may be N and R5B may be H. In such examples, the bond between XB and X1 is a single bond. 10 Optionally, exactly one XA is O. Alternatively, each XA may be C. R5A1 and R5A3 may together represent a -CH2- group bridging ring A, such that group L has a structure of: Group L may for example have a structure of: o 5 Example Compounds Examples of PARP1 inhibitor compounds provided herein include: Medical Uses 10 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, 15 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 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. 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 immunotherapeuticagent 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. 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 or TDO 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 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. 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 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, A, and 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 compound 1 OH 1001 OH BH3-THF THF, 0 °C 1002 OBn NaH,BnBr DMF, 0 °C to rt \ THF / H2O, rt 1003 LiOH BnO MeMgBr BnO THF, 0 °C 1006 N-0 1005 BnO 1007 Jacques reagent THF, rt NaBH(OAc)3, NaBH3CN, MeOH, 50 °C EDCI, HOBt, Et3N, DCM, rt OH 1004 SCHEME 1 Preparation of methyl 3-(hydroxymethyl)bicyclo[l.l.l]pentane-l-carboxylate (1002) To a solution of 3-(methoxycarbonyl)bicyclo[l.l.l]pentane-l-carboxylic acid 1001 (10 g, 58.8 mmol) in THF (100 mL) was added BH3-THF (118 mL, 118.0 mmol, 1.0 M in THF) at 0 °C under an N2 atmosphere. The reaction mixture was stirred at 0 °C for 2 h. The reaction was quenched with MeOH and concentrated under reduced pressure to give methyl 3-(hydroxymethyl)bicyclo[l.l.l]pentane-l-carboxylate 1002 (8 g, 90 % purity, 78 % yield) as a colourless oil. LCMS (ESI) calcd for C8Hi2O3 [M + H] + m / z 157.08, found 157.10. Preparation of methyl 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylate (1003) To a solution of methyl 3-(hydroxymethyl)bicyclo[l.l.l]pentane-l-carboxylate 1002 (7.9 g, 50.6 mmol) in DMF (150 mL) was added NaH (6.1 g, 151.8 mmol, 60 % wt) at 0 °C. The reaction mixture was stirred at 0 °C for 30 min. BnBr (17.3 g, 101.2 mmol) was added dropwise at 0 °C. The reaction mixture was warmed to rt and stirred at rt for 1 h. The reaction mixture was poured into water, then extracted with EtOAc (100 mL x 3). The combined organic layers were washed with brine, dried over Na2SO4, and concentrated under reduced pressure. The residue was purified by flash column chromatography (eluting with PE / EtOAc = 100:0 to 75:25) to afford methyl 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylate 1003 (10.8 g, 90 % purity, 78 % yield) as a colourless oil. Preparation of 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylic acid (1004) LiOH (1.4 g, 56.8 mmol) was added to a solution of methyl 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylate 1003 (7 g, 28.4 mmol) in THF / H2O (100 mL, 3:1). The reaction mixture was stirred at rt for 4 h. THF was removed under reduced pressure and the residue was diluted with water. The mixture was adjusted to pH=4 with 2 N aq. HCI and extracted with EtOAc (200 mL x 2). The combined organic layers were concentrated under reduced pressure to give 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylic acid 1004 (6.5 g, 90 % purity, 88 % yield) as a colourless oil. LCMS (ESI) calcd for C14H16O3 [M + H] + m / z 233.11, found no MS signal. Preparation of 3-((benzyloxy)methyl)-N-methoxy-N-methylbicyclo[l.l.l]pentane-l-carboxamide (1006) To a solution of 3-((benzyloxy)methyl)bicyclo[l.l.l]pentane-l-carboxylic acid 1004 (6.5 g, 28.0 