Niraparib salts

Abstract

We provide novel salts of niraparib. We also provide pharmaceutical compositions containing these salts, as well as methods and uses thereof.

Description

Niraparib salts This invention relates to novel salts of niraparib, pharmaceutical compositions containing such salts and their uses. Niraparib is the International Nonproprietary Name for 2-{4-[(3 S)-piperidin-3-yl]phenyl}-2 H-indazole-7-carboxamide and it has the following chemical structure (“niraparib”). Methods for synthesizing niraparib are given in Jones et al., J. Med. Chem., 52:7170-7185, 2009. Niraparib is an orally available selective poly(ADP-ribose) polymerase (PARP) 1 and 2 inhibitor. Niraparib exhibits IC 50 PARP-1 and PARP-2 inhibitions of 3.8 nM and 2.1 nM, respectively, and in whole cell assays, it inhibits PARP activity (EC 50 = 4 nM) and proliferation of cancer cells with mutant BRCA1 and BRCA2 (CC 50 in the range of 10 to 100 nM) (see Jones et al., J. Med. Chem., 52:7170-7185, 2009). Niraparib is also applicable to treat cancers characterized by defects in certain genes involved in the homologous recombination repair (HRR) pathway (including non-BRCA1 / 2 HRR genes). The activity of niraparib enables it to treat various conditions, including cancer (especially cancers difficult to treat with platinum-based chemotherapy), and conditions such as stroke, autoimmune diabetes, neurological diseases, inflammatory diseases, metabolic diseases and cardiovascular diseases. In recent years, niraparib has been approved for maintenance or treatment of adult patients with recurrent epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer after complete or partial response to platinum-based chemotherapy. The authorized product (ZEJULA™) is a capsule containing 100 mg of niraparib in the form of the monohydrate tosylate salt (niraparib tosylate monohydrate). As a drug substance, niraparib tosylate monohydrate (i.e., 2-{4-[(3 S)-piperidin-3-yl]phenyl}-2 H-Indazole-7-carboxamide 4-methylbenzenesulfonate hydrate (1:1:1) is a white to off-white non-hygroscopic crystalline solid with low water solubility. The method for preparing niraparib tosylate monohydrate includes the method described in PCT / US2018 / 029131. Although niraparib tosylate monohydrate has been successful commercially, there is still a need to provide other forms of niraparib with desired pharmaceutical properties, particularly for formulation into solid (e.g., oral) pharmaceutical dosage forms. Surprisingly, it has now been found that the camphorate, mandelate, and camphorsulfonate salts of niraparib have such desired properties, including improved water solubility, low hygroscopicity, and / or good stability. Accordingly, in one aspect, the present invention provides a salt of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib), which is selected from 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate, and 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate. In aspects and embodiments, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate. In aspects and embodiments, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate. In aspects and embodiments, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate. In aspects and embodiments, the present invention provides a crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of (S)-(+)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 6.5, 11.7, 13.4, 14.1, 14.5, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6, 22.3, 22.8, 24.0, 24.5, 26.9 and 27.6 degrees 2θ when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of (S)-(+)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 11.7, 13.4, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6, 22.8 and 24.0 degrees 2θ when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of (S)-(+)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 13.4, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6 and 24.0 degrees 2θ when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of (S)-(+)-camphorate has an X-ray powder diffraction (XRPD) pattern comprising one or more XRPD diffraction angles at 16.2, 17.5, 20.0, 13.4 and / or 15.2 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of (S)-(+)-camphorate has an XRPD pattern comprising at least two diffraction angles at 16.2, 17.5, 20.0, 13.4 and / or 15.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising at least three diffraction angles at 16.2, 17.5, 20.0, 13.4 and / or 15.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising at least four diffraction angles at 16.2, 17.5, 20.0, 13.4 and / or 15.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at 16.2, 17.5, 20.0, 13.4 and 15.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising one or more XRPD diffraction angles at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising two or more diffraction angles at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising three or more diffraction angles at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at four or more of 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at 20.4, 21.6, 24.0, 11.7 and 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at 16.2, 17.5, 20.0, 13.4, 15.2, 20.4, 21.6, 24.0, 11.7 and 18.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at at least one of 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at at least two of 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate has an XRPD pattern comprising diffraction angles at at least three of 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form has an XRPD pattern comprising diffraction angles at 14.8, 18.0, 22.8 and 27.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form has an XRPD pattern comprising diffraction angles at one or more of 16.2, 17.5, 20.0, 13.4, 15.2, 20.4, 21.6, 24.0, 11.7, 18.0, 22.8, 18.9, 14.5, 14.1, 14.8, 27.6, 26.9, 6.5, 22.3 and / or 24.5 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form has an XRPD pattern comprising diffraction angles having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form is characterized by an XRPD pattern substantially according to Figure 3. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form is characterized by a melting point of about 260 °C to about 270 °C. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate crystalline form is characterized by a melting point of about 264 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 264 °C and / or in which the minimum peak is about 268 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by a DSC thermogram substantially as shown in Figure 5. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by comprising peaks at about 3359 cm -1 、about 1693 cm -1 and about 1649 cm -1 in its infrared spectrum. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by an infrared spectrum substantially as shown in Figure 2. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by adsorbing no more than about 0.3 wt% water up to about 90% relative humidity at about 25 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate is characterized by a GVS thermogram substantially as shown in Figure 6. In aspects and specific examples, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 (R)-(-)-Camphorate In aspects and embodiments, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 (R)-(-)-camphorate. In aspects and embodiments, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 (R)-(-)-camphorate, crystalline form 1. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 The crystalline form of (R)-(-)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 6.5, 11.6, 13.4, 14.0, 14.5, 15.1, 16.2, 17.4, 18.9, 19.9, 20.2, 20.3, 21.5, 21.9, 22.2, 22.3, 23.9, 24.4, and 26.9 degrees 2θ when measured using Cu K radiation. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 The crystalline form of (R)-(-)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 11.6, 13.4, 15.1, 16.2, 17.4, 19.9, 20.2, 20.3, 22.2, 22.3, 24.4, and 26.9 degrees 2θ when measured using Cu K radiation. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 The crystalline form of (R)-(-)-camphorate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 11.6, 15.1, 16.2, 17.4, 19.9, 20.2, 20.3, 22.3, and 24.4 degrees 2θ when measured using Cu K radiation. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising diffraction angles at one or more of 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least two diffraction angles at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least three diffraction angles at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least four diffraction angles at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising diffraction angles at 20.3, 17.4, 16.2, 15.1 and 20.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising diffraction angles at one or more of 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least two diffraction angles at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least three diffraction angles at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising at least four diffraction angles at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising diffraction angles at 24.4, 19.9, 11.6, 22.3 and 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising diffraction angles at 20.3, 17.4, 16.2, 15.1, 20.2, 24.4, 19.9, 11.6, 22.3 and 22.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern comprising a diffraction angle at 16.0 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern that includes a diffraction angle at 21.9 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern that includes diffraction angles at 16.0 and 21.9 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern that includes at least one diffraction angle at 20.3, 17.4, 16.2, 15.1, 20.2, 24.4, 19.9, 11.6, 22.3, 22.2, 13.4, 16.0, 26.9, 6.5, 23.9, 18.9, 14.5, 14.0, 21.9, and / or 21.5 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate has an XRPD pattern that includes diffraction angles with 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by an XRPD pattern substantially as shown in Figure 9. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by a melting point of about 220 °C to about 230 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by a melting point of about 226 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 226 °C and / or in which the minimum peak is about 230 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by a DSC thermogram substantially as shown in Figure 11. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by an infrared spectrum comprising peaks at about 3367 cm -1 、about 1693 cm -1 and about 1648 cm -1 . In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by an infrared spectrum substantially as shown in Figure 8. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 R)-(-)-camphorate is characterized by adsorbing less than about 1 wt% water up to about 90% relative humidity at about 25 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 The crystalline form of (R)-(-)-mandelate is characterized by a GVS thermal analysis graph substantially as shown in Figure 12. In aspects and embodiments, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate. In aspects and embodiments, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( (R)-(-)-mandelate. In aspects and embodiments, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( (R)-(-)-mandelate. In aspects and embodiments, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( (R)-(-)-mandelate form 1. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of: about 4.3, 8.4, 8.6, 8.7, 12.4, 13.7, 14.1, 16.1, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 27.7, 28.0 and 28.7 degrees 2θ when measured using Cu K radiation. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of: about 8.4, 8.6, 8.7, 13.7, 14.1, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 27.7, 28.0 and 28.7 degrees 2θ when measured using Cu K radiation. In an embodiment, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles, selected from the group consisting of about 8.6, 8.7, 13.7, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 28.0 and 28.7 degrees 2θ, when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having one or more diffraction angles at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having at least two diffraction angles at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having at least three diffraction angles at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having at least four diffraction angles at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having diffraction angles at 18.5, 16.4, 17.4, 8.6 and 17.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate has an XRPD pattern having one or more diffraction angles at 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at two or more of 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at three or more of 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at four or more of 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at 8.7, 18.4, 25.1, 27.6 and 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at 18.5, 16.4, 17.4, 8.6, 17.6, 8.7, 18.4, 25.1, 27.6 and 13.7 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(−)-mandelate has an XRPD pattern comprising diffraction angles at one or more of 18.5, 16.4, 17.4, 8.6, 17.6, 8.7, 18.4, 25.1, 27.6, 13.7, 8.4, 28.7, 28.0, 4.3, 21.5, 27.3, 14.1, 27.7, 12.4 and / or 16.1 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate has an XRPD pattern comprising diffraction angles with 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by an XRPD pattern substantially as shown in FIG. 15. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by a melting point of about 190 °C to about 200 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by a melting point of about 197 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 197 °C and / or in which the minimum peak is about 201 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by a DSC thermogram substantially as shown in FIG. 18. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by an infrared spectrum comprising peaks at about 3443 cm -1 、about 3340 cm ‑1 、about 1671 cm- 1 and about 1638 cm -1 . In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by an infrared spectrum substantially as shown in Figure 14. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate is characterized by a DVS thermal analysis chart substantially as shown in Figure 19. In aspects and specific examples, the present invention provides the camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). In aspects and specific examples, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. In aspects and specific examples, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. In aspects and specific examples, the present invention provides a crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by an X-ray powder diffraction (XRPD) pattern having diffraction angles of at least three selected from the group consisting of: about 6.7, 9.5, 11.1, 13.5, 14.3, 16.0, 16.4, 16.7, 16.9, 17.6, 20.3, 22.8, 23.7, 24.3, 24.6, 25.0, 25.2, 25.8, and 26.8 degrees 2θ when measured using Cu K radiation. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The (S)-(+)-camphorsulfonate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 11.1, 13.5, 16.0, 16.4, 16.7, 17.6, 20.3, 23.7, 24.3, 24.6, 25.0, 25.2, and 25.8 degrees 2θ when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate is characterized by an X-ray powder diffraction (XRPD) pattern having at least three diffraction angles selected from the group consisting of about 11.1, 13.5, 16.0, 16.4, 16.7, 17.6, 20.3, 23.7, 24.3, and 24.6 degrees 2θ when measured using Cu K radiation. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at one or more of 16.0, 13.5, 17.6, 24.3, and / or 24.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate has an XRPD pattern comprising at least two diffraction angles at 16.0, 13.5, 17.6, 24.3, and / or 24.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate has an XRPD pattern comprising at least three diffraction angles at 16.0, 13.5, 17.6, 24.3, and / or 24.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate has an XRPD pattern comprising at least four diffraction angles at 16.0, 13.5, 17.6, 24.3, and / or 24.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at 16.0, 13.5, 17.6, 24.3 and 24.6 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising one or more diffraction angles at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising two or more XRPD diffraction angles at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising three or more diffraction angles at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising four or more diffraction angles at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at 11.1, 16.4, 23.7, 16.7 and 20.3 ± 0.2° 2θ. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at 16.0, 13.5, 17.6, 24.3, 24.6, 11.1, 16.4, 23.7, 16.7 and 20.3 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at one or more of 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising at least two diffraction angles at 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising at least three diffraction angles at 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles at at least one of 16.0, 13.5, 17.6, 24.3, 24.6, 11.1, 16.4, 23.7, 16.7, 20.3, 6.7, 25.2, 25.0, 25.8, 26.8, 22.8, 9.5, 16.9, 14.3 and / or 7.7 ±0.2° 2θ. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate has an XRPD pattern comprising diffraction angles having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by an XRPD pattern substantially as shown in Figure 22. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by a melting point of about 235 °C to about 245 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by a melting point of about 239 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 235 °C and / or in which the minimum peak is about 246 °C. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by a DSC thermogram substantially as shown in Figure 24. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by including peaks at about 3467 cm -1 、about 3306 cm ‑1 、about 1724 cm -1 、about 1660 cm -1 and about 1611 cm -1 in its infrared spectrum. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate is characterized by an infrared spectrum substantially as shown in Figure 21. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate is characterized by adsorbing less than about 2% by weight of water at about 25 °C up to about 90% relative humidity. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate is characterized by adsorbing about 1.3% by weight of water at about 25 °C up to about 90% relative humidity. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate is characterized by a GVS thermal analysis graph substantially as shown in Figure 25. In other aspects, the present invention provides a pharmaceutical composition comprising the camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) as defined above, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In other aspects, the present invention provides a pharmaceutical composition comprising the crystalline form of the camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) as defined above, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In a specific example, the pharmaceutical composition comprises 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 The crystalline form of the (S)-(+)-camphorate, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In a specific example, the pharmaceutical composition comprises 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 The crystalline form of (R)-(-)-camphorate, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In a specific example, the pharmaceutical composition comprises 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( The crystalline form of (R)-(-)-mandelate, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In a specific example, the pharmaceutical composition comprises 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of (S)-(+)-camphorsulfonate, and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition is suitable for oral administration. In other aspects, the present invention provides a 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate, or a pharmaceutical composition thereof as defined above, which is used in therapy. In a specific example, the present invention provides a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate, or a pharmaceutical composition thereof as defined above, which is used in therapy. In other aspects, the present invention provides the use of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate, or a pharmaceutical composition thereof as defined above, for the manufacture of a medicament. In a specific example, the present invention provides the use of a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate, or a pharmaceutical composition thereof as defined above, for the manufacture of a medicament. In other aspects, the present invention provides a method for treating cancer, stroke, autoimmune diabetes, neurological diseases, inflammatory diseases, metabolic diseases or cardiovascular diseases in a human in need thereof, the method comprising administering to the human an effective amount of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate or 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate as defined above, or a pharmaceutical composition as defined above. In a specific example, the method comprises administering to the human an effective amount of a crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate or 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate as defined above, or a pharmaceutical composition as defined above. In a specific example, the method is a method for treating cancer. In a specific example, the cancer is associated with BRCA1 and / or BRCA2 mutations. In a specific example, the cancer is associated with ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L or associated with mutations in XRCC2 or any combination thereof. In a specific example, the cancer is epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer. In other aspects, the present invention provides a 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate or 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate as defined above, or a pharmaceutical composition as defined above, which is used in the method as defined above. In a specific example, a crystalline form of a 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate or 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate as defined above, or a pharmaceutical composition as defined above, which is used in the method as defined above. In other aspects, the present invention provides the use of a camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) as defined above, or a pharmaceutical composition as defined above, for the manufacture of a medicament for use in a method as defined above. In a specific example, the present invention provides a crystalline form of a camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) as defined above, or a pharmaceutical composition as defined above, for the manufacture of a medicament for use in a method as defined above. Cross-reference to related applications This application claims the benefit of U.S. Provisional Application No. 62 / 740,872, filed Oct. 3, 2018, which is incorporated herein by reference in its entirety. Although specific embodiments of the invention will now be described with reference to the description and examples, it should be understood that such embodiments are illustrative only and represent only a few of the many possible specific embodiments that may represent the application of the principles of the invention. Given the benefits of the present invention, various changes and modifications will be apparent to those skilled in the art and are considered to be within the spirit and scope of the invention as further defined in the appended claims. Definitions Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. Although any methods and materials similar or equivalent to those described herein may be used to practice or test the present invention, exemplary methods, components, and materials are now described. All technical