mmol) in DCM (100 mL) was added N,O-dimethylhydroxylamine hydrochloride 1005 (3.4 g, 56.0 mmol), HOBT (7.6 g, 56.0 mmol), Et3N (11.3 g, 112.0 mmol) and EDCI (10.7 g, 56.0 mmol) successively. The reaction mixture was stirred at rt for 2 h. The reaction was washed with water and then extracted with DCM (100 mL x 2). The combined organic layers were concentrated under reduced pressure. The residue was purified by flash column chromatography (eluting with PE / DCM = 100:0 to 20:80) to afford 3-((benzyloxy)methyl)-N-methoxy-N-methylbicyclo[l.l.l]pentane-l-carboxamide 1006 (6.8 g, 90 % purity, 79 % yield) as a colourless oil. LCMS (ESI) calcd for Ci6H2iNO3 [M + H] + m / z 276.15, found 276.05. Preparation of l-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)ethan-l-one (1007) To a solution of 3-((benzyloxy)methyl)-N-methoxy-N-methylbicyclo[l.l.l]pentane-l-carboxamide 1006 (6.7 g, 24.3 mmol) in THF (150 mL) was added MeMgBr (16.2 mL, 48.6 mmol, 3.0 M in THF) at 0 °C under N2 atmosphere. The reaction mixture was stirred at 0 °C for 1 h. The reaction mixture was quenched with water, then extracted with EtOAc (150 mL x 3). The combined organic layers were concentrated under reduced pressure. The residue was purified by flash column chromatography (eluting with PE / DCM = 100:0 to 30:70) to afford 1-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)ethan-l-one 1007 (4.5 g, 90 % purity, 72 % yield) as a colourless oil. Preparation of l-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-bromoethan-l-one (1008) To a solution of l-(3-((benzyloxy)methyl) bicyclo[l.l.l]pentan-l-yl)ethan-l-one 1007 (4.3 g, 18.7 mmol) in THF (80 mL) was added phenyltrimethylammonium tribromide ("Jacques reagent", 6.3 g, 16.8 mmol) at rt. The reaction mixture was stirred at rt for 1 h. The mixture was filtered through a Celite pad, and the filtrate was concentrated. The residue was purified by flash column chromatography (eluting with PE / DCM = 100:0 to 50:50) to afford 1-(3- ((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-bromoethan-l-one 1008 (3.2 g, 90 % purity, 49 % yield) as a yellow oil. Preparation of ethyl l-(2-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-oxoethyl)-3-fluoro-1 H-pyrrole-2-carboxylate (1010) To a solution of l-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-bromoethan-l-one 1008 (550 mg, 1.8 mmol) in DMF (10 mL) was added ethyl 3-fluoro-lH-pyrrole-2-carboxylate 1009 (255 mg, 1.8 mmol) and CS2CO3 (1.2 g, 3.6 mmol) successively. The reaction mixture was stirred at rt for 2 h. The reaction mixture was poured into water, then extracted with EtOAc (20 mL x 3). The combined organic layers were washed with brine, dried over Na2SO4 and concentrated under reduced pressure. The residue was purified by flash column chromatography (eluting with PE / EtOAc = 100:0 to 70:30) to afford ethyl 1-(2-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-oxoethyl)-3-fluoro-lH-pyrrole-2-carboxylate 1010 (580 mg, 90 % purity, 79 % yield) as a yellow oil. LCMS (ESI) calcd for C22H24FNO4 [M + H] + m / z 386.17, found 386.10. Preparation of 3-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-8-fluoropyrrolo[l,2-a]pyrazin-l(2H)-one (1011) A solution of ethyl l-(2-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-2-oxoethyl)-3-fluoro-lH-pyrrole-2-carboxylate 1010 (580 mg, 1.5 mmol) and NH4OAC (1.2 g, 15.0 mmol) in EtOH (25 mL) was stirred at 100 °C for 12 h in a steel bomb. The reaction solution was cooled to rt and concentrated under reduced pressure. The residue was purified by flash column chromatography (eluting with PE / EtOAc = 100:0 to 50:50) to afford 3-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-8-fluoropyrrolo[l,2-a]pyrazin-l(2H)-one 1011 (400 mg, 90 % purity, 70 % yield) as a white solid. LCMS (ESI) calcd for C20H19FN2O2 [M + H] + m / z 339.14, found 339.05. Preparation of 8-fluoro-3-(3-(hydroxymethyl)bicyclo[l.l.l]pentan-l-yl)pyrrolo[l,2-a]pyrazin-l(2H)-one (1012) To a solution of 3-(3-((benzyloxy)methyl)bicyclo[l.l.l]pentan-l-yl)-8-fluoropyrrolo[l,2-a]pyrazin-l(2H)-one 1011 (400 mg, 1.2 mmol) in TFA (8 mL) was added TfOH (1 mL) at rt. The reaction mixture was stirred at rt for 30 min. The reaction solution was blown dry with N2 and the residue was adjusted to pH=7 with saturated aq. NaHCOs and extracted with EtOAc (20 mL x 3). The combined organic layers were concentrated under reduced pressure. The residue was dissolved in MeOH (10 mL) and K2CO3 (817 mg, 5.9 mmol) was added, and the reaction mixture was stirred at rt for further 30 min. The reaction solution was filtered through a Celite pad, and the filtrate was concentrated. The residue was purified by flash column chromatography (eluting with PE / EtOAc = 100:0 to 30:70) to afford 8-fluoro-3-(3-(hydroxymethyl)bicyclo[l.l.l]pentan-l-yl)pyrrolo[l,2-a]pyrazin-l(2H)-one 1012 (300 mg, 80 % purity, 81 % yield) as a white solid. LCMS (ESI) calcd for C13H13FN2O2 [M + H] + m / z 249.10, found 249.05. Preparation           of           3-(8-fluoro-l-oxo-l,2-dihydropyrrolo[l,2-a]pyrazin-3- yl)bicyclo[l.l.l]pentane-l-carbaldehyde (1013) To a solution of 8-fluoro-3-(3-(hydroxymethyl)bicyclo[l.l.l]pentan-l-yl)pyrrolo[l,2-a]pyrazin-l(2H)-one 1012 (240 mg, 1.0 mmol) in DCE (10 mL) was added Mn02 (841 mg, 9.7 mmol). The reaction mixture was stirred at 60 °C for 24 h. The reaction solution was cooled to rt and filtered through a Celite pad, and the filtrate was concentrated. The residue was purified by flash column chromatography (eluting with PE / EtOAc = 100:0 to 0:100) to afford 3-(8-fluoro-l-oxo-l,2-dihydropyrrolo[l,2-a]pyrazin-3-yl)bicyclo[l.l.l]pentane-l-carbaldehyde 1013 (70 mg, 80 % purity, 23 % yield) as a colourless oil. LCMS (ESI) calcd for C13H11FN2O2 [M + H2O + H] + m / z 265.08, found 264.95. Preparation of 6-fluoro-5-(4-((3-(8-fluoro-l-oxo-l,2-dihydropyrrolo[l,2-a]pyrazin-3-yl)bicyclo[l.l.l]pentan-l-yl)methyl)piperazin-l-yl)-N-methylpicolinamide (Compound 1) To a solution of 3-(8-fluoro-l-oxo-l,2-dihydropyrrolo[l,2-a]pyrazin-3-yl)bicyclo[l.l.l]pentane-l-carbaldehyde 1013 (35 mg, 0.1 mmol) in MeOH (3 mL) was added 6-fluoro-N-methyl-5-(piperazin-l-yl)picolinamide 1014 (51 mg, 0.2 mmol), NaBH(0Ac)3 (60 mg, 0.3 mmol) and NaBHsCN (9 mg, 0.1 mmol) successively under stirring. The reaction mixture was stirred at 50 °C for 2 h. The reaction solution was cooled to rt and quenched with water (1 mL). The mixture was concentrated under reduced pressure and the residue was purified by prep-HPLC (column: Gemini - C18 150 x 21.2 mm, 5 urn; mobile phase: ACN - H2O (0.05 % NH3); gradient: 35 - 75) to obtain 6-fluoro-5-(4-((3-(8-fluoro-l-oxo-l,2-dihydropyrrolo[l,2-a]pyrazin-3-yl)bicyclo[l.l.l]pentan-l-yl)methyl)piperazin-l-yl)-N-methylpicolinamide Compound 1 (20.2 mg, 98 % purity, 29 % yield) as a white solid. TH NMR (400 MHz, DMSO-d6, ppm) 6: 10.42 (s, 1 H), 8.48-8.28 (m, 1 H), 7.85 (dd, J = 8.0, 1.2 Hz, 1 H), 7.64-7.50 (m, 1 H), 7.27-7.14 (m, 1 H), 6.94 (s, 1 H), 6.38 (d, J= 3.2 Hz, 1 H), 3.23-3.07 (m, 4 H), 2.76 (d, J = 4.8 Hz, 3 H), 2.62-2.54 (m, 4 H), 2.48 (m, 2 H), 1.97 (s, 6 H). LCMS (ESI) calcd for C24H26F2N6O2 [M + H] + m / z 469.21, found 469.30. Example 2: 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 2A. 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 Na2CO3 / HCO3 coating buffer at pH 9.6, overnight at 4 °C, in order to achieve a final immobilisation per well of 0.3 mg. 