and patent publications cited herein are incorporated herein by reference in their entirety. Nothing in this application should be construed as an admission that the present invention is not entitled to antedate such disclosure by virtue of prior invention. Unless otherwise indicated, the practice of the present invention will employ conventional chemical synthesis, tissue culture, immunology, molecular biology, microbiology, cell biology, and recombinant DNA techniques within the skill of the art (see, e.g., Michael R. Green and Joseph Sambrook, Molecular Cloning; 4th Edition, Cold Spring Harbor Laboratory Press 2012). Numeric indications (including ranges) of, for example, pH values, temperature, time, concentration, molecular weight, etc., are approximate values that vary by increments of 0.1 or 1.0 (+) or (-) as appropriate. It is to be understood that, although not always explicitly stated, the term “about” is present before all numeric indications. It is also to be understood that, although not always explicitly stated, the reagents described herein are exemplary only and that equivalents thereof are known in the art. Unless the context clearly indicates otherwise, as used in this specification and the appended claims, the singular forms “a” and “the” include plural references. For example, the term “cell” includes plural cells, including mixtures thereof. As used herein, the term “or” is to be understood as inclusive unless explicitly stated or obvious from the context. The term “comprising” is used herein to mean the phrase “comprising but not limited to” and may be interchanged with that phrase. As used herein and unless otherwise specified, the terms "about" and "substantially," when used in connection with the dosage, amount, or weight percentage of a component of a composition or dosage form, mean a dosage, amount, or weight percentage that provides a pharmacological effect equivalent to that obtained by the specified dosage, amount, or weight percentage and is recognized by one of ordinary skill in the art. Specifically, the terms "about" and "substantially," when used in this context, encompass a dosage, amount, or weight percentage within 15%, more specifically within 10%, and even more specifically within 5% of the specified dosage, amount, or weight percentage. As used herein and unless otherwise specified, the terms "about" and "substantially," when used in connection with a numerical value or range of values that serves to characterize a particular solid form (e.g., a particular temperature or temperature range, such as those describing melting, dehydration, desolvation, or glass transition temperature; a mass change, such as a mass change as a function of temperature or humidity; a solvent or water content, expressed, for example, as a mass or percentage; or a peak position or diffraction angle, such as in IR or Raman spectroscopy or XRPD analysis), indicate that the value or range of values may deviate to an extent that is considered reasonable by one of ordinary skill in the art but still describes the particular solid form. Specifically, in a particular embodiment, the terms "about" and "substantially," when used in this context, indicate that the numerical value or range of values may vary within 20%, 10%, 9%, 8%, 7%, 6%, 5%, 4%, 3%, 2%, 1.5%, 1%, 0.5%, or 0.25% of the stated value or range of values. With respect to XRPD, if the value is not explicitly indicated as as such, it is given as ±0.2 degrees 2θ. As used herein, the term "comprising" is intended to mean that the compositions and methods include the recited elements, but do not exclude other elements. "Consisting essentially of," when used to define compositions and methods, shall mean that for the purposes recited, no other elements of basic significance are included in the combination. Thus, a composition consisting essentially of the elements as defined herein will not exclude contaminants and pharmaceutically acceptable carriers from the separation and purification methods, such as phosphate buffered saline, preservatives, and the like. "Consisting of" shall mean excluding trace elements in excess of other components and significant method steps for administering the compositions of the invention or method steps for producing the compositions or achieving the desired results. Specific examples defined by each of these transitional terms are within the scope of the present invention. The use of the term "comprising" herein is intended to encompass and disclose the corresponding statements in which the term "comprising" is replaced by "consisting essentially of" or "consisting of." The use of the term "individual" means an animal, preferably a mammal, including a human or non-human. The terms "patient" and "individual" may be used interchangeably. "Administration" is defined herein as the means of providing an agent or a composition containing the agent to an individual in such a way that the agent is inside the body of the individual. Such administration can be by any route, including but not limited to oral, transdermal (e.g., by vaginal, rectal or oral mucosa), by injection (e.g., subcutaneous, intravenous, parenteral, intraperitoneal or into the central nervous system) or by inhalation (e.g., oral or nasal). Pharmaceutical formulations are of course given in a form suitable for each route of administration. "Therapeutically effective amount" or "effective amount" is the amount of a pharmaceutical agent that achieves a pharmacological effect. The term "therapeutically effective amount" includes, for example, a prophylactically effective amount. The "effective amount" of niraparib is the amount needed to achieve the desired pharmacological effect or therapeutic improvement without undue adverse side effects. The effective amount of niraparib will be selected by those skilled in the art depending on the particular patient and disease. It should be understood that the "effective amount" or "therapeutically effective amount" can vary from individual to individual, due to variations in the metabolism of niraparib, the age, weight, general condition of the individual, the condition being treated, the severity of the condition being treated and the judgment of the prescribing physician. As used herein, improving or alleviating the symptoms of a particular disease, disorder or condition by administering a particular compound or pharmaceutical composition means any reduction in severity, delay in onset, slowing of progression or shortening of duration, whether permanent or temporary, continuous or short-lived, attributable to or associated with the administration of the compound or composition. As used herein, the terms "treat / treating / treatment" include relieving, alleviating or improving a disease or condition (such as cancer), symptoms; preventing other symptoms; improving or preventing the metabolic etiology of symptoms; inhibiting a disease or condition, such as preventing the manifestation of a disease or condition; alleviating a disease or condition; causing regression of a disease or condition; alleviating the symptoms caused by a disease or condition; or prophylactically and / or therapeutically arresting the symptoms of a disease or condition. The term "suffering from" in relation to the term "treatment" refers to a patient or individual who has been diagnosed with or is susceptible to a disease. A patient may also be said to "be at risk of suffering from a disease" due to a medical history in their family pedigree or due to the presence of a gene mutation associated with the disease. A patient at risk of a disease has not yet manifested all or some of the characteristic lesions of the disease. As used herein, "weight percentage", "wt%", "percentage by weight", "weight %" and variations thereof refer to the concentration of a substance in the form of the weight of the substance divided by the total weight of the composition and multiplied by 100. The terms "amorphous", "amorphous form" and related terms as used herein mean that the substance, component or product under discussion is substantially amorphous as determined by X-ray diffraction. In some embodiments, a sample of a substance containing an amorphous form may be substantially free of other amorphous forms and / or crystalline forms. As used herein, the term "crystalline" and related terms, when used to describe a substance, component, product, or form, mean that the substance, component, or product is substantially crystalline as determined by X-ray diffraction (see, e.g., Remington’s Pharmaceutical Sciences, 22nd Edition, Pharmaceutical Press, 2012; The United States Pharmacopoeia, 30th Edition, 2011). As used herein, the terms "crystal form", "crystalline form", and related terms refer to a crystalline solid form that includes a compound and may refer to a specific single-component or multi-component crystal form, including but not limited to polymorphs, solvates, hydrates, or other molecular complexes, salts, solvates of salts, hydrates of salts, or other molecular complexes of salts, or polymorphs thereof. As used herein, the terms "polymorph", "polymorphic form", and related terms refer to two or more crystal forms that include the same molecule, molecules, or ions. Due to differences in the arrangement or conformation of the molecules or ions in the crystal lattice, different polymorphs can have different physical properties, such as melting temperature, heat of fusion, solubility, dissolution rate, and / or vibrational spectra. The differences in the physical properties exhibited by polymorphs affect the following pharmaceutical parameters: such as storage stability, compressibility, and density (important in the manufacture of formulations and products) and dissolution rate (an important factor in bioavailability). Differences in stability can be caused by chemical reactivity ( e.g., differential oxidation, such that a dosage form containing one polymorph discolors more rapidly than a dosage form containing another polymorph) or mechanical characteristics (e.g., a tablet breaks during storage due to the transformation of a kinetically favored polymorph to a thermodynamically more stable polymorph) or both (e.g., a tablet of one polymorph is more likely to crack at high humidity). Due to solubility / dissolution differences, in extreme cases, some polymorphic transformations can result in ineffectiveness, or in the other extreme case, non-toxicity, which can result in a higher or lower incidence of undesirable side effects, or a change in the severity of undesirable side effects. Additionally, the physical properties of the crystal can be important in processing; for example, one polymorph may be more likely to form a solvate or may be difficult to filter and wash free of impurities (e.g., the particle shape and size distribution may be different between polymorphs). If a relative ion (especially an anion within a salt) mentioned herein has one or more stereoisomers and no specific stereochemistry of the relative ion is mentioned, the reference is intended to cover all stereoisomers of the relative ion and mixtures thereof. Stereoisomers include enantiomeric and diastereomeric forms and mixtures thereof. For example, the term "mandelate" mentioned herein without a stereochemical name is intended to mean ( (R)-α-hydroxyphenylacetic acid, ( S)-α-hydroxyphenylacetic acid, and mixtures thereof, including their racemic mixtures. Techniques for characterizing crystalline and amorphous forms include, but are not limited to, thermogravimetric analysis (TGA), melting point, differential scanning calorimetry (DSC), X-ray powder diffraction (XRPD), single crystal X-ray diffraction, vibrational spectroscopy such as infrared (IR) and Raman spectroscopy, solid state and solution nuclear magnetic resonance (NMR) spectroscopy, optical microscopy (such as polarized light microscopy), hot stage optical microscopy, scanning electron microscopy (SEM), electron crystallography, dynamic vapor sorption (DVS) and quantitative analysis, particle size analysis (PSA), surface area analysis, solubility studies, and dissolution studies. The exemplary experimental values described herein may vary according to standard measures in the art, such as the exemplary variations described herein. In the case where the characteristics of a crystalline form are one or more XRPD diffraction angles and unless otherwise specified, it should be understood that the XRPD pattern is obtained under standard conditions (such as those described herein), and the 2θ values may vary according to standard measures in the art. For example, the 2θ values described herein may vary by ± 0.2°. Additionally, in the case where the characteristics of a crystalline form are one or more specified XRPD diffraction angles, those diffraction angles will generally represent diffraction angles in the diffraction pattern with a relative intensity of at least 1%, such as at least 2%, 5%, or 10%. The description of a specific example of a variable or aspect herein includes that specific example as any single specific example or in combination with any other specific example or part thereof. Any composition or method provided herein can be combined with one or more of any other compositions and methods provided herein. The following abbreviations are used in the text: ℃ = degrees Celsius; DMSO = dimethyl sulfoxide; DSC = differential scanning calorimetry; ESI = electrospray ionization; FT-IR = Fourier transform-infrared (spectroscopy); GVS = gravimetric vapor sorption; h = hour; HPLC = high performance liquid chromatography; Hz = Hertz; 2-MeTHF = 2-methyltetrahydrofuran; MHz = megahertz; min = minute; MS = mass spectrometry; NMR = nuclear magnetic resonance; rt / RT = room temperature; SXRD = single crystal X-ray diffraction; TBME = tert-butyl methyl ether; THF = tetrahydrofuran Salt The present invention relates to novel salt forms of the drug 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) which have the desired properties of pharmaceutical formulations such as, for example, improved water solubility, low hygroscopicity and / or good stability. Accordingly, the present invention provides a camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). In particular, the present invention provides a camphorate, mandelate or camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form, such as detailed herein. Also described herein are exemplary crystalline forms of salts of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Also described herein are exemplary X-ray powder diffraction (XRPD) patterns. In a specific example, the XRPD pattern is measured using Cu K radiation. In a specific example, the XRPD pattern is characterized by certain diffraction angles (peaks) as described herein. Niraparib camphorate In one aspect, the present invention provides a camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ("niraparib camphorate"). In a preferred aspect, the present invention provides crystalline niraparib camphorate. The camphorate may be selected from (1 R,3 S)-(+)-camphorate, (1 S,3 R)-(+)-camphorate, (+ / -)-camphorate and mixtures thereof. In one specific example, the camphorate is (1 R,3 (S)-(+)-camphorate (hereinafter referred to as “(+)-camphorate”). (+)-Camphorate contains ionized form of (1 R,3 S)-(+)-camphoric acid, which has the following structure: . As can be seen from this aspect, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (+)-camphorate, for example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (+)-camphorate. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (+)-camphorate includes 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (+)-camphorate of Form 1, as described herein for example. In a specific example, the crystalline form (Crystalline Form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at one or more (e.g., one, two, three, four, or five) 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, and / or 15.2°. In other specific examples, the crystalline form of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at at least two 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, and / or 15.2°. In other specific examples, the crystalline form (Crystalline Form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at at least three 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, and / or 15.2°. In other specific examples, the crystalline form (Crystalline Form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at at least four 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, and / or 15.2°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at a 2θ value of 16.2°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle at a 2θ value of 17.5°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2° and 17.5°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, and 20.0°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, and 13.4°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, and 15.2°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by an XRPD diffraction angle or angles (such as one, two, three, four, or five) at 2θ values of 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by at least two XRPD diffraction angles at 2θ values of 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by at least three XRPD diffraction angles at 2θ values of 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by at least four XRPD diffraction angles at 2θ values of 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by one or more (e.g., six, seven, eight, nine, or ten) XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by at least six XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by at least seven XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by at least eight XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In other specific examples, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by at least nine XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and / or 18.0°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, and 20.4°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, and 21.6°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, and 24.0°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, and 11.7°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, and 18.0°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by one or more (such as ten, eleven, twelve, thirteen, fourteen, or fifteen) XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, and 14.8°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by at least ten; at least eleven; at least twelve; at least thirteen; or at least fourteen XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, and / or 14.8°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, and 14.8°. In a specific example, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by one or more (e.g., fifteen, sixteen, seventeen, eighteen, nineteen, or twenty) XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, 14.8°, 27.6°, 26.9°, 6.5°, 22.3°, and / or 24.5°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by at least fifteen; at least sixteen; at least seventeen; at least eighteen; or at least nineteen XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, 14.8°, 27.6°, 26.9°, 6.5°, 22.3°, and / or 24.5°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (+)-camphorate is characterized by XRPD diffraction angles at 2θ values of 16.2°, 17.5°, 20.0°, 13.4°, 15.2°, 20.4°, 21.6°, 24.0°, 11.7°, 18.0°, 22.8°, 18.9°, 14.5°, 14.1°, 14.8°, 27.6°, 26.9°, 6.5°, 22.3°, and 24.5°. In any of the specific examples mentioned above, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (+)-camphorate may contain diffraction angles at 2θ values of 14.8°, 18.0°, 22.8°, and 27.6°. In a specific example, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (+)-camphorate contains at least two diffraction angles at 2θ values of 14.8°, 18.0°, 22.8°, and / or 27.6°. In other specific examples, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (+)-camphorate contains at least three diffraction angles at 2θ values of 14.8°, 18.0°, 22.8°, and / or 27.6°. In a specific example, the XRPD pattern of the crystalline form of niraparib (+)-camphorate (crystalline form 1) contains diffraction angles at 2θ values of 18.0° and / or 22.8°. In other specific examples, the XRPD pattern of the crystalline form of niraparib (+)-camphorate (crystalline form 1) contains diffraction angles at 2θ values of 14.8°, 18.0°, and 22.8°. In other specific examples, the XRPD pattern of the crystalline form of niraparib (+)-camphorate (crystalline form 1) contains diffraction angles at 2θ values of 18.0°, 22.8°, and 27.6°. In other specific examples, the XRPD pattern of the crystalline form of niraparib (+)-camphorate (crystalline form 1) contains diffraction angles at 2θ values of 14.8°, 18.0°, 22.8°, and 27.6°. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by having XRPD diffraction angles with 2θ values (and optionally relative intensity values) substantially as described in Table 1 of Example 4. In a specific example, the position of the XRPD diffraction angle is within ± 0.2000° 2θ of the value specified in Table 1, and / or the d-spacing is within ±0.20000 Å or ±0.10000 Å of the value specified in Table 1. In a specific example, the height and / or area of the diffraction angle is within ± 10% or ± 5% of the specified value in Table 1. In a specific example, the relative intensity is within ± 10% or ± 5% of the specified value in Table 1 In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by the XRPD pattern shown (or substantially shown) in Figure 3. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by a melting point of about 260°C to about 270°C. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by a melting point of about 264°C. For example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) may be characterized by a DSC thermal analysis graph in which the melting onset point (endothermic peak) is about 264°C and / or in which the minimum peak is about 268°C. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) may be characterized by having a DSC thermal analysis graph as shown (or substantially shown) in Figure 5. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by having, for example, peaks at about 3359 cm -1 at the peak, about 1693 cm -1 at the peak and about 1649 cm -1The infrared spectrum of the peak at the position. In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by having an FT-IR spectrum as shown in Figure 2 (or substantially shown). In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by being non-hygroscopic. Hygroscopicity can be measured, for example, by GVS (such as described in the following examples). Thus, in a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) can be characterized by adsorbing less than 1% by weight of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) is characterized by adsorbing about 0.3% by weight of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) can be characterized by the GVS thermal analysis graph as shown in Figure 6 (or substantially shown). In a specific example, the crystalline form of niraparib (+)-camphorate (crystalline form 1) can be characterized by being stable under conditions of high temperature and / or humidity. In a specific example, substantially all ( e.g., at least 90%, at least 95%, at least 99% or about 100%) of the crystalline form of niraparib (+)-camphorate (crystalline form 1) remains in the same form (e.g., when evaluated by XRPD) when exposed to 90% relative humidity at room temperature (e.g., about 25 °C). In other specific examples, substantially all (e.g., at least 90%, at least 95%, at least 99% or about 100%) of the crystalline form of niraparib (+)-camphorate (crystalline form 1) remains in the same form (e.g., when evaluated by XRPD) when exposed to 90% relative humidity at high temperature (e.g., about 30 °C, 40 °C, 50 °C, 60 °C or 75 °C). The crystalline form of niraparib (+)-camphorate (crystalline form 1) can further be characterized by any combination of the characteristic stability, melting point, FT-IR spectrum, differential scanning calorimetry thermal analysis graph, gravimetric vapor sorption thermal analysis graph or XRPD diffraction angle values as described herein. In a specific example, the molar ratio of niraparib to camphoric acid in the salt is about 1:1. In another specific example, the camphorate is (1 S,3 R)-(-)-camphorate (hereinafter referred to as "(-)-camphorate"). (-)-Camphorate contains the ionized form of (1 S,3 R)-(-)-camphoric acid, which has the following structure: As can be seen from this aspect, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (-)-camphorate, such as the crystalline form of niraparib (-)-camphorate. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (-)-camphorate includes the crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (-)-camphorate, as described herein. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of one or more (such as one, two, three, four, or five) of 20.3°, 17.4°, 16.2°, 15.1°, and 20.2°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of at least two of 20.3°, 17.4°, 16.2°, 15.1°, and / or 20.2°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of at least three of 20.3°, 17.4°, 16.2°, 15.1°, and / or 20.2°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of at least four of 20.3°, 17.4°, 16.2°, 15.1°, and / or 20.2°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by the XRPD diffraction angle at the 2θ value of 20.3°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by the XRPD diffraction angles at the 2θ values of 20.3° and 17.4°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by the XRPD diffraction angles at the 2θ values of 20.3°, 17.4°, and 16.2°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by the XRPD diffraction angles at the 2θ values of 20.3°, 17.4°, and 15.1°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by the XRPD diffraction angles at the 2θ values of 20.3°, 17.4°, 16.2°, and 15.1°. In a specific example, the crystalline form of niraparib (-)-camphorate is characterized by the XRPD diffraction angles at the 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, and 20.2°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by one or more (e.g., one, two, three, four, or five) XRPD diffraction angles at 2θ values of 24.4°, 19.9°, 11.6°, 22.3°, and 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least two XRPD diffraction angles at 2θ values of 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least three XRPD diffraction angles at 2θ values of 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least four XRPD diffraction angles at 2θ values of 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In a specific example, the crystalline form of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of 24.4°, 19.9°, 11.6°, 22.3°, and 22.2°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by one or more (e.g., six, seven, eight, nine, or ten) XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate is characterized by at least six XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least seven XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate is characterized by at least eight XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least nine XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and / or 22.2°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, and 24.4°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, and 19.9°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, and 11.6°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, and 22.3°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, and 22.2°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by one or more (e.g., ten, eleven, twelve, thirteen, fourteen, or fifteen) XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, and 23.9°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by at least ten; at least eleven; at least twelve; at least thirteen; or at least fourteen XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, and / or 23.9°. In other specific examples, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, and 23.9°. In a specific example, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by one or more (e.g., fifteen, sixteen, seventeen, eighteen, nineteen, or twenty) XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, 23.9°, 18.9°, 14.5°, 14.0°, 21.9°, and 21.5°. In other specific examples, the crystalline form of niraparib (-)-camphorate is characterized by at least fifteen; at least sixteen; at least seventeen; at least eighteen; or at least nineteen XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, 23.9°, 18.9°, 14.5°, 14.0°, 21.9°, and / or 21.5°. In other specific examples, the crystalline form (crystalline form 1) of niraparib (-)-camphorate is characterized by XRPD diffraction angles at 2θ values of 20.3°, 17.4°, 16.2°, 15.1°, 20.2°, 24.4°, 19.9°, 11.6°, 22.3°, 22.2°, 13.4°, 16.0°, 26.9°, 6.5°, 23.9°, 18.9°, 14.5°, 14.0°, 21.9°, and 21.5°. In any of the specific examples mentioned above, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (-)-camphorate may contain diffraction angles at 2θ values of 16.0° and / or 21.9°. In a specific example, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (-)-camphorate contains a diffraction angle at a 2θ value of 16.0°. In other specific examples, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (-)-camphorate contains a diffraction angle at a 2θ value of 21.9°. In other specific examples, the XRPD pattern of the crystalline form (crystalline form 1) of niraparib (+)-camphorate contains diffraction angles at 2θ values of 16.0° and 21.9°. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by having XRPD diffraction angles with 2θ values (and optionally relative intensity values) substantially as described in Table 2 of Example 4. In a specific example, the positions of the XRPD diffraction angles are within ±0.2000° 2θ of the values specified in Table 2, and / or the d-spacing is within ±0.20000 Å or ±0.10000 Å of the values specified in Table 2. In a specific example, the height and / or area of the diffraction angles are within ±10% or ±5% of the specified values in Table 2. In a specific example, the relative intensity is within ±10% or ±5% of the specified values in Table 2. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by the XRPD pattern shown (or substantially shown) in Figure 9. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by a melting point of about 220°C to about 230°C. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by a melting point of about 226°C. For example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) may be characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 226°C and / or in which the minimum peak is about 230°C. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) may be characterized by having a DSC thermogram as shown (or substantially shown) in Figure 11. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by having peaks at about 3367 cm -1 when measured using, for example, the FT-IR method as described herein, a peak at about 1693 cm -1 and a peak at about 1648 cm -1 in the infrared spectrum. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by having an FT-IR spectrum as shown (or substantially shown) in Figure 8. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by non-hygroscopicity. Hygroscopicity can be measured, for example, by GVS (as described in the following examples). Thus, in a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) can be characterized by adsorbing less than 1 wt% of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) is characterized by adsorbing about 0.2 wt% of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) can be characterized by the GVS thermogram shown (or substantially shown) in Figure 12. In a specific example, the crystalline form of niraparib (-)-camphorate (crystalline form 1) can be characterized by being stable under conditions of high temperature and / or humidity. In a specific example, substantially all (e.g., at least 90%, at least 95%, at least 99% or about 100%) of the crystalline form of niraparib (-)-camphorate (crystalline form 1) remains in the same form (e.g., as evaluated by XRPD) when exposed to 90% relative humidity at room temperature (e.g., about 25 °C). In other specific examples, substantially all (e.g., at least 90%, at least 95%, at least 99% or about 100%) of the crystalline form of niraparib (-)-camphorate (crystalline form 1) remains in the same form (e.g., as evaluated by XRPD) when exposed to 90% relative humidity at high temperature (e.g., about 30 °C, 40 °C, 50 °C, 60 °C or 75 °C). The crystalline form of niraparib (-)-camphorate (crystalline form 1) can further be characterized by any combination of the characteristic stability, melting point, FT-IR spectrum, differential scanning calorimetry thermogram, gravimetric vapor sorption thermogram or XRPD diffraction angle values as described herein. In a specific example, the molar ratio of niraparib to camphoric acid in the salt is about 1:1. Niraparib mandelate In another aspect, the present invention provides a mandelate salt of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (「niraparib mandelate」). The mandelate salt comprises ionized mandelic acid, α-hydroxyphenylacetic acid. In a preferred aspect, the present invention provides a crystalline form of a mandelate salt of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). The mandelate salt can be selected from ( (R)-(-)-mandelate, ( (S)-(+)-mandelate, (racemic)-mandelate and mixtures thereof. In a specific example, the mandelate is ( R)-(-)-mandelate. ( The ( R)-(-)-mandelate includes the ionized form of ( R)-(-)-mandelic acid, which has the following structure: As can be seen from this aspect, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate, for example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate. In a specific example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate includes the 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate of Form 1 as described herein. In a specific example, the crystalline form (Crystal Form 1) of niraparib ( R)-(-)-mandelate is characterized by an XRPD diffraction angle at one or more (e.g., one, two, three, four, or five) 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, and / or 17.6°. In other specific examples, the crystalline form ( R)-(-)-mandelate of niraparib is characterized by an XRPD diffraction angle at at least two 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, and / or 17.6°. In other specific examples, the crystalline form of niraparib ( R)-(-)-mandelate is characterized by an XRPD diffraction angle at at least three 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, and / or 17.6°. In other specific examples, the crystalline form ( R)-(-)-mandelate of niraparib is characterized by an XRPD diffraction angle at at least four 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, and / or 17.6°. In a specific example, the crystalline form of niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by an XRPD diffraction angle at a 2θ value of 16.4°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5° and 16.4°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4° and 17.4°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4° and 8.6°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6° and 17.6°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by one or more (e.g., one, two, three, four or five) XRPD diffraction angles at 2θ values of 8.7°, 18.4°, 25.1°, 27.6 and / or 13.7°. In other specific examples, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by at least two XRPD diffraction angles at 2θ values of 8.7°, 18.4°, 25.1°, 27.6° and / or 13.7°. In other specific examples, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by at least three XRPD diffraction angles at 2θ values of 8.7°, 18.4°, 25.1°, 27.6° and / or 13.7°. In other specific examples, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by at least four XRPD diffraction angles at 2θ values of 8.7°, 18.4°, 25.1°, 27.6° and / or 13.7°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 8.7°, 18.4°, 25.1°, 27.6° and 13.7°. In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of one or more (e.g., six, seven, eight, nine, or ten) of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and / or 13.7°. In other embodiments, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of at least six of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and / or 13.7°. In other embodiments, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of at least seven of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and / or 13.7°. In other embodiments, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of at least eight of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and / or 13.7°. In other embodiments, niraparib ( The crystalline form of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of at least nine of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and / or 13.7°. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, and 8.7°. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, and 18.4°. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, and 25.1°. In an embodiment, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, and 27.6°. In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, and 13.7°. In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by one or more (such as ten, eleven, twelve, thirteen, fourteen, or fifteen) XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, and / or 21.5°. In other specific examples, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by at least ten; at least eleven; at least twelve; at least thirteen; or at least fourteen XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, and / or 21.5°. In other specific examples, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, and 21.5°. In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by one or more (such as fifteen, sixteen, seventeen, eighteen, nineteen, or twenty) XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, 21.5°, 27.3°, 14.1°, 27.7°, 12.4°, and / or 16.1°. In other specific examples, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by at least fifteen; at least sixteen; at least seventeen; at least eighteen; or at least nineteen 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, 21.5°, 27.3°, 14.1°, 27.7°, 12.4°, and / or 16.1° in the XRPD diffraction angle. In other embodiments, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 18.5°, 16.4°, 17.4°, 8.6°, 17.6°, 8.7°, 18.4°, 25.1°, 27.6°, 13.7°, 8.4°, 28.7°, 28.0°, 4.3°, 21.5°, 27.3°, 14.1°, 27.7°, 12.4°, and 16.1°. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by having XRPD diffraction angles with 2θ values (and optionally relative intensity values) substantially as described in Table 3 of Example 4. In an embodiment, the position of the XRPD diffraction angle is within ± 0.2000° 2θ of the value specified in Table 3, and / or the d-spacing is within ±0.20000 Å or ±0.10000 Å of the value specified in Table 3. In an embodiment, the height and / or area of the diffraction angle is within ± 10% or ± 5% of the specified value in Table 3. In an embodiment, the relative intensity is within ± 10% or ± 5% of the specified value in Table 3. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by the XRPD pattern shown (or substantially shown) in Figure 15. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by a melting point of about 190°C to about 200°C. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by a melting point of about 197°C. In an embodiment, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) is characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 197°C and / or in which the minimum peak is about 201°C. In an embodiment, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate can be characterized by having a DSC thermal analysis graph as shown in Figure 18 (or substantially shown). In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by having an infrared spectrum including peaks at about 3443 cm -1 when measured using the FT-IR method as described herein, for example, peaks at about 3340 cm -1 peaks at about 1671 cm -1 and peaks at about 1638 cm -1 when measured using the FT-IR method as described herein, for example. In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by having an FT-IR spectrum as shown in Figure 14 (or substantially shown). In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by being non-hygroscopic. Hygroscopicity can be measured, for example, by GVS (as described in the following examples). Thus, in a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate can be characterized by adsorbing less than 1% by weight of water up to 90% relative humidity (for example, at 25 °C). In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate is characterized by adsorbing about 0.5% by weight of water up to 90% relative humidity (for example, at 25 °C). In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate can be characterized by having a DVS thermal analysis graph as shown in Figure 19 (or substantially shown). In a specific example, niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate can be characterized by being stable under conditions of high temperature and / or humidity. In a specific example, substantially all (for example, at least 90%, at least 95%, at least 99% or about 100%) of niraparib ( The crystalline form (crystalline form 1) of (R)-(-)-mandelate remains in the same form (for example, when evaluated by XRPD) when exposed to 90% relative humidity at room temperature (for example, about 25 °C). In other specific examples, substantially all (for example, at least 90%, at least 95%, at least 99% or about 100%) of niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) maintains the same form (e.g., as determined by XRPD) when exposed to 90% relative humidity at elevated temperatures (e.g., about 30 °C, 40 °C, 50 °C, 60 °C, or 75 °C). In a specific example, niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) may be characterized by the structure shown (or substantially shown) in Figure 18. Niraparib ( The crystalline form of (R)-(-)-mandelate (crystalline form 1) may further be characterized by any combination of the characteristic stability, melting point, FT-IR spectrum, differential scanning calorimetry thermogram, dynamic vapor sorption isotherm, structure as determined by single crystal X-ray crystallography, or XRPD diffraction angle values as described herein. Niraparib camphorsulfonate In another aspect, the present invention provides a camphorsulfonate salt of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (「niraparib camphorsulfonate」). The camphorsulfonate salt comprises the ionized form of 7,7-dimethyl-2-oxobicyclo[2.2.1]hept-1-yl)methanesulfonic acid. In a preferred aspect, the present invention provides crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate. The camphorsulfonate salt may be selected from (1 S)-(+)-camphorsulfonate, (1 R)-(-)-camphorsulfonate, (racemic)-camphorsulfonate, and mixtures thereof. In one specific example, the camphorsulfonate salt is (1 S)-(+)-camphorsulfonate. The (1 S)-(+)-camphorsulfonate comprises the ionized form of (1 S)-(+)-7,7-dimethyl-2-oxobicyclo[2.2.1]hept-1-yl)methanesulfonic acid, which has the following structure: As can be seen from this aspect, the present invention provides 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate, for example, the crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. In a specific example, 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 The crystalline form of the (S)-(+)-camphorsulfonate salt comprises 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 of the (S)-(+)-camphorsulfonate salt, as described herein. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by an XRPD diffraction angle at one or more (e.g., one, two, three, four, or five) 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, and / or 24.6°. In other specific examples, niraparib (1 The crystalline form of the (S)-(+)-camphorsulfonate salt is characterized by an XRPD diffraction angle at at least two 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, and / or 24.6°. In other specific examples, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by an XRPD diffraction angle at at least three 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, and / or 24.6°. In other specific examples, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by an XRPD diffraction angle at at least four 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, and / or 24.6°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by an XRPD diffraction angle at a 2θ value of 16.0°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by XRPD diffraction angles at 2θ values of 16.0° and 13.5°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by XRPD diffraction angles at 2θ values of 16.0° and 17.6°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, and 17.6°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of the (S)-(+)-camphorsulfonate salt is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, and 24.3°. In a specific example, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, and 24.6°. In a specific example, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by one or more (e.g., one, two, three, four, or five) XRPD diffraction angles at 2θ values of 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other specific examples, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by at least two XRPD diffraction angles at 2θ values of 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other specific examples, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by at least three XRPD diffraction angles at 2θ values of 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other specific examples, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by at least four XRPD diffraction angles at 2θ values of 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In a specific example, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by XRPD diffraction angles at 2θ values of 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In a specific example, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate (crystalline form 1) is characterized by one or more (e.g., six, seven, eight, nine, or ten) XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other specific examples, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate is characterized by at least six XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other specific examples, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of at least seven of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other embodiments, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of at least eight of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In other embodiments, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of at least nine of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and / or 20.3°. In an embodiment, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, and 11.1°. In an embodiment, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, and 16.4°. In an embodiment, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, and 23.7°. In an embodiment, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, and 16.7°. In an embodiment, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, and 20.3°. In an embodiment, niraparib (1 The crystalline form (Crystal Form 1) of (S)-(+)-camphorsulfonate is characterized by one or more (e.g., ten, eleven, twelve, thirteen, fourteen, or fifteen) XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, and / or 26.8°. In other embodiments, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate is characterized by at least ten; at least eleven; at least twelve; at least thirteen; or at least fourteen XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, and / or 26.8°. In other embodiments, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, and / or 26.8°. In an embodiment, niraparib 1 The crystalline form (Crystal Form 1) of (S)-(+)-camphorsulfonate is characterized by one or more (e.g., fifteen, sixteen, seventeen, eighteen, nineteen, or twenty) XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, 26.8°, 22.8°, 9.5°, 16.9°, 14.3°, and / or 7.7°. In other embodiments, niraparib (1 The crystalline form (Crystal Form 1) of (S)-(+)-camphorsulfonate is characterized by at least fifteen; at least sixteen; at least seventeen; at least eighteen; or at least nineteen XRPD diffraction angles at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, 26.8°, 22.8°, 9.5°, 16.9°, 14.3°, and / or 7.7°. In other embodiments, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by diffraction angles in the XRPD at 2θ values of 16.0°, 13.5°, 17.6°, 24.3°, 24.6°, 11.1°, 16.4°, 23.7°, 16.7°, 20.3°, 6.7°, 25.2°, 25.0°, 25.8°, 26.8°, 22.8°, 9.5°, 16.9°, 14.3°, and 7.7°. In any of the specific examples mentioned above, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate may contain diffraction angles at 2θ values of 6.7°, 16.4°, 23.7°, and / or 25.2°. In a specific example, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate contains at least two diffraction angles at 2θ values of 6.7°, 16.4°, 23.7°, and / or 25.2°. In other specific examples, niraparib (1 The XRPD pattern of the crystalline form of (S)-(+)-camphorsulfonate contains at least three diffraction angles at 2θ values of 6.7°, 16.4°, 23.7°, and / or 25.2°. In a specific example, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate contains a diffraction angle at a 2θ value of 16.4°. In a specific example, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate contains diffraction angles at 2θ values of 16.4° and 23.7°. In a specific example, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate contains diffraction angles at 2θ values of 6.7°, 16.4°, and 23.7°. In a specific example, niraparib (1 The XRPD pattern of the crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate contains diffraction angles at 2θ values of 6.7°, 16.4°, 23.7°, and 25.2°. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by XRPD diffraction angles having substantially the 2θ values (and optionally relative intensity values) as described in Table 4 of Example 4. In a specific example, the positions of the XRPD diffraction angles are within ± 0.2000° 2θ of the values specified in Table 4, and / or the d-spacing is within ±0.20000 Å or ±0.10000 Å of the values specified in Table 4. In a specific example, the height and / or area of the diffraction angle is within ± 10% or ± 5% of the specified values in Table 4. In a specific example, the relative intensity is within ± 10% or ± 5% of the specified values in Table 4. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by the XRPD pattern shown (or substantially shown) in Figure 22. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by a melting point of about 235 °C to about 245 °C. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by a melting point of about 239 °C. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by a DSC thermogram in which the melting onset point (endothermic peak) is about 235 °C and / or in which the minimum peak is about 246 °C. In a specific example, niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate may be characterized by a DSC thermogram shown (or substantially shown) as in Figure 24. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by having, for example, peaks at about 3467 cm -1 when measured using the FT-IR method as described herein, peaks at about 3306 cm -1 when measured using the FT-IR method as described herein, peaks at about 1724 cm -1 when measured using the FT-IR method as described herein, peaks at about 1660 cm -1 when measured using the FT-IR method as described herein, peaks at about 1611 cm -1 when measured using the FT-IR method as described herein, and an infrared spectrum with peaks at about 1611 cm. In a specific example, niraparib (1 The crystalline form (crystalline form 1) of (S)-(+)-camphorsulfonate is characterized by having an FT-IR spectrum shown (or substantially shown) as in Figure 21. In a specific example, the crystalline form (crystalline form 1) of niraparib (1 S)-(+)-camphorsulfonate is characterized by being slightly hygroscopic. The hygroscopicity can be measured, for example, by GVS (as described in the following examples). Thus, in a specific example, niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) may be characterized by adsorbing less than 2% by weight of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) is characterized by adsorbing about 1.3% by weight of water up to 90% relative humidity (e.g., at 25 °C). In a specific example, niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) may be characterized by the GVS thermal analysis graph shown (or substantially shown) in Figure 25. In a specific example, niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) may be characterized by being stable under conditions of high temperature and / or humidity. In a specific example, substantially all (e.g., at least 90%, at least 95%, at least 99% or about 100%) of niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) remains in the same form (e.g., when evaluated by XRPD) when exposed to 90% relative humidity at room temperature (e.g., about 25 °C). In other specific examples, substantially all (e.g., at least 90%, at least 95%, at least 99% or about 100%) of niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) remains in the same form (e.g., when evaluated by XRPD) when exposed to 90% relative humidity at high temperature (e.g., about 30 °C, 40 °C, 50 °C, 60 °C or 75 °C). Niraparib (1 S)-(+)-camphorsulfonate crystalline form (crystalline form 1) may further be characterized by any combination of the characteristic stability, melting point, FT-IR spectrum, differential scanning calorimetry thermal analysis graph, gravimetric vapor sorption thermal analysis graph or XRPD diffraction angle values as described herein. Solubility The niraparib salts of the present invention have the desired properties of pharmaceutical formulations, including in particular the desired dissolution properties. From this aspect, the present invention provides camphoric acid salts of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib), mandelic acid salts of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) or camphorsulfonic acid salts of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) having a solubility of at least 1 mg / mL in an aqueous medium ( as described herein, for example). "Aqueous medium" means a liquid medium containing water and optionally one or more ionic species acting as buffers and / or pH regulators. In the case where another solvent such as an organic solvent is present in the medium, this preferably represents a solution of less than 50% by volume (for example, less than 20% by volume, less than 15% by volume, less than 10% by volume, less than 5% by volume or less than 1% by volume). Exemplary aqueous media include water and the buffer solutions described in Example 10. In a specific example, the 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salt has a solubility of at least 1 mg / mL in an aqueous medium, where the aqueous medium has a pH value between 1 and 7. In a specific example, the niraparib salt has a solubility of at least 1 mg / mL in an aqueous medium, where the aqueous medium has a pH value between 1 and 5, such as between 1 and 3, between 1 and 2 or about 1. In other specific examples, the niraparib salt has a solubility of at least 1 mg / mL in an aqueous medium, where the aqueous medium has a pH value of about 4.5 or about 6.8. In a specific example, the aqueous medium has a pH value less than 7. In a specific example, the aqueous medium does not consist solely of water. In a specific example, the solubility of the niraparib salt is at least 1.2 mg / mL. In a specific example, the solubility of the niraparib salt is at least 1.5 mg / mL, such as at least 2.0, 2.5, 3.0, 3.5, 4.0, 4.5 or 5.0 mg / mL. In a specific example, the solubility of the niraparib salt is at least 7 mg / mL, such as at least 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 or 20 mg / mL. In a specific example, the solubility of the niraparib salt is at least 25 mg / mL, such as at least 30, 35, 40, 45, 50, 60, 70, 80, 90 or 100 mg / mL. In a specific example, the solubility of the niraparib salt is at least 125 mg / mL, such as at least 150, 175 or 200 mg / mL. In a specific example, the solubility of crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate (such as defined herein, such as niraparib (1 R,3 S)-(+)-camphorate) is at least 1 mg / mL (such as about 1.2 mg / mL) in an aqueous medium having a pH value of about 6.8. In a specific example, the solubility of niraparib camphorate is at least 10 mg / mL (such as at least 15 mg / mL, at least 20 mg / mL, or about 21 mg / mL) in an aqueous medium having a pH value of about 1. In a specific example, the solubility of crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate (such as defined herein, such as niraparib ( R)-(-)-mandelate) is at least 5 mg / mL (such as about 7.8 mg / mL) in an aqueous medium having a pH value of about 6.8. In a specific example, the solubility of niraparib mandelate is at least 10 mg / mL (such as at least 20 mg / mL, at least 30 mg / mL, at least 40 mg / mL, or about 45 mg / mL) in water. In a specific example, the solubility of niraparib mandelate is at least 20 mg / mL (such as at least 30 mg / mL, at least 40 mg / mL, at least 50 mg / mL, or about 54 mg / mL) in an aqueous medium having a pH value of about 4.5. In a specific example, the solubility of niraparib mandelate is at least 50 mg / mL (such as at least 75 mg / mL, at least 100 mg / mL, at least 125 mg / mL, at least 150 mg / mL, or about 163 mg / mL) in an aqueous medium having a pH value of about 1. In a specific example, the solubility of crystalline form 1 of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate (such as defined herein, such as niraparib (1 The crystalline form of (S)-(+)-camphorsulfonate has a solubility of at least 1 mg / mL (such as at least 1.5 mg / mL or about 1.7 mg / mL) in an aqueous medium having a pH value of about 6.8. In a specific example, the solubility of niraparib camphorsulfonate in water is at least 2.5 mg / mL (such as at least 3.0 mg / mL, at least 4.0 mg / mL, at least 5.0 mg / mL or about 5.9 mg / mL). In a specific example, the solubility of niraparib camphorsulfonate in an aqueous medium having a pH value of about 4.5 is at least 3.0 mg / mL (such as at least 4.0 mg / mL, at least 5.0 mg / mL, at least 6.0 mg / mL or about 7.1 mg / mL). In a specific example, the solubility of niraparib camphorsulfonate in an aqueous medium having a pH value of about 1 is at least 5.0 mg / mL (such as at least 7.5 mg / mL, at least 10.0 mg / mL or about 11.5 mg / mL). The method for determining the solubility of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salts as defined herein is obvious to those skilled in the art. In a specific example, the method for determining the solubility of the salts as defined herein is the method described in Example 10. Pharmaceutical composition In another aspect, the present invention provides a pharmaceutical composition comprising the camphorate, mandelate or camphorsulfonate (such as the salts described herein) of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) and at least one pharmaceutically acceptable excipient. In a specific example, the pharmaceutical composition comprises crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate (such as the crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (+)-camphorate or crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (-)-camphorate) described herein. In a specific example, the pharmaceutical composition comprises crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate (such as the crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( (R)-(-)-mandelate). In a specific example, the pharmaceutical composition comprises crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate (such as crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) described herein (1 S)-(+)-camphorsulfonate). In a specific example, the pharmaceutical composition comprises about 20-80 wt% of the niraparib salt, such as for example about 45-70 wt%, about 40-50 wt%, about 45-55 wt%, about 50-60 wt%, about 55-65 wt%, about 60-70 wt%, about 65-75 wt%, about 70-80 wt% or about 40-60 wt% of the niraparib salt (wherein wt% is calculated based on the weight of the niraparib free base present in the salt and is in the form of a percentage of the weight of the pharmaceutical composition). The pharmaceutical composition comprises at least one pharmaceutically acceptable excipient. The pharmaceutically acceptable excipient can be any such excipient known in the art, including for example those described in Remington's Pharmaceutical Sciences, Mack Publishing Co. (edited by A. R. Gennaro 1985). The pharmaceutical composition of the compound of the present invention can be prepared by conventional means known in the art, including for example mixing at least one compound of the present invention with a pharmaceutically acceptable excipient. Exemplary pharmaceutically acceptable excipients for the purposes of the pharmaceutical compositions disclosed herein include but are not limited to binders, disintegrants, superdisintegrants, lubricants, diluents, fillers, flavoring agents, glidants, absorbents, solubilizers, chelating agents, emulsifiers, thickeners, dispersants, stabilizers, suspending agents, adsorbents, granulating agents, preservatives, buffers, coloring agents and sweetening agents or combinations thereof. In a specific example, the pharmaceutically acceptable excipient comprises hydroxypropyl methylcellulose, such as low-substituted hydroxypropyl cellulose. In a specific example, the pharmaceutically acceptable excipient comprises lactose, such as lactose monohydrate. In a specific example, the pharmaceutically acceptable excipient comprises magnesium stearate. In some specific examples, the pharmaceutically acceptable excipient is lactose monohydrate and magnesium stearate. Various suitable fillers or diluents include, but are not limited to, calcium carbonate (Barcroft™, MagGran™, Millicarb™, Pharma-Carb™, Precarb™, Sturcal™, Vivapres Ca™), calcium hydrogen phosphate anhydrous (Emcompress Anhydrous™, Fujicalin™), calcium hydrogen phosphate dihydrate (Calstar™, Di-Cafos™, Emcompress™), calcium phosphate (Tri-Cafos™, TRI-TAB™), calcium sulfate (Destab™, Drierite™, Snow White™, Cal-Tab™, Compactrol™), powdered cellulose (Arbocel™, Elcema™, Sanacet™), silicified microcrystalline cellulose, cellulose acetate, compressible sugar (Di-Pac™), powdered sugar, dextran binder (Candex™, Emdex™), dextrin (Avedex™, Caloreen™, Primogran W™), dextrose (Caridex™, Dextrofin™, Tab fine D-IOO™), fructose (Fructofin™, Krystar™), kaolin (Lion™, Sim 90™), lactitol (Finlac DC™, Finlac MCX™), lactose (Anhydrox™, CapsuLac™, Fast-Flo™, FlowLac™, GranuLac™, InhaLac™, Lactochem™, Lactohaie™, Lactopress™, Microfme™, Microtose™, Pharmatose™, Prisma Lac™, Respitose™, SacheLac™, SorboLac™, Super-Tab™, Tablettose™, Wyndale™, Zeparox™), lactose monohydrate, magnesium carbonate, magnesium oxide (MagGran MO™), maltodextrin (C*Dry MD™, Lycatab DSH™, Maldex™, Maitagran™, Maltrin™, Maltrin QD™, Paselli MD 10 PH™, Star-Dri™), maltose (Advantose 100™), mannitol (Mannogem™, Pearlitol™), microcrystalline cellulose (Avicel PH™, Celex™, Celphere™, Ceolus KG™, Emcocel™, Pharmacel™, Tabulose™, Vivapur™), polydextrose (Litesse™), polydimethylsiloxane (Dow CorningQ7-2243 LVA™, Cow Corning Q7-2587™, Sentry Simethicone™), sodium alginate (Keltone™, Protanal™), sodium chloride (Alberger™), sorbitol (Liponec 70-NC™, Liponic 76-NCv, Meritol™, Neosorb™, Sorbitol Instant™, Sorbogem™), starch (Flufiex W™, Instant Pure-Cote™, Melojei™, Meritena Paygel 55™, Perfectamyl D6PH™, Pure-Cote™, Pure-Dent™, Pure-Gel™, Pure-Set™, Purity 21™, Purity 826™, Tablet White™), pregelatinized starch, sucrose, trehalose, and xylitol, or a mixture thereof. In a specific example, the filler comprises lactose monohydrate. In a specific example, the composition comprises about 5-90% by weight of a filler, for example, the filler is present in an amount of about 10-80% by weight, about 15-70% by weight, about 20-60% by weight, or about 25-50% by weight. For example, the composition may comprise about 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, or 80% by weight of the filler. In a specific example, the composition comprises about 25 mg to about 1000 mg of the filler, for example, the filler is present in an amount of about 50 mg to about 750 mg, about 100 mg to about 600 mg, about 150 mg to about 500 mg, or about 200 mg to about 450 mg. For example, the composition may comprise about 250, 275, 300, 325, 350, 375, 400, 425, 450, 475, or 500 mg of the filler. Various applicable lubricants include, but are not limited to, calcium stearate (HyQual™), glycerol monostearate (Imwitor™ 191 and 900, Kessco GMS5™, 450 and 600, Myvaplex 600P™, Myvatex™, Rita GMS™, Stepan GMS™, Tegin™, Tegin™ 503 and 515, Tegin 4100™, Tegin M™, Unimate GMS™), glyceryl behenate (Compritol 888 ATO™), glyceryl palmitostearate (Precirol ATO 5™), hydrogenated castor oil (Castorwax MP 80™, Croduret™, Cutina HR™, Fancol™, Simulsol 1293™), hydrogenated vegetable oil type I 0 (Sterotex™, Dynasan P60™, Hydrocote™, Lipovol HS-K™, Sterotex HM™), magnesium lauryl sulfate, magnesium stearate, medium-chain triglycerides (Captex 300™, Labrafac CC™, Miglyol 810™, Neobee M5™, Nesatol™, Waglinol 3 / 9280™), poloxamer (Pluronic™, Synperonic™), polyethylene glycol (Carbowax Sentry™, Lipo™, Lipoxol™, Lutrol E™, Pluriol E™), sodium benzoate (Antimol™), sodium chloride, sodium lauryl sulfate (Elfan 240™, Texapon Kl 2P™), sodium stearyl fumarate (Pruv™), stearic acid (Hystrene™, industrene™, Kortacid 1895™, Pristerene™), talc (Altaic™, Luzenac™, Luzenac Pharma™, Magsil Osmanthus™, 0 Magsil Star™, Superiore™), sucrose stearate (Surfhope SE Pharma D-1803 F™), and zinc stearate (HyQual™), or mixtures thereof. Examples of suitable lubricants include, but are not limited to, magnesium stearate, calcium stearate, zinc stearate, stearic acid, talc, glyceryl behenate, polyethylene glycol, polyethylene oxide polymer, sodium lauryl sulfate, magnesium lauryl sulfate, sodium oleate, sodium stearyl fumarate, DL-leucine, colloidal silica. In a specific example, the lubricant comprises magnesium stearate. In a specific example, the composition comprises about 0.1 - 5% by weight of a lubricant. For example, the lubricant is present in an amount of about 0.2 - 2% by weight, about 0.3 - 1% by weight, about 0.4 - 0.75% by weight, or about 0.5 - 0.7% by weight. For instance, the composition may comprise about 0.3% by weight, 0.4% by weight, 0.5% by weight, 0.6% by weight, 0.7% by weight, or 0.8% by weight of the lubricant. In a specific example, the composition comprises about 0.01 mg to about 10 mg of the lubricant. For example, the lubricant is present in an amount of about 0.01 mg to 0.05 mg, 0.05 mg to 0.1 mg, 0.1 mg to 0.2 mg, 0.2 mg to 0.25 mg, 0.25 mg to 0.5 mg, 0.5 mg to 0.75 mg, 0.7 mg to 0.95 mg, 0.9 mg to 1.15 mg, 1.1 mg to 1.35 mg, 1.3 mg to 1.5 mg, 1.5 mg to 1.75 mg, 1.75 to 1.95 mg, 1.9 mg to 2.15 mg, 2.1 mg to 2.35 mg, 2.3 mg to 2.55 mg, 2.5 mg to 2.75 mg, 2.7 mg to 3.0 mg, 2.9 mg to 3.15 mg, 3.1 mg to 3.35 mg, 3.3 mg to 3.5 mg, 3.5 mg to 3.75 mg, 3.7 mg to 4.0 mg, 4.0 mg to 4.5 mg, 4.5 mg to 5.0 mg, 5.0 mg to 5.5 mg, 5.5 mg to 6.0 mg, 6.0 mg to 6.5 mg, 6.5 mg to 7.0 mg, 7.0 mg to 7.5 mg, 7.5 mg to 8.0 mg, 8.0 mg to 8.5 mg, 8.5 mg to 9.0 mg, 9.0 mg to 9.5 mg, or 9.5 mg to 10.0 mg. For instance, the composition may comprise about 0.01 mg, 0.05 mg, 0.1 mg, 0.2 mg, 0.25 mg, 0.5 mg, 0.7 mg, 0.9 mg, 1.1 mg, 1.3 mg, 1.5 mg, 1.7 mg, 1.9 mg, 2. mg, 2.3 mg, 2.5 mg, 2.75 mg, 3.0 mg, 3.1 mg, 3.3 mg, 3.5 mg, 3.7 mg, 4.0 mg, 4.5 mg, 5.0 mg, 5.5 mg, 6.0 mg, 6.5 mg, 7.0 mg, 7.5 mg, 8.0 mg, 8.5 mg, 9.0 mg, 9.5 mg, or 10.0 mg of the lubricant. Various suitable disintegrants include, but are not limited to, alginic acid (Protacid™, Satialgine H8™), calcium phosphate (TRI-TAB™), calcium carboxymethylcellulose (ECG 505™), sodium carboxymethylcellulose (Akucell™, Finnfix™, Nymcel Tylose CB™), colloidal silicon dioxide (Aerosil™, Cab-O-Sil™, Wacker HDK™), croscarmellose sodium (Ac-Di-Sol™, Pharmacel XL™, Primellose™, Solutab™, Vivasol™), crospovidone (Collison CL™, Collison CL-M™, Polyplasdone XL™), sodium docusate, guar gum (Meyprodor™, Meyprofm™, Meyproguar™), low-substituted hydroxypropyl cellulose, magnesium aluminum silicate (Magnabite™, Neusilin™, Pharmsorb™, Veegum™), methylcellulose (Methocel™, Metolose™), microcrystalline cellulose (Avicel PH™, Ceoius KG™, Emcoel™, Ethispheres™, Fibrocel™, Pharmacel™, Vivapur™), povidone (Collison™, Plasdone™), sodium alginate (Kelcosol™, Ketone™, Protanal™), sodium starch glycolate, polacrilin potassium (Amberlite IRP88™), siliconized microcrystalline cellulose (ProSotv™), starch (Aytex P™, Fluftex W™, Melojel™, Meritena™, Paygel 55™, Perfectamyl D6PH™, Pure-Bind™, Pure-Cote™, Pure-Dent™, Purity 21™, Purity 826™, Tablet White™) or pregelatinized starch (Lycatab PGS™, Merigel™, National 78-1551™, Pharma-Gel™, Prejel™, Sepistab ST 200™, Spress B820™, Starch 1500 G™, Tablitz™, Unipure LD™), or mixtures thereof. In a specific example, the composition comprises from about 0 to about 10% by weight of a disintegrant. Various applicable glidants include, but are not limited to, calcium phosphate (TRI-TAB™), calcium silicate, powdered cellulose (Sanacel™, Solka-Floe™), colloidal silica (Aerosil™, Cab-O-Sil M-5P™, Wacker HDK™), magnesium silicate, magnesium trisilicate, starch (Melojel™, Meritena™, Paygel 55™, Perfectamyl D6PH™, Pure-Bind™, Pure-Cote™, Pure-Dent™, Pure-Gel™, Pure-Set™, Purity 21™, Purity 826™, Tablet White™), and talc (Luzenac Pharma™, Magsil Osmanthus™, Magsil Star™, Superiore™), or mixtures thereof. In a specific example, the composition contains from about 0 to about 15% by weight of a glidant. Pharmaceutically acceptable surfactants include, but are not limited to, nonionic and ionic surfactants applicable to pharmaceutical dosage forms. Ionic surfactants can include one or more of anionic, cationic, or zwitterionic surfactants. Various applicable surfactants include, but are not limited to, sodium lauryl sulfate, monooleate, monolaurate, monopalmitate, monostearate, or another ester of polyoxyethylene sorbitan, dioctyl sodium sulfosuccinate, lecithin, stearyl alcohol, cetostearyl alcohol, cholesterol, polyoxyethylene castor oil, polyoxyethylene fatty acid glycerol esters, poloxamer, or any other commercially available co-processing surfactant, such as SEPITRAP® 80 or SEPITRAP® 4000, and mixtures thereof. In a specific example, the composition contains from about 0 to about 5% by weight of a surfactant. In a specific example, the solid pharmaceutical composition of the present invention contains the camphorate, mandelate, or camphorsulfonate of niraparib (such as the salts described herein), a diluent, and a lubricant. In a specific example, the solid pharmaceutical composition contains the camphorate, mandelate, or camphorsulfonate of niraparib (such as the crystalline salts described herein), lactose monohydrate, and magnesium stearate. In a specific example, the solid pharmaceutical composition of the present invention contains (by weight of the composition) from about 20 - 60% of the salt of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib), from about 20 - 80% of a diluent, and from about 0.1 - 5% of a lubricant. In a specific example, the pharmaceutical composition contains (by weight of the composition) from about 40 - 60% of the niraparib salt, from about 40 - 70% of a diluent (such as lactose monohydrate), and from about 0.2 - 2% of a lubricant (such as magnesium stearate). The pharmaceutical composition can be formulated using, for example, different proportions of hydroxypropyl methylcellulose to provide the desired release characteristics, other polymeric matrices, liposomes and / or microspheres to provide a slow, delayed or controlled release of the active ingredient therein. The pharmaceutical composition may also optionally contain opacifying agents and may be a composition that releases the active ingredient only or preferentially in a certain part of the gastrointestinal tract in a delayed manner, for example by using an enteric coating. Examples of embedding compositions include polymeric materials and waxes. When appropriate, the active ingredient may also be in the form of microencapsulation with one or more pharmaceutically