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 ml 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 ml of 10 mM 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 ml 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 ml 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 ml 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 ms). 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: Duplex Sequences 5'-ACCCTGCTGTGGGC / ideoxyU / GGAGAACAAGGTGAT-3' (SEQID NO:1) 5'-ATCACCTTGTTCTCCAHGCCCACAGCAGGGT-3' (SEQID NO:2) 5' -ACCCTGCTGTGGGCGGAGAACAAGGTGAT-3' (SEQID NO:3) I II I I I I I I I I I I I I I I I I 3'-TGGGACGACACCCGHACCTCTTGTTCCACTA-5' Example 2B. 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: IC50 = (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 2C. 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 (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. 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 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 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 2. TABLE 1 Results of Parp 1 / 2 assays for selected compounds (DELFIA and Probe Displacement HTRF) Compound PARP1 DELFIA PARP1 HTRF PARP2 HTRF Selectivity 1 ++++ ++++ + +++ 2 ++++ ++++ - +++ TABLE 2 Results of Parp 1 / 2 assays for selected compounds (NanoBRET) Compound PARP1 NanoBRET PARP2 NanoBRET Selectivity 1 ++++ - +++ 2 ++++ - +++ Key DELFIA, Probe Displacement HTRF and NanoBRET assay categories: - indicates IC50 or Kd value above 10 pM + indicates IC50 or Kd value above 1 pM up to 10 pM ++ indicates IC50 or Kd value above 100 nM up to 1 pM +++ indicates IC50 or Kd value above 10 nM up to 100 nM ++++ indicates IC50 or Kd value of 10 nM or less NT: not tested 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 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). 5 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 10 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:y is 0 or 1;each XD is independently selected from C, O, N, and S, and XET and XEB are each independently selected from C and N, with the proviso that ring D is a heteroaromaticring;each R1 is independently absent or selected from Handa substituted or unsubstitutedorganic group;R2 and R3 are each independently selected from H and a substituted or unsubstituted organic group;R4 is absent or selected from H and a substituted or unsubstituted organic group; andL is a group having a structure of:7 RR(XjpN B >\ BZ (X )q5B RI1R5C5Bwherein:a dashed line represents a bond selected from a single bond and a double bond;X1 and X2 are each independently selected from C and N;each XA, XB, and Xc is independently selected from C, N, O, and S;m is 0,1, or 2, and n is 1 or 2, with the proviso that m + n is 1, 2, or 3;up to one pair of R5A groups together represent a group bridging ring A, and each other R5A group is independently absent, H, or selected from a substituted or unsubstituted organic group;j is 1 or 2;each R7 is independently selected from H and a substituted or unsubstituted organic group;p is 1, 2 or 3;q is 1, 2, or 3;up to one pair of R5B groups together represent a bond or group bridging ring B, and each other R5B group is independently absent, H, or selected from a substituted or unsubstituted organic group;r is 1, 2, 3, or 4, and s is 1, 2, 3, or 4, with the proviso that r + s is 3 or 4;each R5C is independently absent or selected from H and a substituted or unsubstituted organic group;R6 is H or a substituted or unsubstituted organic group; andQ is a bond or a 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;andR8 is independently selected from H and a substituted or unsubstituted organic group.

2. The PARP1 inhibitor compound according to claim 1, wherein R4 and each R1 is independently absent or selected from:H;a halogen;a nitrile group;a Cl to C6 acyclic alkyl group;a C3 to C6 cyclic 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; andR22 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 R4 and each R1 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 is independently absent or H.

6. The PARP1 inhibitor compound according to any preceding claim, wherein R4 is a substituted or unsubstituted organic group;optionally wherein R4 is selected from Cl; F; and a halomethyl group, such as CF3.

7. The PARP1 inhibitor compound according to any preceding claim, wherein R2 isselected from H; halogen, optionally F or Cl; Cl to C3 alkyl, optionally isopropyl or cyclopropyl; Cl to C3 haloalkyl, optionally -CH2F, -CHF2, -CF3, -CH2CF3, or -CH2CH2F; Cl to C3 alcohol, optionally -CH2CH2OH; Cl to C3 alkoxy, optionally methoxy, methoxymethyl, or methoxyethyl; or Cl to C3 aminoalkyl.

8. The PARP1 inhibitor compound according to claim 7, wherein R2 is H.

9. The PARP1 inhibitor compound according to any preceding claim, wherein R3 isselected from H, Cl to C3 alkyl, and Cl to C3 haloalkyl.

10. The PARP1 inhibitor compound according to claim 9, wherein R3 is H.

11. The PARP1 inhibitor compound according to any preceding claim, wherein each XD isindependently selected from C and N.

12. The PARP1 inhibitor compound according to any preceding claim, wherein at least one ofXETand XEB is C.

13. The PARP1 inhibitor compound according to claim 12, having a structure of:

14. The PARP1 inhibitor compound according to claim 13, having a structure selectedfrom:G415. The PARP1 inhibitor compound according to claim 14, having a structure of G1 or G2.

16. The PARP1 inhibitor compound according to claim 14 or claim 15, having a structureselected from:HlH2H3H4H6H1717. The PARP1 inhibitor compound according to claim 16, having a structure selected fromHl, H2, H3, H4, H5, and H6.

18. The PARP1 inhibitor compound according to claim 12, having a structure of:19.The PARP1 inhibitor compound according to claim18, having astructure selectedfrom:20.The PARP1 inhibitor compound according to claim 19, having a structure selectedfrom:

21. The PARP1 inhibitor compound according to claim 12, wherein XET and XEB are each C,and wherein at least one XD is N, O, or S.

22. The PARP1 inhibitor compound according to claim 21, having a structure selectedfrom:

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

24. The PARP1 inhibitor compound according to any preceding claim, wherein each XA isindependently selected from C and O, with the proviso that ring A is free of 0-0 bonds.

25. The PARP1 inhibitor compound according to any preceding claim, wherein each R5A isindependently absent or H.

26. The PARP1 inhibitor compound according to any preceding claim, wherein n + m = 2.

27. The PARP1 inhibitor compound according to claim 26, wherein ring A has a structureof:(to ring E)wherein:each XA is independently selected from C and O;when an XA is O:both corresponding R5A2 groups are absent;when an XA is C:each corresponding R5A2 group is independently selected from H and a substituted or unsubstituted organic group, andoptionally each corresponding R5A2 group is H;R5A1 and R5A3 are each independently selected from H and a substituted or unsubstituted organic group; or wherein R5A1 and R5A3 together represent a group bridging ring A.

28. The PARP1 inhibitor compound according to claim 27, wherein R5A1 is H and R5A3 is H.

29. The PARP1 inhibitor compound according to claim 28, wherein ring A has a structureselected from:AltransA230. The PARP1 inhibitor compound according to claim 27, wherein ring A has a structureof:

31. The PARP1 inhibitor compound according to claim 30, wherein ring A has a structureselected from:(to ring E)A3optionally wherein ring A has structure A3.

32. The PARP1 inhibitor compound according to any of claims 1 to 25, wherein n + m = 1.

33. The PARP1 inhibitor compound according to claim 32, wherein ring A has a structureof:

34. The PARP1 inhibitor compound according to claim 33, wherein ring A has a structure selected from:(to ring E).(to ring E)(to ring E)A5cisA5trans35. The PARP1 inhibitor compound according to any of claims 1 to 25, wherein n + m = 3.

36. The PARP1 inhibitor compound according to claim 35, wherein ring A has a structureof:(to ring E)wherein:each XA is independently selected from C and O, with the proviso that ring A is free of 0-0 bonds; andwhen an XA is 0, both corresponding R5A groups are absent.