acceptable carriers, excipients or diluents well known in the art (see, for example, Remington’s). The compounds of the present invention can be formulated for sustained delivery according to methods well known to those of ordinary skill in the art. Examples of such formulations can be found in U.S. Patents 3,119,742; 3,492,397; 3,538,214; 4,060,598; and 4,173,626. Synthesis The salts of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) of the present invention can be prepared, for example, from niraparib free base by slurrying the niraparib free base in the presence of a suitable acid. The niraparib salts of the present invention can be prepared in crystalline form. Various techniques can be used to obtain the salts in crystalline form. These techniques include, for example, preparation from a solvent system by solvent evaporation, cooling and / or addition of one or more antisolvents (such as TBME). These techniques can also include heating the salt, for example, near or above its melting point and then cooling. Solution crystallization can be carried out with or without seeding. Exemplary solvents for preparing the crystalline salts of niraparib disclosed herein include acetone, acetonitrile, ethanol, ethyl acetate, methanol, THF and mixtures thereof. In some cases, the crystalline salts of the present invention can be obtained by recrystallization from an organic solvent such as methanol. Methods for preparing the niraparib salts (including crystalline salts) of the present invention are shown in the following examples. Alternative methods for preparing the niraparib salts and their crystalline forms of the present invention will be apparent to those of ordinary skill in the art in light of their common general knowledge and the teachings of this application. For example, those of ordinary skill in the art will understand that the amorphous form of the niraparib salts of the present invention can be obtained by, for example, spray drying a solution of the appropriate salt. Medical Indications The 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salts and pharmaceutical compositions described herein are suitable for use in therapy, particularly for the therapeutic treatment of PARP-1 and PARP-2 mediated conditions in an individual. Methods for treating PARP-1 and PARP-2 mediated conditions are described in WO 2018 / 005818. In certain embodiments, the niraparib salts described herein may provide improved therapeutic benefits compared to administering different forms of niraparib (such as crystalline niraparib tosylate monohydrate). In embodiments, the improved therapeutic benefits may be a change (such as a decrease) in the incidence and / or severity of undesirable side effects observed with different forms of niraparib. In embodiments, the undesirable side effects are thrombocytopenia, anemia, neutropenia, leukopenia, palpitations, nausea, constipation, vomiting, abdominal pain / distension, mucositis / stomatitis, diarrhea, dyspepsia, dry mouth, fatigue / asthenia, decreased appetite, urinary tract infection, elevated AST / ALT, myalgia, back pain, joint pain, headache, dizziness, taste disorder, insomnia, anxiety, nasopharyngitis, dyspnea, cough, rash, or hypertension. In embodiments, the undesirable side effects are hematological side effects (such as thrombocytopenia, anemia, neutropenia, or leukopenia). In embodiments, the undesirable side effects are non-hematological side effects. In embodiments, the undesirable side effects are cardiovascular effects (such as palpitations). In embodiments, the undesirable side effects are gastrointestinal disorders (such as nausea, constipation, vomiting, abdominal pain / distension, mucositis / stomatitis, diarrhea, dyspepsia, or dry mouth). In embodiments, the undesirable side effects are fatigue or asthenia. In embodiments, the undesirable side effects are metabolic or nutritional disorders (such as decreased appetite). In embodiments, the undesirable side effects are infections or contagions (such as urinary tract infection). In embodiments, the undesirable side effects are elevated AST / ALT. In embodiments, the undesirable side effects are musculoskeletal or connective tissue disorders (such as myalgia, back pain, joint pain). In embodiments, the undesirable side effects are neurological disorders (headache, dizziness, or taste disorder). In embodiments, the undesirable side effects are psychiatric disorders (such as insomnia or anxiety). In embodiments, the undesirable side effects are respiratory, thoracic, or mediastinal disorders (such as nasopharyngitis, dyspnea, or cough). In embodiments, the undesirable side effects are skin or subcutaneous tissue disorders (such as rash). In embodiments, the undesirable side effects are vascular disorders (such as hypertension). In embodiments, the undesirable side effects are myelodysplastic syndrome / acute myeloid leukemia. In embodiments, the undesirable side effects are myelosuppression. Individuals to be treated according to the methods described herein include vertebrates such as mammals. In preferred embodiments, the mammal is a human patient. In one aspect, the invention provides the camphorate, mandelate, or camphorsulfonate of niraparib (such as the salts described herein) for use in therapy. Also provided is the use of the camphorate, mandelate, or camphorsulfonate of niraparib (such as the salts described herein) for the manufacture of a medicament. In another aspect, the present invention provides a method for treating cancer, stroke, autoimmune diabetes, neurological disease, inflammatory disease, metabolic disease or cardiovascular disease in an individual, the method comprising administering to the individual an effective amount of the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein). Also provided are the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein) for use in a method of treating cancer, stroke, autoimmune diabetes, neurological disease, inflammatory disease, metabolic disease or cardiovascular disease. Further provided is the use of the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein) for the manufacture of a medicament for use in a method of treating cancer, stroke, autoimmune diabetes, neurological disease, inflammatory disease, metabolic disease or cardiovascular disease. In another aspect, the present invention provides a method for treating PARP-1 and / or PARP-2 mediated conditions in an individual, the method comprising administering to the individual an effective amount of the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein). Also provided are the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein) for use in a method of treating PARP-1 and / or PARP-2 mediated conditions. Further provided is the use of the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein) for the manufacture of a medicament for use in a method of treating PARP-1 and / or PARP-2 mediated conditions. Tumor conditions ( Cancer ) PARP inhibitors have demonstrated activity as monotherapy against tumors with existing DNA repair defects such as BRCA1 and BRCA2 and as combination therapy when co-administered with anti-cancer agents that induce DNA damage. Despite some progress in the treatment of ovarian cancer, most patients ultimately relapse and the subsequent response to additional treatment is usually of limited duration. Women with germline BRCA1 or BRCA2 mutations have an increased risk of developing high grade serous ovarian cancer (HGSOC), and their tumors appear to be particularly sensitive to treatment with PARP inhibitors. Additionally, published scientific literature has shown that patients with platinum-sensitive HGSOC who do not have germline BRCA1 or BRCA2 mutations may also derive clinical benefit from PARP inhibitor treatment. Because PARP inhibitors block DNA repair, in cancer cells having In the case of BRCA mutations, PARP inhibition causes synthetic lethality. For this reason, patients with germline mutations in the BRCA gene show significant clinical benefit after treatment with PARP inhibitors. In one embodiment, the condition to be treated is cancer, especially related to DNA repair defects, such as those related to BRCA1 and / or BRCA2 mutations. In an embodiment, the cancer is a recurrent cancer. In an embodiment, the cancer is breast cancer, ovarian cancer, cervical cancer, epithelial ovarian cancer, fallopian tube cancer, primary peritoneal cancer, endometrial cancer, prostate cancer, testicular cancer, pancreatic cancer, esophageal cancer, head and neck cancer, gastric cancer, bladder cancer, lung cancer (such as adenocarcinoma, NSCLC and SCLC), bone cancer (such as osteosarcoma), colon cancer, rectal cancer, thyroid cancer, brain and central nervous system cancer, glioblastoma, neuroblastoma, neuroendocrine cancer, rhabdoid cancer, keratoacanthoma, epidermoid cancer, seminoma, melanoma, sarcoma (such as liposarcoma), bladder cancer, liver cancer (such as hepatocellular carcinoma), renal cancer (such as renal cell carcinoma), myeloid disorders (such as AML, CML, myelodysplastic syndrome and promyelocytic leukemia) and lymphoid disorders (such as leukemia, multiple myeloma, mantle cell lymphoma, ALL, CLL, B-cell lymphoma, T-cell lymphoma, Hodgkin's lymphoma, non-Hodgkin's lymphoma, hairy cell lymphoma), which can be treated with the compounds and methods described herein. The cancer can be selected from head and neck cancer, breast cancer (such as metastatic breast cancer), prostate cancer (such as metastatic prostate cancer), testicular cancer, ovarian cancer, endometrial cancer, colon cancer, rectal cancer, lung cancer (such as non-small cell lung cancer), bladder cancer, pancreatic cancer (such as metastatic pancreatic cancer), brain and central nervous system cancer (such as primary malignant brain tumor), neuroendocrine cancer, rhabdoid cancer, gynecological cancer, peritoneal cancer, skin cancer, thyroid cancer, esophageal cancer, cervical cancer, gastric cancer, liver cancer, gastric cancer, renal cell carcinoma, cholangiocarcinoma, blood cancer, bone cancer and blood cancer. In an embodiment, the cancer is selected from colorectal cancer, colon cancer, head and neck cancer, seminoma, sarcoma, lung cancer, lung adenocarcinoma, bladder cancer, Barrett's adenocarcinoma, renal cancer, epidermoid cancer and liver cancer. In an embodiment, the cancer is selected from glioblastoma, astrocytoma, melanoma (such as metastatic melanoma), mesothelioma, myeloma, keratoacanthoma, neuroblastoma, histiocytic lymphoma and lymphocytic leukemia. In an embodiment, the cancer is a solid tumor (such as a malignant solid tumor), which can be an advanced solid tumor. In a specific example, the cancer is a gynecological cancer, such as selected from ovarian cancer, cancer of the fallopian tube, peritoneal cancer, and breast cancer. In some specific examples, the gynecological cancer is related to HRD and / or BRCA1 / 2 mutations. In some specific examples, the gynecological cancer is platinum-sensitive. In other specific examples, the gynecological cancer is not platinum-sensitive. In a specific example, the gynecological cancer previously had (e.g., partial or complete) response to platinum-based therapy but later developed drug resistance to platinum-based therapy. In a specific example, the cancer is ovarian cancer (e.g., epithelial ovarian cancer), cancer of the fallopian tube, or peritoneal cancer (e.g., primary peritoneal cancer). In other specific examples, the cancer is breast cancer. In some specific examples, the method of the present invention treats an individual with ovarian cancer. In some specific examples, the method of the present invention treats an individual with epithelial ovarian cancer. In some specific examples, the method of the present invention treats an individual with fallopian tube cancer. In some specific examples, the method of the present invention treats an individual with primary peritoneal cancer. In some specific examples, the method of the present invention treats an individual with recurrent ovarian cancer. In some specific examples, the method of the present invention treats an individual with recurrent epithelial ovarian cancer. In some specific examples, the method of the present invention treats an individual with recurrent fallopian tube cancer. In some specific examples, the method of the present invention treats an individual with recurrent primary peritoneal cancer. In some specific examples, the method of the present invention treats an individual with recurrent ovarian cancer after having a complete or partial response to chemotherapy (such as platinum-based chemotherapy). In some specific examples, the method of the present invention treats an individual with recurrent epithelial ovarian cancer after having a complete or partial response to chemotherapy (such as platinum-based chemotherapy). In some specific examples, the method of the present invention treats an individual with recurrent fallopian tube cancer after having a complete or partial response to chemotherapy (such as platinum-based chemotherapy). In some specific examples, the method of the present invention treats an individual with recurrent primary peritoneal cancer after having a complete or partial response to chemotherapy (such as platinum-based chemotherapy). In some embodiments, the methods of the invention treat individuals with recurrent ovarian cancer, recurrent epithelial ovarian cancer, recurrent fallopian tube cancer, and / or recurrent primary peritoneal cancer after a complete or partial response to platinum-based chemotherapy, wherein the individuals begin treatment no later than 8 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 7 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 6 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 6 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 5 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 4 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 3 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 2 weeks after their most recent platinum-containing treatment course. For example, an individual may begin treatment with niraparib about 1 week after their most recent platinum-containing treatment course. In embodiments, the method treats cancer in individuals exhibiting a positive HRD status. In some embodiments, an additional characteristic of the individual is the absence of BRCA1 and / or mutations in BRCA2. A positive HRD status can be determined by quantifying the number of chromosomal aberration regions indicated in a patient sample. In some embodiments, a tumor sample from an individual has a positive HRD status. In other embodiments, the method treats cancer in individuals exhibiting absence of HRD, such as individuals with platinum-sensitive recurrent ovarian cancer. The characteristic of absence of HRD can be the lack of chromosomal aberrations (detectable changes in chromosomal DNA that can belong to at least one of three overlapping categories: loss of heterozygosity, allelic imbalance (such as telomeric allelic imbalance), or large-scale transitions). In embodiments, the methods described herein treat cancer associated with a defect in at least one gene involved in a DNA repair pathway. There are various pathways for DNA repair, including base excision repair (BER), direct repair (DR), double-strand break (DSB) repair, homologous recombination repair (HRR), mismatch repair (MMR), nucleotide excision repair (NER), and non-homologous end joining (NHEJ) repair; disruption of these pathways can lead to the development and / or growth of cancer. See, for example, Kelley et al., Future Oncol., 10(7):1215-1237, 2014. Exemplary genes involved in DNA repair pathways are described in Table A. Table A. DNA Repair Genes In a specific example, the method treatment shows the absence of BRCA1 and germline mutations of BRCA2 in individuals with cancer. In some specific examples, the method treatment shows the absence of BRCA1 and germline mutations of BRCA2 in individuals with platinum-sensitive tumors having cancer. In one aspect, the present invention is characterized by a method for treating cancer, which comprises: identifying a cancer patient with a defect in at least one of the genes listed in Table A. In a specific example, the method treatment described herein is not related to treating cancer associated with a defect in at least one gene involved in the homologous recombination repair (HRR) pathway. In a specific example, the defect is non-BRCA defect. In a specific example, the defect is in two or more, three or more, four or more, five or more, six or more, seven or more, eight or more, nine or more, ten or more, eleven or more, twelve or more, thirteen or more, fourteen or more, fifteen or more, sixteen or more, seventeen or more, eighteen or more, nineteen or more, twenty or more, twenty-one or more, twenty-two or more, twenty-three or more, twenty-four or more, twenty-five or more, twenty-six or more, twenty-seven or more, twenty-eight or more, twenty-nine or more or thirty or more genes selected from the group consisting of: RFC2, XRCC6, POLD2, PCNA, RPA1, RPA2, ERCC3, UNG, ERCC5, MLH1, LIG1, MSH6, POLD4, RFC5, DDB2 / / / LHX3, POLD1, FANCG, POLB, XRCC1, MPG, ERCC1, TDG、 FANCA、 RFC4、 RFC3、 APEX2、 RAD1、 EXO1、 FEN1、 MLH3、 MGMT、 RAD51、 XRCC4、 RECQL、 ERCC8、 FANCC、 OGG1、 MRE11A、 RAD52、 WRN、 XPA、 BLM、 MSH3、 POLE2、 RAD51C、 LIG4、 ERCC6、 LIG3、 RAD17、 XRCC2、 MUTYH、 RFC1、 RAD50、 DDB1、 XRCC5、 PARP1、 POLE3、 XPC、 MSH2、 RPA3、 MBD4、 NTHL1、 PMS2 / / / PMS2CL、 UNG2、 APEX1、 ERCC4、 RECQL5、 MSH5、 POLD3、 ERCC2、 RECQL4, PMS1, ZFP276, POLE, XRCC3, NBN, SMUG1, FANCF, NEIL1, FANCE, ATM, ATR, BAP1, BARD1, BRIP1, PALB2, RAD51B, RAD51D and RAD54L. In a specific example, cancer patients with HRR defects attributable to at least one of the sixteen genes listed in Table B may benefit from the methods described herein. Table B. Non- BRCA1 / 2 HRR pathway genes In a specific example, defects in genes involved in the HRR pathway are identified using a pre-specified gene set. In a specific example, the pre-specified gene panel includes the genes listed in Table A or Table B or any combination thereof. In a specific example, the pre-specified gene panel comprises: ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L and XRCC2 and at least one of any combination thereof; and BRCA1 and At least one of BRCA2. In a specific example, the pre-specified gene panel comprises: ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L and each of XRCC2; and BRCA1 and at least one of BRCA2. In a specific example, the pre-specified gene panel comprises ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L, XRCC2, BRCA1 and BRCA2. In a specific example, the method is monotherapy. In other specific examples, the method is combination therapy. In a specific example, the method is a combination therapy, in which the administration of the camphorate, mandelate or camphorsulfonate of niraparib (such as the salts described herein) is combined with a second therapy that induces DNA damage. In a specific example, the second therapy includes radiosensitization (administration of ionizing radiation) and / or chemosensitization (administration of one or more DNA-damaging agents). The DNA-damaging agent can be selected, for example, from DNA methylating agents (such as, for example, dacarbazine or temozolomide), topoisomerase I inhibitors (such as, for example, camptothecin, topotecan or irinotecan), and cytotoxic agents (such as, for example, platinum-based drugs, such as cisplatin or carboplatin). The administration of the niraparib salt can be carried out before, during and / or after the second therapy. The therapy of such combination therapy can be easily determined by a clinician. Non-oncological conditions In a specific example, the method of the present invention is used to treat a condition of an individual selected from neurological or neurodegenerative diseases, inflammatory diseases, metabolic diseases, and cardiovascular diseases or conditions. Examples of such diseases are described by Curtin et al. ( Mol Aspects Med. (2013) 34(6):1217-1256). In one specific example, the method treats an individual suffering from a stroke or at risk of suffering from a stroke. In another specific example, the method treats an individual suffering from traumatic brain injury. In another specific example, the method treats an individual suffering from autoimmune diabetes or at risk of suffering from autoimmune diabetes. In a specific example, the neurodegenerative disease is Parkinson's disease. In a specific example, the inflammatory disease is asthma or multiple sclerosis. In a specific example, the cardiovascular disease or condition is myocardial infarction, circulatory shock, multiple injuries or acute respiratory distress syndrome. Administration and dosage The 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salts as described herein can be formulated into pharmaceutical compositions for oral, buccal, parenteral (e.g., intravenous, intraperitoneal, intramuscular or subcutaneous), topical, rectal or intranasal administration or in a form suitable for administration by inhalation or insufflation. Such modes of administration and methods of preparing suitable pharmaceutical compositions are described, for example, in Gibaldi’s Drug Delivery Systems in Pharmaceutical Care (1st Edition, American Society of 15 Health-System Pharmacists 2007). In a specific example, an exemplary dosing regimen for niraparib is to orally receive one or more 100 mg doses once daily (e.g., two doses equivalent to a total daily dose of 200 mg or three doses equivalent to a total daily dose of 300 mg). Patients can be encouraged to take their doses at approximately the same time each day. Bedtime dosing can be a potential method for controlling nausea. In some embodiments, the method of the present invention treats an individual suffering from cancer with niraparib or a pharmaceutically acceptable salt thereof at a dose of 1 mg, 5 mg, 10 mg, 20 mg, 25 mg, 35 mg, 50 mg, 75 mg, 100 mg, 125 mg, 150 mg, 175 mg, 200 mg, 225 mg, 250 mg to 275 mg, 300 mg, 325 mg, 350 mg 375 mg, 400 mg, 425 mg, 450 mg, 475 mg, 500 mg, 550 mg, 600 mg, 650 mg, 700 mg, 750 mg, 800 mg, 850 mg, 900 mg, 950 mg, 1000 mg, 1050 mg, 1100 mg, 1150 mg, 1200 mg, 1250 mg, 1300 mg, 1350 mg, 1400 mg, 1450 mg, 1500 mg, 1550 mg, 1600 mg, 1650 mg, 1700 mg, 1750 mg, 1800 mg, 1850 mg, 1900 mg, 1950 mg or 2000 mg once a day, twice a day or three times a day. In some embodiments, the method of the present invention treats an individual suffering from cancer with niraparib or a pharmaceutically acceptable salt thereof at a dose of 150 mg to 175 mg, 170 mg to 195 mg, 190 mg to 215 mg, 210 mg to 235 mg, 230 mg to 255 mg, 250 mg to 275 mg, 270 to 295 mg, 290 mg to 315 mg, 310 mg to 335 mg, 330 mg to 355 mg, 350 mg to 375 mg or 370 mg to 400 mg once a day, twice a day or three times a day. In some embodiments, the method of the present invention treats an individual suffering from cancer with niraparib or a pharmaceutically acceptable salt thereof at a dose of 5 mg, 7.5 mg, 10 mg, 12.5 mg, 15 mg, 17.5 mg, 20 mg, 22.5 mg, 25 mg, 27.5 mg, 30 mg, 35 mg, 40 mg, 45 mg, 50 mg, 55 mg, 60 mg, 65 mg, 70 mg, 75 mg, 80 mg, 85 mg, 90 mg, 95 mg or 100 mg once a day, twice a day or three times a day. In some specific examples, the method of the present invention uses niraparib or a pharmaceutically acceptable salt thereof at a dose of about 1 mg to 5 mg, 5 mg to 10 mg, 10 mg to 20 mg, 20 mg to 25 mg, 35 mg to 50 mg, 50 mg to 75 mg, 70 mg to 95 mg, 90 mg to 115 mg, 110 mg to 135 mg, 130 mg to 155 mg, 150 mg to 175 mg, 170 to 195 mg, 190 mg to 215 mg, 210 mg to 235 mg, 230 mg to 255 mg, 250 mg to 275 mg, 270 mg to 300 mg, 290 mg to 315 mg, 310 mg to 335 mg, 330 mg to 355 mg, 350 mg to 375 mg, 370 mg to 400 mg, 400 mg to 450 mg, 450 mg to 500 mg, 500 mg to 550 mg, 550 mg to 600 mg, 600 mg to 650 mg, 650 mg to 700 mg, 700 mg to 750 mg, 750 mg to 800 mg, 800 mg to 850 mg, 850 mg to 900 mg, 900 mg to 950 mg, 950 mg to 1000 mg, 1000 mg to 1050 mg, 1050 mg to 1100 mg, 1100 mg to 1150 mg, 1150 mg to 1200 mg, 1200 mg to about 1250 mg, 1250 mg to 1300 mg, 1300 mg to 1350 mg, 1350 mg to 1400 mg, 1400 mg to 1450 mg, 1450 mg to 1500 mg, 1500 mg to 1550 mg, 1550 mg to 1600 mg, 1600 mg to 1650 mg, 1650 mg to 1700 mg, 1700 mg to 1750 mg, 