37. The PARP1 inhibitor compound according to claim 36, wherein ring A has a structure of:r5A r5A(to ring E)38. The PARP1 inhibitor compound according to claim 36 or claim 37, wherein ring A hasa structure selected from:(to ring E)A6A7transA8cisAll39. The PARP1 inhibitor compound according to any preceding claim wherein each R5B is, when present, H.

40. The PARP1 inhibitor compound according to any preceding claim, wherein each XB is C.

41. The PARP1 inhibitor compound according to any preceding claim, wherein X1 is N.

42. The PARP1 inhibitor compound according to any of claims 1 to 40, wherein X1 is C.

43. The PARP1 inhibitor compound according to any preceding claim, wherein p + q is inthe range 2 to 5.

44. The PARP1 inhibitor according to claim 43, wherein:i) ring B is 7-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstitutedorganic group, optionally wherein each R5B is H; orii) ring B is a 6-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstituted organic group, optionally wherein each R5B is H; oriii) ring B is a 5-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstituted organic group, optionally wherein each R5B is H; oriv) ring B is a 4-membered ring, optionally having a structure of:5B Reach R5B being independently selected from H and a substituted or unsubstituted organic group, optionally wherein each R5B is H.

45. The PARP1 inhibitor compound according to claim 43, wherein:i) ring B is a 7-membered ring, optionally having a structure of:each R5B being independently selected from Hand a substituted or unsubstitutedorganic group, optionally wherein each R5B is H; orii) ring B is a 6-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstituted organic group, optionally wherein each R5B is H; oriii) ring B is a 5-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstitutedorganic group, optionally wherein each R5B is H; oriv) ring B is a 4-membered ring, optionally having a structure of:each R5B being independently selected from H and a substituted or unsubstitutedorganic group, optionally wherein each R5B is H.

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

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

48. The PARP1 inhibitor compound according to claim 47, wherein ring B has a structureof:

49. The PARP1 inhibitor compound according to claim 47, wherein ring B has a structureof:and wherein Q is -O-.

50. The PARP1 inhibitor compound according to any of claims 1 to 42, wherein p + q is 6,and wherein ring B comprises two fused rings.

51. The PARP1 inhibitor compound according to claim 50, wherein ring B has a structure of:

52. The PARP1 inhibitor compound according to claim 51, wherein ring B has a structureof:

53. The PARP1 inhibitor compound according to claim 52, wherein ring B has a structure of:

54. The PARP1 inhibitor compound according to claim 53, wherein ring B has a structureof:

55. The PARP1 inhibitor compound according to any preceding claim, wherein j is 1.

56. The PARP1 inhibitor compound according to any preceding claim, wherein each R7 is independently 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.

57. The PARP1 inhibitor compound according to claim 56, wherein each R7 is independently selected from: H; a halogen, optionally F; a methyl group; and a halomethyl group.

58. The PARP1 inhibitor compound according to claim 57, wherein each R7 is H.

59. The PARP1 inhibitor compound according to any preceding claim, wherein Q is: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-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)-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).

60. The PARP1 inhibitor compound according to claim 59, wherein R8 is selected from H, a Ci-Ce alkyl group, and a Ci-Ce halogenated alkyl group.

61. The PARP1 inhibitor compound according to any of claims 1 to 58, wherein Qis a bond, -O-, or -CH2-.

62. The PARP1 inhibitor according to claim 61, wherein Q is a bond, and at least one of X1 and X2 is C;optionally wherein X1 is N and X2 is C.

63. The PARP1 inhibitor compound according to any preceding claim, wherein ring C is an aromatic ring.

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

65. The PARP1 inhibitor compound according to any preceding claim, wherein each Xc isindependently selected from C and N.

66. The PARP1 inhibitor compound according to claim 65, wherein r + s = 4;optionally wherein r is 2 and s is 2.

67. The PARP1 inhibitor compound according to claim 66, wherein exactly one Xc atom is N, or wherein exactly two Xc atoms are N.

68. The PARP1 inhibitor compound according to claim 67, wherein ring C has a structureof: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 present;when XCo is N, RCo is absent;when XCm is C, RCm is present;when XCm is N, RCm is absent;when present, RCo and RCm are each independently selected from H; a halogen, optionally F; -CN; a methyl group; and a halomethyl group, optionally a fluoromethyl group such as -CF3.

69. The PARP1 inhibitor compound according to claim 68, wherein XCo is C and XCm is N.

70. The PARP1 inhibitor compound according to claim 67, wherein ring C is a pyridinegroup, optionally having a structure selected from:each R5C being independently selected from H and a substituted orunsubstituted organic group.

71. The PARP1 inhibitor compound according to claim 70, wherein ring C is a pyridinegroup having a structure of:

72. The PARP1 inhibitor compound according to claim 67, wherein ring C is a diazinegroup, optionally having a structure selected from:each R5C being independently selectedfrom H and a substituted orunsubstituted organic group.

73. The PARP1 inhibitor compound according to any of claims 1 to 65, wherein r + s = 3.

74. The PARP1 inhibitor compound according to claim 73, 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 orunsubstituted 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.

75. 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, optionally a cyclopropyl group; a Cl to C3 haloalkyl group, optionally a fluoromethyl group such as CF2H or CF3; a Cl to C3 alkoxy group; and a nitrile group.

76. The PARP1 inhibitor compound according to claim 75, wherein the organic group is selected from F, Cl, a nitrile group, a methyl group, and a fluoromethyl group, optionally CF2H.

77. The PARP1 inhibitor compound according to claim 75 or claim 76, wherein exactly one R5C is an organic group.

78. The PARP1 inhibitor compound according to claim 77, wherein exactly one R5C is F.

79. The PARP1 inhibitor compound according to claim 75, wherein when present each R5Cis H.

80. The PARP1 inhibitor compound according to any preceding claim, wherein ring C hasa structure selected from:C2981. The PARP1 inhibitor compound according to claim 80, wherein ring C has a structureselected from:TilT14T17T20T26FT29T21T24HNXT3082. The PARP1 inhibitor compound according to any of claims 1 to 80, wherein R6 is selected 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.

83. The PARP1 inhibitor compound according to claim 82, wherein R6 is selected from -F,-Cl, -CN, -CONH2, -CONMe2, -CONHCOMe, -CONHCH2-CH2OMe, -OCHF2, -NHCOMe, -NHSO2Me,-SO2NHMe,-CONHSO2Me, O84. The PARP1 inhibitor compound according to claim 82, wherein R6 has a structure of:OII 51SAnhwherein R51 is selected from:a Cl to C6 alkyl group, optionally a C3 to C6 cycloalkyl group, a Cl to C3 alkyl group, or a Cl to C3 deuterated alkyl group;a Cl to C3 haloalkyl group, optionally a Cl to C3 fluoroalkyl group; anda 4-, 5-, 6-, or 7-membered saturated heterocyclic group, optionally a 4-, 5- or6-membered cyclic ether group.

85. The PARP1 inhibitor compound according to claim 84, wherein R6 is selected from:

86. The PARP1 inhibitor compound according to claim 85, wherein R6 is -CONHMe.87.The PARP1 inhibitor compound according to claim 86, wherein R6 is88. The PARP1 inhibitor compound for use according to any of claims 1 to 84, wherein R6has a structure of:wherein:each X6 is independently selected from C, N, and O;R61 is absent or H;each R62 is independently absent or selected from H; a halo group, such as F; an oxo group; a Cl to C3 alkyl group; a Cl to C3 haloalkyl group, optionally a Cl to C3 fluoroalkyl group; and -NHR63, wherein R63 is H or a Cl to C3 alkyl group.

89. The PARP1 inhibitor compound for use according to claim 88, wherein R6 is selectedfrom:

90. The PARP1 inhibitor compound according to any preceding claim, wherein when one or more of R1, R2, R3, R4, R5A, 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 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, -CCI3, -CH2CH2F, -CH2CF3, -CH2CCI3, -CH2CBr3, and -CH2CH2CI3);NH2;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 or 4)F-Ph, -NH-(2,3 or 4)CI-Ph, -NH-(2,3 or 4)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 or 4)Pr-Ph, -NH-(2,3 or 4)Bu-Ph, NH-(2,3 or 4)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-C8 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, -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)-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-);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.