1750 mg to 1800 mg, 1800 mg to 1850 mg, 1850 mg to 1900 mg, 1900 mg to 1950 mg or 1950 mg to 2000 mg once a day, twice a day or three times a day to treat an individual suffering from cancer.In some specific examples, the method of the present invention uses niraparib or a pharmaceutically acceptable salt thereof at a dose of about 5 mg to 7.5 mg, 7 mg to 9.5 mg, 9 mg to 11.5 mg, 11 mg to 13.5 mg, 13 mg to 15.5 mg, 15 mg to 17.5 mg, 17 to 19.5 mg, 19 mg to 21.5 mg, 21 mg to 23 / 5 mg, 23 mg to 25.5 mg, 25 mg to 27.5 mg, 27 mg to 30 mg, 30 mg to 35 mg, 35 mg to 40 mg, 40 mg to 45 mg, 45 mg to 50 mg, 50 mg to 55 mg, 55 mg to 60 mg, 60 to 65 mg, 65 mg to 70 mg, 70 mg to 75 mg, 75 mg to 80 mg, 80 mg to 85 mg, 85 mg to 90 mg, 90 mg to 95 mg or 95 mg to 100 mg once, twice or three times a day to treat an individual suffering from cancer. In a preferred specific example, the niraparib salt is formulated for oral administration, for example, in solid form. In a preferred specific example, the pharmaceutical composition is an oral composition, more preferably a solid oral dosage form, such as, for example, tablets, capsules, powders, granules or sachets. The oral composition can be provided in unit dosage form, wherein one or more of each unit dosage are combined to provide an effective amount for administration to an individual. In solid dosage forms for oral administration (such as capsules, tablets, pills, dragees, powders, granules and the like), the active ingredient is mixed with one or more pharmaceutically acceptable excipients as described herein. In the case of capsules, tablets and pills, the pharmaceutical composition may also contain buffering agents. Solid compositions of a similar type can also be prepared using fillers and excipients (such as lactose or milk sugar), as well as high molecular weight polyethylene glycols and the like in soft and hard gelatin capsules. As an example of a pharmaceutical composition provided in capsule form, the composition may contain one or more components that are combined to produce a powder blend for filling the capsule. For example, the powder blend can be filled into a gelatin capsule, such as a size 0 gelatin capsule. In such cases, the term "pharmaceutical composition" should generally be understood to refer to the contents of the capsule, i.e., the powder blend. Tablets can be manufactured by compression or molding, optionally with one or more accessory ingredients. Compressed tablets can be prepared using binders (such as gelatin or hydroxypropyl methylcellulose), lubricants, inert diluents, preservatives, disintegrants (such as sodium starch glycolate or croscarmellose sodium), surfactants, and / or dispersants. Molded tablets can be manufactured by molding a mixture of powdered active ingredients moistened with an inert liquid diluent in a suitable machine. Tablets and other solid dosage forms such as dragees, capsules, pills, and granules can be optionally scored or prepared with coatings and shells, such as enteric coatings and other coatings well known in the art. In embodiments, solid dosage forms for administering a therapeutically effective amount of niraparib to an individual comprise from about 1 mg to about 1000 mg of niraparib salt (calculated as the weight of the niraparib free base equivalent in the salt). In embodiments, the solid dosage form comprises from about 25 mg to about 750 mg of niraparib salt, such as from about 50 mg to about 500 mg, from about 60 mg to about 400 mg, or from about 75 mg to about 300 mg (calculated as the weight of the niraparib free base equivalent in the salt). In other embodiments, the solid dosage form comprises from about 50 to about 300 mg of niraparib salt (calculated as the weight of the niraparib free base equivalent in the salt). In embodiments, the solid dosage form comprises about 50 mg, 75 mg, 100 mg, 125 mg, 150 mg, 175 mg, 200 mg, 225 mg, 250 mg, 275 mg, 300 mg, 325 mg, or 350 mg of niraparib salt (calculated as the weight of the niraparib free base equivalent in the salt). In embodiments, solid dosage forms for administering a therapeutically effective amount of niraparib to an individual comprise greater than about 100 mg of niraparib salt (calculated as the weight of the niraparib free base equivalent in the salt). In embodiments, the solid dosage form comprises greater than about 120 mg, 140 mg, 160 mg, 180 mg, 200 mg, 220 mg, 240 mg, 260 mg, or 280 mg of niraparib salt (calculated as the weight of the niraparib free base equivalent in the salt). In a specific example, the solid dosage form presents as one, two or three unit doses. In a specific example, the solid oral dosage form is administered once, twice or three times a day so as to use a therapeutically effective amount of niraparib in the methods as described herein. In a preferred specific example, the solid dosage form presents as a single unit dose administered once a day, that is, it provides a therapeutically effective daily dose of niraparib (such as, for example, the amount of the salt corresponding to about 300 mg of niraparib free base). In another preferred specific example, the solid dosage form presents as two unit doses administered together or individually, that is, they cooperate to provide a therapeutically effective daily dose of niraparib (such as, for example, about 150 mg per unit dose). In another preferred specific example, the solid dosage form presents as three unit doses administered together or individually, that is, they cooperate to provide a therapeutically effective daily dose of niraparib (such as, for example, about 100 mg per unit dose). For buccal administration, the composition can be in the form of a tablet or a lozenge formulated in a conventional manner. In some specific examples, the pharmaceutical composition is administered by non-oral means, such as by topical application, transdermal application, injection and similar means. In related specific examples, the pharmaceutical composition is administered by injection, infusion or implantation (such as intravenous, intramuscular, intra-arterial, subcutaneous and the like) rather than enterally. In each case, the pharmaceutical composition is preferably stored and / or used in solid form in order to utilize the properties of the niraparib salt. The pharmaceutical composition can be suitable for preparing an injectable formulation for parenteral administration (including using conventional catheterization techniques or infusion). The injectable formulation can be presented in unit dosage forms, for example in ampoules or multi-dose containers, with added preservatives. The composition can take the form of a suspension or an emulsion in an oily or aqueous vehicle, and can contain formulating agents, such as suspending, stabilizing and / or dispersing agents recognized by those skilled in the art. Alternatively, the active ingredient can be in powder form for reconstitution with a suitable vehicle (such as sterile pyrogen-free water) before use. The pharmaceutical composition is suitable for preparing a sterile injectable formulation. Such formulations can be sterilized, for example, by filtration through a bacteria-retaining filter or by incorporating a sterilizing agent in the form of a sterile solid composition, which can be dissolved in sterile water or some other sterile injectable medium immediately before use. To prepare such compositions, the active ingredient is dissolved or suspended in a parenterally acceptable liquid vehicle. Exemplary vehicles and solvents include, but are not limited to, water, water adjusted to a suitable pH by adding a suitable amount of hydrochloric acid, sodium hydroxide, or a suitable buffer, 1,3-butanediol, Ringer's solution, and isotonic sodium chloride solution. The pharmaceutical composition may also contain one or more preservatives, such as methylparaben, ethylparaben, or propylparaben. To improve solubility, a solubilizing enhancer or solubilizer may be added or the solvent may contain 10 - 60% w / w of propylene glycol or the like. The pharmaceutical composition may contain one or more pharmaceutically acceptable sterile isotonic aqueous or non-aqueous solutions, dispersions, suspensions, or emulsions, or sterile powders that can be reconstituted into a sterile injectable solution or dispersion only immediately before use. Such pharmaceutical compositions may contain antioxidants; buffers; bacteriostatic agents; solutes to render the formulation isotonic with the blood of a given recipient; suspending agents; thickening agents; preservatives; and the like. Examples of suitable aqueous and non-aqueous carriers that can be used in the pharmaceutical composition of the present invention include water, ethanol, polyols (such as glycerol, propylene glycol, polyethylene glycol, and the like) and suitable mixtures thereof, vegetable oils (such as olive oil), and injectable organic esters (such as ethyl oleate). Suitable fluidity can be maintained, for example, by using coating materials (such as lecithin), by maintaining the required particle size in the case of a dispersion, and by using surfactants. In some embodiments, to prolong the action of the active ingredient, it is necessary to slow the absorption of the compound from a subcutaneous or intramuscular injection. This can be achieved by using a liquid suspension of a crystalline material having poor water solubility. The absorption rate of the active ingredient depends on its dissolution rate, which in turn depends on the crystal size and crystal form. Alternatively, the absorption of the parenterally administered active ingredient is delayed by dissolving or suspending the compound in an oily vehicle. Additionally, prolonged absorption of the injectable pharmaceutical form can be achieved by including absorption delaying agents (such as aluminum monostearate and gelatin). Controlled-release parenteral compositions can be in the form of aqueous suspensions, microspheres, microcapsules, magnetic microspheres, oil solutions, oil suspensions, emulsions, or the active ingredient can be incorporated into biocompatible carriers, liposomes, nanoparticles, implants or infusion devices. Materials for preparing microspheres and / or microcapsules include, but are not limited to, biodegradable / biodegradable polymers such as polysaccharides, poly(isobutyl cyanoacrylate), poly(2-hydroxyethyl-L-glutamic acid) and poly(lactic acid). Biocompatible carriers that can be used in formulating controlled-release parenteral formulations include carbohydrates (such as dextran), proteins (such as albumin, lipoprotein or antibody). Materials for implants can be non-biodegradable, such as polydimethylsiloxane, or biodegradable, such as poly(caprolactone), poly(lactic acid), poly(glycolic acid) or poly(orthoester). For topical administration, the niraparib salt can be formulated into an ointment or cream. The niraparib salt can also be formulated in the form of a rectal composition, such as a suppository or a retention enema, for example containing a conventional suppository base such as cocoa butter or other glycerides. For intranasal administration or administration by inhalation, the niraparib salt is preferably presented in the form of a solution or suspension from a pump spray container that is squeezed or pumped by the patient or as an aerosol spray from a pressurized container or nebulizer, in the presence of a suitable propellant such as dichlorodifluoromethane, trichlorofluoromethane, dichlorotetrafluoroethane, carbon dioxide or other suitable gas. In the case of a pressurized aerosol, the dosage unit can be determined by a valve that provides a metered amount of delivery. The pressurized container or nebulizer can contain a solution or suspension. Capsules and cartridges (e.g., made of gelatin) for inhalers or insufflators can be formulated to contain a powder mixture of the niraparib salt and a suitable powder base such as lactose or starch. In other aspects, the present invention provides a dosage form or pharmaceutical composition as described herein for use in therapy, for example in a method as defined herein. In other aspects, the present invention provides a product (such as a kit) comprising a plurality of unit doses of a pharmaceutical composition as described herein in a sealed container having written instructions for use. In a specific example, the product further comprises an induction seal, a desiccant or a combination thereof. Combination therapy The crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salt described herein can be suitably used as a monotherapy or in combination therapy with the administration of one or more additional therapeutic agents or treatment lines. For example, the crystalline forms of the 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salts described herein can be administered in combination with surgery, radiotherapy, chemotherapy, immunotherapy, anti-angiogenic agents, or anti-inflammatory agents. In the case where a crystalline form of a 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salt is administered in combination with one or more different therapeutic agents (such as those described herein), the administration of the crystalline form of the niraparib salt can be sequential with the administration of the one or more different therapeutic agents. For example, the administration of the crystalline form of the niraparib salt is carried out before the administration of the one or more different therapeutic agents. In a specific example, the administration of the niraparib tablet composition is carried out after the administration of the one or more different therapeutic agents. In other specific examples, the administration of the crystalline form of the niraparib salt is carried out simultaneously with the administration of the one or more different therapeutic agents. In a specific example, a crystalline form of the niraparib salt described herein is administered in combination with one or more immune checkpoint inhibitors. In a specific example, the checkpoint inhibitor is an agent capable of inhibiting any one of the following: PD-1 (e.g., inhibited via anti-PD-1, anti-PD-L1, or anti-PD-L2 therapy), CTLA-4, TIM-3, TIGIT, LAG (e.g., LAG-3), CEACAM (e.g., CEACAM-1, -3, and / or -5), VISTA, BTLA, LAIR1, CD160, 2B4, CD80, CD86, B7-H3 (CD276), B7-H4 (VTCN1), HVEM (TNFRSF14 or CD270), KIR, A2aR, MHC class I, MHC class II, GALS, adenosine, TGFR (e.g., TGFRβ), B7-H1, B7-H4 (VTCN1), OX-40, CD137, CD40, IDO, or CSF-1R. In a specific example, the checkpoint inhibitor is a small molecule, nucleic acid, polypeptide (e.g., antibody), carbohydrate, lipid, metal, or toxin. In a specific example, the checkpoint inhibitor is an antibody, antibody conjugate, or antigen-binding fragment thereof. In a specific example, the immune checkpoint inhibitor is a PD-1 inhibitor. In a specific example, the PD-1 inhibitor is a small molecule, nucleic acid, polypeptide (such as an antibody, antibody conjugate or antigen-binding fragment thereof), carbohydrate, lipid, metal or toxin. In a specific example, the PD-1 inhibitor is a PD-1 binder (such as an antibody, antibody conjugate or antigen-binding fragment thereof). In a specific example, the PD-1 binder is an antibody, antibody conjugate or antigen-binding fragment thereof. In a specific example, the PD-1 binder is TSR-042, nivolumab, pembrolizumab, atezolizumab, durvalumab, avelumab, PDR-001, tislelizumab (BGB-A317), cemiplimab (REGN2810), LY-3300054, JNJ-63723283, MGA012, BI-754091, IBI-308, camrelizumab (HR-301210), BCD-100, JS-001, CX-072, BGB-A333, AMP-514 (MEDI-0680), AGEN-2034, CS1001, Sym-021, SHR-1316, PF-06801591, LZM009, KN-035, AB122, genolimzumab (CBT-501), FAZ-053, CK-301, AK 104 or GLS-010. In a specific example, the PD-1 inhibitor is a PD-L1 or PD-L2 binder, such as durvalumab, atezolizumab, avelumab, BGB-A333, SHR-1316, FAZ-053, CK-301 or a PD-L1 millamolecule, or a derivative thereof. In a specific example, the anti-PD-1 agent is pembrolizumab. In a specific example, the anti-PD-1 agent is nivolumab. In some specific examples, the PD-1 antibody agent is disclosed in International Patent Application Publication Nos. WO2014 / 179664, WO 2018 / 085468 or WO 2018 / 129559. In other specific examples, the PD-1 antibody agent is administered according to the methods disclosed in International Patent Application Publication Nos. WO2014 / 179664, WO 2018 / 085468 or WO 2018 / 129559. In a specific example, the anti-PD-1 agent is TSR-042. In a specific example, the immune checkpoint inhibitor is a TIM-3 inhibitor. In a specific example, the TIM-3 inhibitor is a small molecule, nucleic acid, polypeptide (such as an antibody, antibody conjugate or antigen-binding fragment thereof), carbohydrate, lipid, metal or toxin. In a specific example, the TIM-3 inhibitor is a TIM-3 binder (such as an antibody, antibody conjugate or antigen-binding fragment thereof). In a specific example, the TIM-3 binder is an antibody, antibody conjugate or antigen-binding fragment thereof. In some specific examples, the TIM-3 antibody agent is MBG453, LY3321367, Sym023, TSR-022 or a derivative thereof. In some specific examples, the TIM-3 antibody agent is disclosed in International Patent Application Publication No. WO2016 / 161270, No. WO 2018 / 085469 or No. WO 2018 / 129553. In some specific examples, the TIM-3 antibody agent is administered as disclosed in International Patent Application Publication No. WO2016 / 161270, No. WO 2018 / 085469 or No. WO 2018 / 129553. In some specific examples, the TIM-3 antibody agent is TSR-022. In a specific example, the immune checkpoint inhibitor is a LAG-3 inhibitor. In a specific example, the anti-LAG-3 agent is an antibody, an antibody conjugate, or an antigen-binding fragment thereof. In a specific example, the anti-LAG-3 agent is a small molecule, nucleic acid, polypeptide (such as an antibody), carbohydrate, lipid, metal, or toxin. In a specific example, the anti-LAG-3 agent is a small molecule. In a specific example, the anti-LAG-3 agent is a LAG-3 binder. In a specific example, the anti-LAG-3 agent is an antibody, an antibody conjugate, or an antigen-binding fragment thereof. In a specific example, the anti-LAG-3 agent is IMP321, relatlimab (BMS-986016), BI 754111, GSK2831781 (IMP-731), Novartis LAG525 (IMP701), REGN3767, MK-4280, MGD-013, GSK-2831781, FS-118, XmAb22841, INCAGN-2385, FS-18, ENUM-006, AVA-017, AM-0003, Avacta PD-L1 / LAG-3 bispecific affamer, iOnctura anti-LAG-3 antibody, Arcus anti-LAG-3 antibody, or Sym022 or TSR-033. In some specific examples, the LAG-3 antibody agent is disclosed in International Patent Application Publication No. WO2016 / 126858 or International Patent Application No. PCT / US18 / 30027. In some specific examples, the LAG-3 antibody agent is administered as disclosed in International Patent Application Publication No. WO2016 / 126858 or International Patent Application No. PCT / US18 / 30027. In a specific example, the LAG-3 antibody agent is TSR-033. In a specific example, the niraparib tablet composition is administered in combination with a PD-1 inhibitor (such as TSR-042, pembrolizumab or nivolumab). In a specific example, the niraparib tablet composition is administered in combination with a TIM-3 inhibitor (such as TSR-022). In a specific example, the niraparib tablet composition is administered in combination with a LAG-3 inhibitor (such as TSR-033). In a specific example, the niraparib tablet composition is administered in combination with a PD-1 inhibitor (such as TSR-042, pembrolizumab or nivolumab) and a TIM-3 inhibitor (such as TSR-022). In a specific example, the niraparib tablet composition is administered in combination with a PD-1 inhibitor (such as TSR-042, pembrolizumab or nivolumab) and a LAG-3 inhibitor (such as TSR-033). In a specific example, the niraparib tablet composition is administered in combination with a TIM-3 inhibitor (such as TSR-022) and a LAG-3 inhibitor (such as TSR-033). In a specific example, the niraparib tablet composition is administered in combination with a PD-1 inhibitor (such as TSR-042, pembrolizumab or nivolumab), a TIM-3 inhibitor (such as TSR-022) and a LAG-3 inhibitor (such as TSR-033). In a specific example, the niraparib tablet composition is administered in combination with one or more chemotherapeutic agents. In a specific example, the niraparib tablet composition is administered in combination with a platinum-based chemotherapeutic agent (such as one or more of cisplatin, carboplatin, oxaliplatin, nedaplatin, triplatinum tetranitrate, phenanthriplatin, picoplatin and satraplatin). In a specific example, the niraparib tablet composition is administered in combination with a chemotherapeutic agent, which is aminoglutethimide, amsacrine, anastrozole, asparaginase, bcg, bicalutamide, bleomycin, buserelin, busulfan, campothecin, capecitabine, carboplatin, carmustine, chlorambucil, cisplatin, cladribine, clodronate, colchicine, cyclophosphamide, cyproterone, cytarabine, dacarbazine, dactinomycin, daunorubicin, dienestrol, diethylstilbestrol, docetaxel, doxorubicin, epirubicin, estradiol, estramnustine, etoposide, exemestane, filgrastim, fludarabine, fludrocortisone, fluorouracil, fluoxymesterone, flutamide, gemcitabine, genistein, goserelin, hydroxyurea, idarubicin, ifosfamide, imatinib, interferon, irinotecan, ironotecan, letrozole, leucovorin, leuprolide, levamisole, lomustine, mechlorethamine, medroxyprogesterone, megestrol,Melphalan, mercaptopurine, mesna, methotrexate, mitomycin, mitotane, mitoxantrone, nilutamide, nocodazole, octreotide, oxaliplatin, paclitaxel, pamidronate, pentostatin, plicamycin, porfimer, procarbazine, raltitrexed, rituximab, streptozocin, suramin, tamoxifen, temozolomide, teniposide, testosterone, thioguanine, thiotepa, titanium dichloride bis(cyclopentadienyl), topotecan, trastuzumab, tretinoin, vinblastine, vincristine, vindesine or vinorelbine. In a specific example, the niraparib tablet composition is administered in combination with a second agent, which is a regulatory T cell (Treg) inhibitor, a macrophage inhibitor, an antigen-specific immune response enhancer, an antigen-specific immune response enhancer, an anti-angiogenic agent, a chemotherapeutic agent, or a combination thereof. In a specific example, the second agent is any second agent described in International Application No. PCT / US18 / 33437, which is incorporated herein by reference in its entirety. In a specific example, the macrophage inhibitor is selected from the group consisting of: macrophage recruitment inhibitors (such as anti-CCL2 / CCR2 agents, anti-IL6 agents, anti-M-CSFR agents, and combinations thereof), M2 macrophage anti-survival agents, M1 macrophage enhancers, M2 to M1 polarizers, macrophage activity inhibitors, and combinations thereof. In a specific example, the macrophage recruitment inhibitors are selected from the group consisting of: trabectedin, RS102895, PF-04136309, CNTO888, MLN1202, siltuximab, JNJ-28312141, GW2580, IMC-CS4 (LY3022855), emactuzumab, AMG820, pexidartinib, linifanib, OSI-930, CEP-32496, PLX7846, BLZ945, ARRY-382, JNJ-40346527, MCS110, PLX3397, PLX6134, PD-0360324, FPA008, and combinations thereof. In a specific example, the M2 macrophage anti-survival agents are selected from the group consisting of MMP inhibitors, clodronate, zoledronic acid, dichloromethylene bisphosphonate, trabectedin, dasatinib, retinoic acid, attenuated bacteria (such as Shigella flexneri (Shigella flexneri) , Salmonella typhimurium (Salmonella typhimurium), Listeria monocytogens ( Listeria monocytogens), Chlamydia psittaci ( Chlamydia psittaci), Legionella pneumophila ( Legionella pneumophila)) and combinations thereof. In a specific example, the M1 macrophage enhancer or M2 to M1 polarizer is selected from the group consisting of: anti-CD40 agent, anti-IL-10R agent, CD47 antagonist (such as Hu5F9-G4, CC-90002 and CD47-Fc fusion protein TTI-621), PolyI:C, LPS, monophosphoryl A, imiquimod, R-848, CpG-ODN, IFN-α, IFN-β, IFN-γ, GM-CSF, IL-12, IL-2, IL-15, Tα1, ibrutinib, EF-022 and combinations thereof. In a specific example, the macrophage activity inhibitor is selected from the group consisting of: STAT3 inhibitor, STAT6 inhibitor or anti-tumor agent (such as the macrophage activity inhibitor is WP1066, sunitinib, sorafenib, STA-21, IS3 295, S3I-M2001, AS1517499, leflunomide, TMC-264, histidine-rich