91. The PARP1 inhibitor compound for use according to claim 90, wherein each R5A, R5B, and 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 CF3or CHF2),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, anda Ci-Ce alkoxy group;wherein, 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-.

92. The PARP1 inhibitor compound according to any of claims 1 to 23, wherein group L has a structure of:wherein:R5A1 is H and R5A3 is H, or R5A1 and R5A3 together represent a -CH2 group bridging ring A;each XA is independently selected from C and O;when an XA is O, each corresponding R5A is absent;when an XA is C, each corresponding R5A is H;XB is a carbon atom;X1 is selected from C and N;when X1 is C, R5B is absent and the bond between XB and X1 is a double bond;when X1 is N, R5B is H and the bond between XB and X1 is a single bond;each Xc is independently selected from C and N;when an Xc is N, the corresponding R5C is absent;when an Xc is C, each R5C is as defined in any of claims 75 to 79;and R6 is as defined in any of claims 82 to 89.

93. The PARP1 inhibitor compound according to claim 92, wherein group L has a structure of:

94. The PARP1 inhibitor compound according to claim 93, wherein group L has a structureof:

95. The PARP1 inhibitor compound according to any of claims 92 to 94, wherein X1 is Nand R5B is H.

96. The PARP1 inhibitor compound according to any of claims 92 to 95, wherein exactly one XA is O; or wherein each XA is C.

97. The PARP1 inhibitor compound according to any of claims 92 to 96, wherein R5A1 andR5A3 together represent a -CH2- group bridging ring A, such that group L has a structure of:

98. The PARP1 inhibitor compound according to any preceding claim, wherein group L hasa structure of:

99. The PARP1 inhibitor compound according to claim 1, which is selected from:

100. 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, or a racemic mixture, or a tautomer of the compound.

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

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

103. The PARP1 inhibitor compound for use according to claim 102, which is for use in treating a cancer.

104. The PARP1 inhibitor compound for use according to claim 103, 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-TumorSyndromes, 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.

105. The PARP1 inhibitor compound for use according to claim 103 or claim 104, wherein the cancer is deficient in a DNA damage response repair pathway, such as Homologous Recombination dependent DNA Double Strand Break DNA repair activity.

106. The PARP1 inhibitor compound for use according to any of claims 103 to 105, wherein the cancer is deficient in BRCA1 and / or BRCA2 function.

107. The PARP1 inhibitor compound for use according to any of claims 103 to 106, which is to be administered in conjunction with a furtheragent fortreating 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.

108. The PARP1 inhibitor compound for use according to claim 107, 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 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.

109. A pharmaceutical composition comprising a PARP1 inhibitor compound as defined in any of claims 1 to 101.

110. A pharmaceutical composition according to claim 109, 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.

111. The pharmaceutical composition according to claim 109 or claim 110, 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.

112. The pharmaceutical composition according to claim 111, 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.

113. The pharmaceutical composition according to any of claims 109 to 112, for use in treating a cancer.

114. A pharmaceutical kit for treating a cancer, which pharmaceutical kit comprises:a) a PARP1 inhibitor compound as defined in any of claims 1 to 101; andb) 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 antimicrotubule 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.

115. 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.

116. The method according to claim 115, wherein the patient is an animal, preferably a mammal, optionally a human, canine, equine or feline; and preferably a human.

117. A method of synthesising a PARP1 inhibitor compound as defined in any of claims 1 to 101, which 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.

118. A method according to claim 117 wherein the first reactant comprises rings D, E, and 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.

119. A method according to claim 118, wherein the reactive group precursor comprises a carbonyl group, an alkyl halide, or an alkyl sulfonate.

120. A method according to any of claims 117 to 119, wherein the reaction comprises alkylation, reductive amination or amide formation so as to form group L.

121. A method according to claim 120, wherein the first reactant comprises rings D, E, A, and B, and the second reactant comprises a ring C derivative bearing a leaving group such as a halide or sulfonate.

122. A method according to claim 121, wherein the reaction comprises a nucleophilic substitution reaction, such as a nucleophilic aromatic substitution reaction, so as to form group L.

123. The method according to any of claims 117 to 122, further comprising separating structural isomers of the PARP1 inhibitor compound using chiral supercritical fluid chromatography and / or chiral high-performance liquid chromatography.127

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