glycoprotein (HRG), copper chelate (CuNG), 5,6-dimethyldibenzopyranone-4-acetic acid (MDXAA), vadimezan (ASA404), cisplatin, silibinin, proton pump inhibitor pantoprazole (PPZ) or CNI-1493, or a combination thereof). In a specific example, the macrophage inhibitor is an anti-IL-1α agent (such as xilonix). In a specific example, the regulatory T cell (Treg) inhibitor is selected from the group consisting of: Treg ablation agents, Treg migration inhibitors, Treg function inhibitors, and combinations thereof. In a specific example, the Treg ablation agent is selected from the group consisting of: cyclophosphamide, paclitaxel, imatinib, sunitinib, sorafenib, dasatinib, temozolomide, daclizumab, denileukin diftitox, and combinations thereof. In a specific example, the Treg migration inhibitor is selected from the group consisting of: AMD3100, mogamulizumab, casuarinin, fucoidan, and combinations thereof. In a specific example, the Treg function inhibitor is selected from the group consisting of: anti-CTLA4 agents (such as ipilimumab, tremelimumab), anti-OX40 agents, anti-GITR agents, adenosine receptor antagonists (such as caffeine, theophylline, theobromine, and 8-phenylxanthine), P60, and combinations thereof. In a specific example, the antigen-specific immune response enhancer is selected from the group consisting of: anti-PD-1 agents, anti-PD-L1 agents, glucocorticoid-induced TNFR-related protein (GITR) stimulants, anti-CTLA4 agents, anti-TIM-3 agents, anti-LAG-3 agents, anti-IDO agents, agents that enhance tumor antigen presentation (such as personalized cancer vaccines, autologous antigen-presenting cells, autologous dendritic cells, artificial antigen-presenting cells), chemokine signaling agents, anti-VEGF agents, cytokine signal stimulants, and combinations thereof. In a specific example, the GITR stimulant is selected from the group consisting of: DTA-1, mGITRL, pGITRL, and combinations thereof. In a specific example, the anti-CTLA4 agent is selected from the group consisting of: ipilimumab, tremelimumab, and combinations thereof. In a specific example, the chemokine signal transducer is selected from the group consisting of: CXCL16, CXCR6 chemokine receptor (CD186) agonist, and combinations thereof. In a specific example, the anti-VEGF agent is selected from the group consisting of: bevacizumab, pazopanib, sunitinib, sorafenib, axitinib, ponatinib, regorafenib, cabozantinib, vandetanib, ramucirumab, lenvatinib, ziv-aflibercept, and combinations thereof. In a specific example, the cytokine signal stimulant is interleukin or interferon. In a specific example, the interleukin is selected from the group consisting of: IL-2, IL-1, IL-7, IL-15, IL-12, IL-18, and combinations thereof. In a specific example, the interferon is IFNα. In a specific example, the antigen-specific immune response enhancer is selected from the group consisting of: flavonoids (such as flavonoid glycosides), lidocaine, lamotrigine, sulfamethoxazole, phenytoin, carbamazepine, sulfamethoxazole, phenytoin, allopurinol, paracetamol, mepivacaine, p-phenylenediamine, ciprofloxacin, and moxifloxacin. In a specific example, the anti-angiogenic agent is TNP-470, platelet factor 4, thrombospondin-1, tissue inhibitors of metalloproteinases (TIMP1 and TIMP2), prolactin, angiostatin, endostatin, soluble bFGF receptor, transforming growth factor β, interferon α, soluble KDR and FLT-1 receptors, placental proliferin-related protein, and combinations thereof. In a specific example, the anti-angiogenic agent reduces the production of pro-angiogenic factors, inhibits the interaction between pro-angiogenic factors and pro-angiogenic receptors, inhibits the function of pro-angiogenic factors, inhibits the function of pro-angiogenic factor receptors, reduces blood flow by disrupting blood vessels, inhibits vessel sprouting, or any combination thereof. In a specific example, the anti-angiogenic agent is a small organic molecule or an inorganic molecule; saccharin; oligosaccharide; polysaccharide; carbohydrate; peptide; protein; peptide analogue; peptide derivative; lipid; antibody; antibody fragment, peptidomimetic; nucleic acid; nucleic acid analogue; nucleic acid derivative; extract made from biological materials; naturally occurring or synthetic composition; metal; toxin; or any combination thereof.In a specific example, the anti-angiogenic agent is selected from the group consisting of: bevacizumab, itraconazole, carboxyamidotriazole, TNP-470, fumagillin, CM101, IL-12, platelet factor-4, suramin, SU5416, thrombospondin, angiostatic steroid, heparin, cartilage-derived angiogenesis inhibitor, matrix metalloproteinase inhibitor, angiostatin, endostatin, 2-methoxyestradiol, tecogalan, tetrathiomolybdate, thrombospondin, thalidomide, prolactin, αVβ3 inhibitor, lenalidomide, linomide, ramucirumab, tasquinimod, ranibizumab, sorafenib, sunitinib, pazopanib, everolimus, tissue inhibitors of metalloproteinases (TIMP1 and TIMP2), soluble receptor for bFGF, transforming growth factor β, interferon α, soluble KDR and FLT-1 receptors, placental proliferin-related protein, pazopanib, sunitinib, sorafenib, axitinib, ponatinib, cabozantinib, regorafenib, vandetanib, lenvatinib, semaxanib, SU6668, vatalanib, tivozanib, cediranib, protamine, heparin, steroid, ascorbic acid ether, sulfated polysaccharide DS 4152, fumagillin, AGM 12470, neovastat, RO4929097, MRK-003, MK-0752, PF03084014, MEDI0639, curcumin, 3,3'-diindolylmethane (DIM), resveratrol, 3,5-bis(2,4-difluorobenzylidene)-4-piperidone (DiFiD) and epigallocatechin-3-gallate (EGCG), and honokiol, OMP-21M18, navicixizumab (OMP-305B83), Flt. 2-11 , CBO-P11, Je-11, V1, and any combination thereof. In some specific examples, the anti-angiogenic agent inhibits the DLL4 / Notch signaling pathway. In some specific examples, the angiogenesis inhibitor that inhibits the DLL4 / Notch signaling pathway is a gamma-secretase inhibitor (GSI), siRNA, or a monoclonal antibody against the Notch receptor or ligand. In some specific examples, the anti-angiogenic agent is selected from the group consisting of: RO4929097, MRK-003, MK-0752, PF03084014, MEDI0639, curcumin, 3,3'-diindolylmethane (DIM), resveratrol, 3,5-bis(2,4-difluorobenzylidene)-4-piperidone (DiFiD), and epigallocatechin-3-gallate (EGCG), honokiol, and any combination thereof. In some specific examples, the anti-angiogenic agent inhibits the vascular endothelial growth factor (VEGF) / vascular endothelial growth factor receptor (VEGFR) pathway. In some specific examples, the anti-angiogenic agent is selected from the group consisting of: Akt inhibitor, calcineurin autoimmunosuppressive peptide, ET-18-OCH3, Go 6983, NG-nitro-L-arginine methyl ester, p21-activated kinase inhibitor, cPLA2α inhibitor, PI-103, PP2, SB 203580, U0126, VEGFR tyrosine kinase inhibitor V, VEGFR2 kinase inhibitor VI, VEGFR2 kinase inhibitor III, ZM 336372, and any combination thereof. In some specific examples, the anti-angiogenic agent inhibits VEGF family proteins and / or VEGFR family proteins. In some specific examples, the VEGF family proteins include VEGF-A, VEGF-B, VEGF-C, VEGF-D, placental growth factor (PlGF), VEGF-E (Orf-VEGF), Trimeresurus flavoviridis svVEGF, or any combination thereof. In some specific examples, the anti-angiogenic agent is bevacizumab, ranibizumab, OPT-302, aflibercept, or any combination thereof. In some specific examples, the anti-angiogenic agent is Flt2-11, CBO-P11, Je-11, V1, or any combination thereof. In some specific examples, the anti-angiogenic agent is pazopanib, sunitinib, sorafenib, axitinib, ponatinib, cabozantinib, regorafenib, vandetanib, lenvatinib, semaxanib, SU6668, vantanib, tivozanib, cediranib, or any combination thereof. As generally described herein, the following non-limiting examples are provided to further illustrate the present invention. Exemplary Aspects and Embodiments of the Present Invention Exemplary aspects and embodiments of the present invention are described herein and include items 1 to 125. Item 1. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) salt selected from niraparib camphorate, niraparib mandelate, and niraparib camphorsulfonate. Item 2. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorate. Item 3. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate. Item 4. A crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate. Item 5. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 R,3 S)-(+)-camphorate, Form 1. Item 6. The niraparib (1 R,3 S)-(+)-camphorate, Form 1 as in Item 5, which has an X-ray powder diffraction (XRPD) pattern comprising one or more XRPD peaks at 16.2, 17.5, 20.0, 13.4, and / or 15.2 ± 0.2° 2θ. Item 7. The niraparib (1 R,3 S)-(+)-camphorate of Form 1 as in Item 5 or Item 6, which has an XRPD pattern comprising at least two peaks at 16.2, 17.5, 20.0, 13.4, and / or 15.2 ± 0.2° 2θ. Item 8. The niraparib (1 R,3 S)-(+)-camphorate, Form 1 as in any one of Items 5 to 7, which has an XRPD pattern comprising at least three peaks at 16.2, 17.5, 20.0, 13.4, and / or 15.2 ± 0.2° 2θ. Item 9. The niraparib (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks at at least four of 16.2, 17.5, 20.0, 13.4 and / or 15.2 ± 0.2° 2θ. Item 10. Niraparib as in any one of Items 5 to 9 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks at 16.2, 17.5, 20.0, 13.4 and 15.2 ± 0.2° 2θ. Item 11. Niraparib as in any one of Items 5 to 10 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising one or more XRPD peaks at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. Item 12. Niraparib as in any one of Items 5 to 11 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising two or more peaks at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. Item 13. Niraparib as in any one of Items 5 to 12 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising three or more peaks at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. Item 14. Niraparib of crystalline form 1 as in any one of Items 5 to 13 (1 R,3 The (S)-(+)-camphorate, which has an XRPD pattern comprising four or more peaks at 20.4, 21.6, 24.0, 11.7 and / or 18.0 ± 0.2° 2θ. Item 15. Niraparib as in any one of Items 5 to 14 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks at 20.4, 21.6, 24.0, 11.7 and 18.0 ± 0.2° 2θ. Item 16. Niraparib as in any one of Items 5 to 15 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks at 16.2, 17.5, 20.0, 13.4, 15.2, 20.4, 21.6, 24.0, 11.7 and 18.0 ± 0.2° 2θ. Item 17. Niraparib as in any one of Items 5 to 16 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising at least one peak at 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. Item 18. Niraparib as in any one of Items 5 to 17 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising at least two peaks at 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. Item 19. Niraparib as in any one of Items 5 to 18 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising at least three peaks at 14.8, 18.0, 22.8 and / or 27.6 ± 0.2° 2θ. Item 20. Niraparib as in any one of Items 5 to 19 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks at 14.8, 18.0, 22.8 and 27.6 ± 0.2° 2θ. Item 21. Niraparib as in any one of Items 5 to 20 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising one or more peaks at 16.2, 17.5, 20.0, 13.4, 15.2, 20.4, 21.6, 24.0, 11.7, 18.0, 22.8, 18.9, 14.5, 14.1, 14.8, 27.6, 26.9, 6.5, 22.3 and / or 24.5 ± 0.2° 2θ. Item 22. Niraparib as in any one of Items 5 to 21 (1 R,3 Crystalline Form 1 of (S)-(+)-camphorate, which has an XRPD pattern comprising peaks having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: Item 23. Niraparib as in any one of Items 5 to 22 (1 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by an XRPD pattern substantially as shown in Figure 3. Item 24. Niraparib (1 as in any one of Items 5 to 23 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by a melting point of about 260 °C to about 270 °C. Item 25. Niraparib (1 as in any one of Items 5 to 24 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by a melting point of about 264 °C. Item 26. Niraparib (1 as in any one of Items 5 to 25 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by a DSC thermogram in which the melting onset (endothermic peak) is about 264 °C and / or in which the minimum peak is about 268 °C. Item 27. Niraparib (1 as in any one of Items 5 to 26 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by a DSC thermogram substantially as shown in Figure 5. Item 28. Niraparib (1 as in any one of Items 5 to 27 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by an infrared spectrum comprising peaks at about 3359 cm -1 about 1693 cm -1 and about 1649 cm -1 Item 29. Niraparib (1 as in any one of Items 5 to 28 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by an infrared spectrum substantially as shown in Figure 2. Item 30. Niraparib (1 as in any one of Items 5 to 29 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by adsorbing no more than about 0.3 wt% of water at about 25 °C up to about 90% relative humidity. Item 31. Niraparib (1 as in any one of Items 5 to 30 R,3 The crystalline form 1 of (S)-(+)-camphorate, characterized by a GVS thermogram substantially as shown in Figure 6. Item 32. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S,3 (R)-(-)-Camphorate. Item 33. A crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (Niraparib) (1 S,3 (R)-(-)-Camphorate. Item 34. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (Niraparib) (1 S,3 Crystal form 1 of (R)-(-)-camphorate. Item 35. Niraparib as in item 34 (1 S,3 Crystal form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at one or more of 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. Item 36. Niraparib as in item 34 or item 35 (1 S,3 Crystal form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least two peaks at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. Item 37. Niraparib as in any one of items 34 to 36 (1 S,3 Crystal form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least three peaks at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. Item 38. Niraparib as in any one of items 34 to 37 (1 S,3 Crystal form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least four peaks at 20.3, 17.4, 16.2, 15.1 and / or 20.2 ± 0.2° 2θ. Item 39. Niraparib as in any one of items 34 to 38 (1 S,3 Crystal form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at 20.3, 17.4, 16.2, 15.1 and 20.2 ± 0.2° 2θ. Item 40. Niraparib as in any one of items 34 to 39 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at one or more of 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. Item 41. Niraparib as in any one of items 34 to 40 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least two peaks at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. Item 42. Niraparib as in any one of items 34 to 41 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least three peaks at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. Item 43. Niraparib as in any one of items 34 to 42 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least four peaks at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. Item 44. Niraparib as in any one of items 34 to 43 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at 24.4, 19.9, 11.6, 22.3 and / or 22.2 ± 0.2° 2θ. Item 45. Niraparib as in any one of items 34 to 44 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at 20.3, 17.4, 16.2, 15.1, 20.2, 24.4, 19.9, 11.6, 22.3 and 22.2 ± 0.2° 2θ. Item 46. Niraparib as in any one of items 34 to 45 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising a peak at 16.0 ± 0.2° 2θ. Item 47. Niraparib as in any one of items 34 to 46 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising a peak at 21.9 ± 0.2° 2θ. Item 48. Niraparib as in any one of items 34 to 47 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks at 16.0 and 21.9 ± 0.2° 2θ. Item 49. Niraparib according to any one of Items 34 to 48 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising at least one peak at 20.3, 17.4, 16.2, 15.1, 20.2, 24.4, 19.9, 11.6, 22.3, 22.2, 13.4, 16.0, 26.9, 6.5, 23.9, 18.9, 14.5, 14.0, 21.9 and / or 21.5 ± 0.2° 2θ. Item 50. Niraparib according to any one of Items 34 to 49 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which has an XRPD pattern comprising peaks having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: Item 51. Niraparib according to any one of Items 34 to 50 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which is characterized by an XRPD pattern substantially as shown in Figure 9. Item 52. Niraparib according to any one of Items 34 to 51 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which is characterized by a melting point of about 220°C to about 230°C. Item 53. Niraparib according to any one of Items 34 to 52 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which is characterized by a melting point of about 226°C. Item 54. Niraparib according to any one of Items 34 to 53 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which is characterized by a DSC thermogram in which the melting onset point (endothermic peak) is about 226°C and / or in which the minimum peak is about 230°C. Item 55. Niraparib according to any one of Items 34 to 54 (1 S,3 Crystalline Form 1 of (R)-(-)-camphorate, which is characterized by a DSC thermogram substantially as shown in Figure 11. Item 56. Niraparib according to any one of Items 34 to 55 (1 S,3 The crystalline form 1 of (R)-(-)-camphorate, characterized by comprising infrared spectra with peaks at about 3367 cm -1 , about 1693 cm -1 and about 1648 cm -1 . Item 57. Niraparib (1 S,3 R)-(-)-camphorate crystalline form 1, characterized by an infrared spectrum substantially as shown in Figure 8. Item 58. Niraparib (1 S,3 R)-(-)-camphorate crystalline form 1, characterized by adsorbing less than about 1 wt% water up to about 90% relative humidity at about 25 °C. Item 59. Niraparib (1 S,3 R)-(-)-camphorate crystalline form 1, characterized by a GVS thermal analysis chart substantially as shown in Figure 12. Item 60. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) mandelate. Item 61. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate. Item 62. A crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate. Item 63. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) ( R)-(-)-mandelate crystalline form 1. Item 64. Niraparib ( R)-(-)-mandelate crystalline form 1 as in Item 63, which has an XRPD pattern comprising peaks at one or more of 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. Item 65. Niraparib ( R)-(-)-mandelate crystalline form 1 as in Item 63 or Item 64, which has an XRPD pattern comprising at least two peaks at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. Item 66. Niraparib ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks at least at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. Item 67. Niraparib as described in any one of Items 63 to 66 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising at least four peaks at 18.5, 16.4, 17.4, 8.6 and / or 17.6 ± 0.2° 2θ. Item 68. Niraparib as described in any one of Items 63 to 67 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks at 18.5, 16.4, 17.4, 8.6 and 17.6 ± 0.2° 2θ. Item 69. Niraparib as described in any one of Items 63 to 68 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising one or more peaks at 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. Item 70. Niraparib as described in any one of Items 63 to 69 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising two or more peaks at 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. Item 71. Niraparib as described in any one of Items 63 to 70 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising three or more peaks at 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. Item 72. Niraparib as described in any one of Items 63 to 71 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising four or more peaks at 8.7, 18.4, 25.1, 27.6 and / or 13.7 ± 0.2° 2θ. Item 73. Niraparib as described in any one of Items 63 to 72 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks at 8.7, 18.4, 25.1, 27.6 and 13.7 ± 0.2° 2θ. Item 74. Niraparib as described in any one of Items 63 to 73 ( The crystalline form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks at 18.5, 16.4, 17.4, 8.6, 17.6, 8.7, 18.4, 25.1, 27.6 and 13.7 ± 0.2° 2θ. Item 75. Niraparib as described in any one of Items 63 to 74 ( Crystalline Form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks at 18.5, 16.4, 17.4, 8.6, 17.6, 8.7, 18.4, 25.1, 27.6, 13.7, 8.4, 28.7, 28.0, 4.3, 21.5, 27.3, 14.1, 27.7, 12.4 and / or 16.1 ± 0.2° 2θ. Item 76. Niraparib according to any one of Items 63 to 75 ( Crystalline Form 1 of (R)-(-)-mandelate, which has an XRPD pattern comprising peaks having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: Item 77. Niraparib according to any one of Items 63 to 76 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by an XRPD pattern substantially as shown in Figure 15. Item 78. Niraparib according to any one of Items 63 to 77 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by a melting point of about 190 °C to about 200 °C. Item 79. Niraparib according to any one of Items 63 to 78 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by a melting point of about 197 °C. Item 80. Niraparib according to any one of Items 63 to 79 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by a DSC thermogram in which the melting onset point (endothermic peak) is about 197 °C and / or in which the minimum peak is about 201 °C. Item 81. Niraparib according to any one of Items 63 to 80 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by a DSC thermogram substantially as shown in Figure 18. Item 82. Niraparib according to any one of Items 63 to 81 ( Crystalline Form 1 of (R)-(-)-mandelate, which is characterized by an infrared spectrum comprising peaks at about 3443 cm -1 about 3340 cm -1 about 1671 cm -1 and about 1638 cm -1 Item 83. Niraparib according to any one of Items 63 to 82 ( The crystalline form 1 of (R)-(-)-mandelate, characterized by an infrared spectrum substantially as shown in Figure 14. Item 84. Niraparib as described in any one of Items 63 to 83 ( The crystalline form 1 of (R)-(-)-mandelate, characterized by a DVS thermal analysis chart substantially as shown in Figure 19. Item 85. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) camphorsulfonate. Item 86. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. Item 87. A crystalline 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate. Item 88. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (1 S)-(+)-camphorsulfonate crystalline form 1. Item 89. Niraparib as described in Item 88 (1 S)-(+)-camphorsulfonate crystalline form 1, which has an XRPD pattern comprising peaks at one or more of 16.0, 13.5, 17.6, 24.3 and / or 24.6 ± 0.2° 2θ. Item 90. Niraparib as described in Item 88 or Item 89 (1 S)-(+)-camphorsulfonate crystalline form 1, which has an XRPD pattern comprising at least two peaks at 16.0, 13.5, 17.6, 24.3 and / or 24.6 ± 0.2° 2θ. Item 91. Niraparib as described in any one of Items 88 to 90 (1 S)-(+)-camphorsulfonate crystalline form 1, which has an XRPD pattern comprising at least three peaks at 16.0, 13.5, 17.6, 24.3 and / or 24.6 ± 0.2° 2θ. Item 92. Niraparib as described in any one of Items 88 to 91 (1 S)-(+)-camphorsulfonate crystalline form 1, which has an XRPD pattern comprising at least four peaks at 16.0, 13.5, 17.6, 24.3 and / or 24.6 ± 0.2° 2θ. Item 93. Niraparib as described in any one of Items 88 to 92 (1 S)-(+)-camphorsulfonate crystalline form 1, which has an XRPD pattern comprising peaks at 16.0, 13.5, 17.6, 24.3 and / or 24.6 ± 0.2° 2θ. Item 94. Niraparib as described in any one of Items 88 to 93 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at one or more of 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. Item 95. Niraparib as in any one of Items 88 to 94 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising two or more XRPD peaks at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. Item 96. Niraparib as in any one of Items 88 to 95 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising three or more peaks at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. Item 97. Niraparib as in any one of Items 88 to 96 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising four or more peaks at 11.1, 16.4, 23.7, 16.7 and / or 20.3 ± 0.2° 2θ. Item 98. Niraparib as in any one of Items 88 to 97 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at 11.1, 16.4, 23.7, 16.7 and 20.3 ± 0.2° 2θ. Item 99. Niraparib as in any one of Items 88 to 98 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at 16.0, 13.5, 17.6, 24.3, 24.6, 11.1, 16.4, 23.7, 16.7 and 20.3 ± 0.2° 2θ. Item 100. Niraparib as in any one of Items 88 to 99 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising one or more XRPD peaks at 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. Item 101. Niraparib as in any one of Items 88 to 100 (1 Crystalline Form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising at least two peaks at 6.7, 16.4, 23.7 and / or 25.2 ± 0.2° 2θ. Item 102. Niraparib as in any one of Items 88 to 101 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at at least three of 6.7, 16.4, 23.7, and / or 25.2 ± 0.2° 2θ. Item 103. Niraparib as in any one of Items 88 to 102 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at 6.7, 16.4, 23.7, and 25.2 ± 0.2° 2θ. Item 104. Niraparib as in any one of Items 88 to 103 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks at at least one of 16.0, 13.5, 17.6, 24.3, 24.6, 11.1, 16.4, 23.7, 16.7, 20.3, 6.7, 25.2, 25.0, 25.8, 26.8, 22.8, 9.5, 16.9, 14.3, and / or 7.7 ± 0.2° 2θ. Item 105. Niraparib as in any one of Items 88 to 104 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which has an XRPD pattern comprising peaks having 2θ values (± 0.2° 2θ) according to the following table and optionally relative intensities: Item 106. Niraparib as in any one of Items 88 to 105 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by an XRPD pattern substantially as shown in Figure 22. Item 107. Niraparib as in any one of Items 88 to 106 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by a melting point of about 235°C to about 245°C. Item 108. Niraparib as in any one of Items 88 to 107 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by a melting point of about 239°C. Item 109. Niraparib as in any one of Items 88 to 108 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by a DSC thermal analysis graph in which the melting start point (endothermic peak) is about 235°C and / or in which the minimum peak is about 246°C. Item 110. Niraparib as in any one of Items 88 to 109 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by a DSC thermal analysis graph substantially as shown in Figure 24. Item 111. Niraparib as in any one of Items 88 to 110 (1 The crystalline form 1 of (S)-(+)-camphorsulfonate, which is characterized by containing about 3467 cm -1 , about 3306 cm -1 , about 1724 cm -1 , about 1660 cm -1 and about 1611 cm -1 infrared spectrum of the peaks of. Item 112. Niraparib (1 S)-(+)-camphorsulfonate crystalline form 1, characterized by an infrared spectrum substantially as shown in Figure 21. Item 113. Niraparib (1 S)-(+)-camphorsulfonate crystalline form 1, characterized by adsorbing less than about 2% by weight of water at about 25 °C up to about 90% relative humidity. Item 114. Niraparib (1 S)-(+)-camphorsulfonate crystalline form 1, characterized by adsorbing about 1.3% by weight of water at about 25 °C up to about 90% relative humidity. Item 115. As described in items 88 to 114, niraparib (1 S)-(+)-camphorsulfonate crystalline form 1, characterized by a GVS thermal analysis chart substantially as shown in Figure 25. Item 116. A pharmaceutical composition comprising niraparib camphorate, niraparib mandelate or niraparib camphorsulfonate according to any one of items 1 to 115 and at least one pharmaceutically acceptable excipient. Item 117. Niraparib camphorate, niraparib mandelate or niraparib camphorsulfonate according to any one of items 1 to 115 or the pharmaceutical composition according to item 116, which is used in therapy. Item 118. Use of niraparib camphorate, niraparib mandelate or niraparib camphorsulfonate according to any one of items 1 to 115 or the pharmaceutical composition according to item 116 for the manufacture of a medicament. Item 119. A method for treating cancer, stroke, autoimmune diabetes, neurological disease, inflammatory disease, metabolic disease or cardiovascular disease in an individual, the method comprising administering to the individual an effective amount of niraparib camphorate, niraparib mandelate or niraparib camphorsulfonate according to any one of items 1 to 115 or the pharmaceutical composition according to item 116. Item 120. The method according to item 119, wherein the method is a method for treating cancer. Item 121. The method according to item 120, wherein the cancer is related to BRCA1 and / or Related to BRCA2 mutations. Item 122. The method according to item 120 or 121, wherein the cancer is related to ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L or mutations of XRCC2 or any combination thereof. Item 123. The method according to any one of items 120 to 122, wherein the cancer is epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer. Item 124. The nilaparib camphorate, nilaparib mandelate or nilaparib camphorsulfonate according to any one of items 1 to 115 or the pharmaceutical composition according to item 116, which is used in the method according to any one of items 119 to 123. Item 125. Use of a nilaparib camphorate, nilaparib mandelate or nilaparib camphorsulfonate according to any one of items 1 to 115 or the pharmaceutical composition according to item 116 for manufacturing a medicament for use in the method according to any one of items 119 to 123. ( Example ) Analysis procedure X Ray powder diffraction (XRPD) XRPD analysis is usually carried out on a PANalytical X’pert pro, scanning the sample between 3 and 35° 2θ. The material is gently ground to release any aggregates and loaded onto a porous plate supported by a Kapton or Mylar polymer film. Then, the porous plate is placed in the diffractometer and a 40 kV / 40 mA generator setting is used, using Cu K radiation (α 1 λ = 1.54060 Å; α 2= 1.54443 Å; β = 1.39225 Å; α 1 : α 2 Ratio = 0.5) was analyzed. Unless otherwise specified, XRPD analysis was performed at room temperature and pressure and at a relative humidity of about 30 - 50% (e.g., about 40% relative humidity). NMR Analysis The NMR method was typically performed on a Bruker AVIIIHD spectrometer equipped with a DCH cryoprobe. Experiments were performed in deuterated DMSO and each sample was prepared at a concentration of about 10 mM. Unless otherwise specified, NMR spectra were obtained at room temperature (e.g., approximately 300K). High Performance Liquid Chromatography - Ultraviolet Detection (HPLC-UV) HPLC was typically performed using the following parameters: Column: Waters Symmetry C18, 150×3.9 mm, 5 µm Column temperature: 40°C Autosampler temperature: 5°C UV wavelength: 220 nm Injection volume: 4.3 µL Flow rate: 1.962 mL / min Mobile phase A: Aqueous solution of 0.1% perchloric acid Mobile phase B: Acetonitrile The gradient program typically used was: Polarizing Microscopy ( PLM) The presence of crystallinity (birefringence) was typically determined using an Olympus BX50 polarizing microscope equipped with a Motic camera and image capture software (Motic Images Plus 2.0). Unless otherwise specified, all images were recorded using a 20× objective. Fourier Transform Infrared Spectroscopy (FT-IR) Fourier transform infrared spectroscopy was typically performed on a Bruker ALPHA P spectrometer. An adequate amount of material was placed at the center of the spectrometer's disk and spectra were obtained using the following parameters: Resolution: 4 cm -1 Background scan time: 16 scans Sample scan time: 16 scans Data collection: 4000 to 400 cm -1 Resultant spectrum: Transmittance Software: OPUS version 6 Thermogravimetric Analysis (TGA) Typically, approximately 5 mg of the material is weighed and placed in an open aluminum pan and loaded into a synchronous thermogravimetric / differential thermal analyzer (TG / DTA) and maintained at room temperature. Then the sample is heated from 20 °C to 350 °C at a rate of 10 °C / min, during which time, the change in sample weight and any differential thermal events (DTA) are recorded. Nitrogen gas with a flow rate of 300 cm 3 / min is used as the purge gas. Differential Scanning Calorimetry (DSC) Typically, approximately 5 mg of the material is weighed and placed in an aluminum DSC pan and sealed non-hermetically with a perforated aluminum lid. Then the sample pan is loaded into a Seiko DSC6200 (equipped with a cooler), cooled and maintained at 20 °C. Once a stable heat flow response is obtained, the sample and reference are heated to melting (if possible) at a scanning rate of 10 °C / min, and the resulting heat flow response is monitored. Nitrogen gas with a flow rate of 50 cm 3 / min is used as the purge gas. Gravimetric Vapor Sorption (GVS) Typically, approximately 10 - 20 mg of the sample is placed on a vapor sorption balance mesh pan and loaded into an IGASorp moisture sorption analyzer balance from Hiden Analytical. The sample is ramped from 40% to 90% relative humidity (RH) in 10% increments, and the sample is maintained at 25 °C at each step until a stable weight has been achieved (98% step completion, minimum step length 30 minutes, maximum step length 60 minutes). After the adsorption cycle is completed, the sample is dried to 0% RH using the same procedure and finally returned to the starting point of 40% RH. Two cycles are performed. The weight changes during the adsorption / desorption cycles are plotted to determine the hygroscopic properties of the sample. Dynamic Vapor Sorption (DVS) Typically, approximately 10 mg of the sample is placed on the mesh pan of a vapor sorption balance and loaded into a DVS-1 / DVS Intrinsic / DVS Advantage dynamic vapor sorption balance from Surface Measurement Systems. The sample is subjected to a ramping profile from 40% to 90% relative humidity (RH) in 10% increments, and the sample is maintained at 25 °C at each step until a stable weight has been achieved (dm / dt 0.004%, minimum step length 30 minutes, maximum step length 500 minutes). After the adsorption cycle is completed, the sample is dried to 0% RH using the same procedure and then returned to 40% RH for a second adsorption cycle. Two cycles are performed. The weight change during the adsorption / desorption cycle is plotted to determine the hygroscopic properties of the sample. Synthesis of Niraparib Tosylate and Niraparib Free Base Niraparib Tosylate Monohydrate Niraparib tosylate monohydrate is obtained from niraparib as described, for example, in WO 2014 / 088983 or PCT / US2018 / 029131. An exemplary XRPD pattern for niraparib tosylate monohydrate is shown in Figure 1. Niraparib free base To a mixture of 50.0 g (97.9 mmol) of niraparib tosylate monohydrate in 2-MeTHF (1 L) at room temperature was added 1% NaOH solution (500 mL). After stirring the mixture for 30 minutes, the aqueous layer was separated and extracted twice with 2-MeTHF (500 mL). The combined organics were then washed with water (1 L). The solution was slowly concentrated under partial vacuum below 30 °C to give approximately 20 mL of a suspension. The mixture was stirred at room temperature for 30 minutes and filtered to give an off-white solid (23.8 g, yield 75.9%). MS (ESI) C 19 H 20 N 4 O Required: 320, Experimental value: 321 [M+H] + . 1 H NMR (500.12 MHz, DMSO-d 6) δ 9.27 (s, 1H), 8.59 (dd, 1H, J=1.8, 4.7 Hz), 8.07 (dd, 1H, J=1.1, 7.0 Hz), 8.04 (d, 2H, J=8.7 Hz), 8.02 (dd, 1H, J=1.1, 8.1 Hz), 7.90 (br. s, 1H), 7.46 (d, 2H, J=8.5 Hz), 7.27 (dd, 1H, J=7.2, 8.3 Hz), 3.00 (br. d, 1H, J=12.1 Hz), 2.94 (br. d, 1H, J=12.1 Hz), 2.70 (m, 1H), 2.51 (m, 2H), 1.91, (d, 1H, J=13.0 Hz), 1.68 (m, 1H), 1.61 (m, 1H), 1.49 (m, 1H). 13 C NMR (125.77 MHz, DMSO-d 6 ) δ 166.1, 146.5, 146.4, 138.0, 130.1, 128.7, 125.8, 123.9, 123.8, 122.3, 121.9, 121.1, 54.0, 46.4, 43.6, 40.6, 40.4, 40.3, 40.1, 39.9, 32.3, 27.0. Embodiment 1 : Niraparib camphorate crystalline salt 1.1 Niraparib (1R,3S)-(+) -Camphorate (Form 1) - "(+)-Camphorate" Niraparib free base (5 g, 15.6 mmol) and methanol (17.5 mL) were weighed into a vial. R, 3 S)-(+)-camphoric acid (16.4 mmol, 1.05 equiv) in THF (16.4 mL) was added and the resulting slurry was thermocycled with stirring for 72 h (4 h at ambient conditions followed by 40 °C for 4 h). After removal from the thermocycle, the solid material present was separated by centrifuge filtration to obtain crude niraparib (1 R, 3 (S)-(+)-Camphorate (5.69 g). Crude niraparib (1 R, 3 S)-(+)-Camphorate (5.24 g) and (1 R, 3 S)-(+)-Camphoric acid (4.0 g; 12.5 mmol; 0.8 eq) was slurried in methanol (200 mL) at 40 °C. After stirring for approximately 0.5 h, the batch was cooled to room temperature and stirred for an additional 24 h. The resulting slurry was stored in the refrigerator for 24 h, after which the solid was separated by filtration and the filtered solid was dried in a vacuum oven at 40 °C for 3 h. This gave niraparib (1 R, 3 S)-(+)-Camphorate (6.48 g, total yield 75.0%) (melting point 264 °C). 1 H NMR (500 MHz, DMSO-d 6 ) δ 9.28 (s, 1H), 8.57 (br. s, 1H), 8.07 (dt, 2H, J=1.9, 8.7 Hz), 8.06 (dd, 1H, J=1.0, 6.9 Hz), 8.02 (dd, 1H, J=1.0, 8.3 Hz), 7.89 (br. s, 1H), 7.49 (d, 2H, J=8.8 Hz), 7.27 (dd, 1H, J=7.1, 8.1 Hz), 3.11 (br. d, 1H, J=12.0 Hz), 3.06 (br. d, 1H, J=12.3 Hz), 2.80 (tt, 1H, J=3.5, 11.3 Hz), 2.75 - 2.56 (m, 3H), 2.39 - 2.27 (m, 1H), 2.05 - 1.88 (m, 2H), 1.79 - 1.54 (m, 4H), 1.41 - 1.32 (m, 1H), 1.18, (s, 3H), 1.11 (s, 3H), 0.80 (s, 3H). FT-IR (cm -1): 3359.44, 3182.612, 3120.66, 2980.97, 2964.28, 2886.27, 2860.66, 2701.37, 2513.23, 1692.94, 1648.76, 1557.44, 1523.02, 1434.04, 1396.55, 1377.75, 1331.85, 1304.91, 1264.73, 1229.82, 1203.47, 1156.66, 1127.69, 1091.44, 1060.29, 1001.87, 946.70, 871.18, 827.13, 794.09, 755.21, 717.77, 678.26, 615.99, 551.87, 535.68, 494.00, 463.87, 411.96. Niraparib (1 R,3 The IR spectrum of (1S,3R)-(+)-camphorate is shown in Figure 2. 1.2 Niraparib (1S,3R)-(-)-camphorate (Form 1) - "(-)-camphorate" To a suspension of niraparib free base (250 mg; 0.78 mmol) in ethanol (2.5 mL) at 40 °C was slowly added a solution of ( 1S, 3R)-(-)-camphoric acid in THF (1.58 mL, 1.0 M, 2.1 equivalents) over 1 hour. The resulting solution was stirred at 40 °C for 1 hour. The resulting suspension was cooled to room temperature over 1 hour. The mixture was filtered and the wet filter cake was dried under vacuum at 40 °C for 3 hours to give niraparib (1 S,3 R)-(-)-camphorate (331 mg) (melting point 226 °C). 1 H NMR (500 MHz, DMSO-d 6) δ 9.28 (s, 1H), 8.58 (br. s, 1H), 8.08 (dt, 2H, J=2.0, 8.6 Hz), 8.07 (dd, 1H, J=1.1, 7.0 Hz), 8.02 (dd, 1H, J=1.1, 8.3 Hz), 7.89 (br. s, 1H), 7.49 (d, 2H, J=8.6 Hz), 7.27 (dd, 1H, J=6.9, 8.2 Hz), 3.11 (br. d, 1H, J=11.9 Hz), 3.05 (br. d, 1H, J=12.5 Hz), 2.88 - 2.75 (m, 1H), 2.75 - 2.56 (m, 3H), 2.40-2.26 (m, 1H), 2.05-1.85 (m, 2H), 1.80-1.52 (m, 4H), 1.42-1.31 (m, 1H), 1.18 (s, 3H), 1.11 (s, 3H), 0.79 (s, 3H). FT-IR (cm -1 ): 3366.88, 3177.98, 3120.30, 3036.66, 2978.54, 2879.58, 2790.08, 2719.08, 2507.15, 2529.46, 2371.80, 2228.38, 2030.21, 1693.10, 1648.46, 1560.66, 1523.93, 1458.02, 1429.67, 1377.32, 1331.43, 1303.71, 1269.54, 1200.70, 1156.87, 1127.25, 1085.34, 8. The IR spectrum of niraparib (1S,3R)-(-)-camphorate is shown in FIG8. Embodiment 2 : Niraparib mandelate crystalline salt At room temperature, a solution of (R)-(-)-mandelic acid in THF (15.8 mL, 1.0 M, 1.05 equiv) was added to a suspension of 5.0 g (15.6 mmol) of niraparib free base in acetonitrile (100 mL) as the bulk solution. The resulting mixture was placed in a heat cycle with stirring for 72 hours (4 hours at room temperature and then 4 hours at 40 °C). The mixture was filtered at room temperature to obtain the title compound (5.9 g). Approximately 5.5 g of the solid was dissolved in MeOH (80 mL) at 40 °C. After cooling to room temperature, 10 - 20 mL of the solvent was evaporated. After 24 hours, significant precipitation was observed. The suspension was stored in the refrigerator for another 24 hours, and then the solid was separated by filtration and the filtered solid was dried in a vacuum oven at 40 °C for 3 hours. This gave the title salt in the form of a crystalline salt (3.8 g, total yield 50.6%) (melting point 197 °C). 1 H NMR (500 MHz, DMSO-d 6 ) δ 9.30 (s, 1H), 8.58 (br. s, 1H), 8.10 (dt, 2H, J = 1.9, 8.7 Hz), 8.08 (dd, 1H, J = 1.1, 6.9 Hz), 8.02 (dd, 1H, J = 1.1, 8.4 Hz), 7.90 (br. s, 1H), 7.48 (d, 2H, J = 8.6 Hz), 7.41 (m, 2H), 7.27 (m, 3H), 7.17 (tt, 1H, J = 1.9, 8.0 Hz), 4.65 (s, 1H), 3.30 - 3.19 (m, 2H), 3.00 - 2.90 (m, 2H), 2.87 - 2.76 (m, 1H), 1.90 - 1.64 (m, 4H). FT-IR (cm -1): 3443.90, 3340.48, 3150.83, 3030.33, 2982.99, 2939.97, 2621.21, 2513.33, 2442.51, 1671.47, 1637.65, 1584.33, 1524.97, 1433.06, 1465.81, 1369.51, 1320.36, 1263.54, 1204.03, 1186.23, 1142.43, 1098.65, 1062.22, 961.17, 905.79, 870.89, 828.56, 764.89, 730.97, 693.15, 674.78, 622.88, 591.13, 555.73, 536.97, 508.16, 455.43, 406.54. The IR spectrum of niraparib (R)-(-)-mandelate is shown in Figure 14. Example 3 : Crystalline niraparib camphorsulfonate At room temperature, a solution of (1 S)-(+)-camphor-10-sulfonic acid in THF (7.9 mL, 1.0 M, 1.05 equivalents) was added to a suspension of niraparib free base (2.5 g; 7.8 mmol) in acetonitrile (100 mL) as the bulk solution. The mixture was placed in a heat cycle (4-hour cycle between ambient temperature and 40 °C) with stirring. The solid was collected by filtration and completely dissolved in methanol (50 mL). Approximately 10 to 20 mL of the solvent in the resulting solution was very slowly evaporated at room temperature for 24 hours. A precipitate was observed. The sample was placed in the refrigerator for 24 hours. The mixture was filtered and the wet filter cake was dried in a vacuum oven to give niraparib camphorsulfonate (1.6 g; yield 37%) (melting point 239 °C) in the form of a crystalline solid. 1 H NMR (500 MHz, DMSO-d 6) δ 9.32 (s, 1H), 8.56 (br. s, 1H), 8.14 (dt, 2H, J=1.9, 8.7 Hz), 8.07 (dd, 1H, J=1.1, 7.0 Hz), 8.03 (dd, 1H, J=1.1, 8.4 Hz), 7.90 (br. s, 1H), 7.56 (d, 2H, J=8.6 Hz), 7.29 (dd, 1H, J=7.1, 8.4 Hz), 3.47 - 3.21 (m, 2H), 3.19 - 3.02 (m, 2H), 2.99 - 2.87 (m, 2H), 2.74 - 2.63 (m, 1H), 2.41 (d, 1H, J=14.7 Hz), 2.24 (dt, 1H, J=4.0, 18.0 Hz), 2.02 - 1.71 (m, 7H), 1.36 - 1.22 (m, 2H), 1.06 (s, 3H), 0.75 (s, 3H). FT-IR (cm -1 ): 3466.56, 3305.79, 3134.98, 2983.48, 2966.85, 2924.72, 2855.25, 2629.88, 2529.59, 2443.22, 1724.23, 1660.68, 1611.04, 1594.54, 1525.74, 1458.86, 1378.40, 1351.19, 1305.30, 1277.01, 1254.07, 1196.23, 1110.37, 1032.65, 941.09, 906.51, 867.55, The IR spectrum of niraparib camphorsulfonate is shown in FIG21 . Embodiment 4 : X Radiation powder diffraction (XRPD) The XRPD patterns of the crystalline solids produced in Examples 1 to 3 are shown in Figures 3, 9, 15 and 22. Niraparib ( The (R)-(-)-mandelate salt was ground until a more homogeneous particle size was achieved prior to XRPD analysis. The crystalline form observed in each case was designated "Form 1". The following Tables 1 to 4 list the XRPD diffraction angles from Figures 3, 9, 15, and 22, respectively. Table 1: XRPD diffraction angles of niraparib (+)-camphorate (Form 1) XRPD diffraction angles Table 2: XRPD diffraction angles of niraparib (-)-camphorate (Form 1) XRPD diffraction angles Table 3: XRPD diffraction angles of niraparib mandelate (Form 1) XRPD diffraction angles Table 4: XRPD diffraction angles of niraparib camphorsulfonate (Form 1) XRPD diffraction angles Example 5 : Melting characteristics DSC was performed on the crystalline solids produced in Examples 1 to 3. The DSC thermograms can be seen in Figures 5, 11, 18, and 24. The following Table 5 lists the parameters from their thermograms. Table 5: Example 6 : Hygroscopicity GVS was performed on the crystalline solids produced in Examples 1 and 3. DVS was performed on the crystalline solid produced in Example 2. The results are shown in Figures 6, 12, 19, and 25. The following Table 6 outlines the % mass increase of the samples observed at 90% RH. The camphorates and mandelates are non-hygroscopic (≤ 0.5% mass increase); the camphorsulfonate is slightly hygroscopic. Table 6: Example 7 : Storage stability Samples of each of the crystalline solids produced in Examples 1 to 3 above were stored at 40 °C and 75% RH for 24 hours and then analyzed by XRPD. All materials remained unchanged after storage at 40 °C / 75% RH for 24 hours. Example 8 : Niraparib (R)-(-)- mandelate ( form 1) single crystal structure SXRD analysis was carried out using monochromatic Cu Kα (λ = 1.54184 Å) radiation on an Agilent Technologies (Dual Source) SuperNova diffractometer. The diffractometer was equipped with an Oxford Cryosystems low-temperature device to enable data collection at 120(1) K and a crystal encapsulated in a protective layer of Paratone oil. The collected data were corrected for absorption effects in a multi-layer crystal model based on Gaussian integration, which was implemented as part of the CrysAlisPro software package (Agilent Technologies, 2014). The structure was solved by the direct method (SHELXS97)1 and refined by least-squares refinement of F2 using the OLEX2 software package (SHELXL97)1. Images were generated via OLEX2.2, and the data collection was analyzed and improved using the ADDSYMM3 program of PLATON4 with the orthorhombic space group P212121 and a search for higher symmetry, but no higher-order symmetry was revealed. All non-hydrogen atoms were located in the Fourier map, and their positions were refined, after which the anisotropic thermal displacement of all non-hydrogen atoms was described. Within the structure, a complete crystallographically independent niraparib unit was found within the asymmetric unit, and the associated mandelate unit was of full stoichiometry. Within the structure, it was found that the parent niraparib molecule was disordered with the associated mandelic acid at two positions, each occupying 50%. No further disorder was noted in the final structure. Within the disordered unit, the following distances were limited to 1.54 Å with an esd of 0.01; C22A - C21 and C22B - C21. Using the riding model, with fixed Uiso, for all C H, C H 2 and N H 2 groups at 1.2 times and for all O The H groups were multiplied by 1.5 to place all hydrogen atoms at the calculated positions. The highest residual Fourier peak was seen at 0.58 from N2 e.Å -3 at approximately 0.30 Å, and the deepest Fourier pit was seen at -0.37 from N 2 e.Å -3 at approximately 1.55 Å. Niraparib (R)-(-)-mandelate improved parameters Example 9 : Optical microscopy The crystalline solids produced in Examples 1 to 3 were evaluated by optical microscopy using visible and PLM. Micrographs are shown in Figures 7, 13, 20 and 26 and the results are summarized in Table 7 below. Table 7: Example 10 : Solubility study The solubility of the crystalline solids produced in Examples 1.1, 2 and 3 above was compared with the solubility of crystalline niraparib tosylate monohydrate (characterized by the XRPD pattern of Figure 1) using the following protocol In the initial procedure (performed three times), small aliquots of the salt were added to deionized water or buffer solution (10 mL) until saturation was reached (initially about 20 mg added), and the resulting slurry was shaken at 37 °C for 24 hours. The following buffers were used (50 mM in each case): pH 1 25 mL of KCl solution (1.49 g, dissolved in 100 mL of water) and 42.5 mL of HCl solution (1.66 mL of concentrated HCl (about 37%), made up to 100 mL with water) were added together and made up to 100 mL with water; pH 4.5 Anhydrous sodium acetate (1.07 g) was dissolved in water (about 150 mL), then 5.9 mL of acetic acid solution (11.6 mL of glacial acetic acid made up to 100 mL with water) was added. The resulting solution was made up to 500 mL with water; and pH 6.8 25 mL of KH 2 PO 4A solution (2.72 g, dissolved in about 80 mL of water and made up to 100 mL with water) and 11.2 mL of NaOH solution (800 mg of sodium hydroxide dissolved in water and diluted to 100 mL) were added together and made up to 100 mL with water. After the first hour, about 20 to 30 mg of the appropriate salt was added to the following samples: (i) (1 R,3 S)-(+)-camphorate in a pH 1 buffer; (ii) ( R)-(-)-mandelate 1 in water, a pH 1 buffer, and a pH 4.5 buffer; and (iii) (1 S)-(+)-camphorsulfonate in all solvents. Each sample was then filtered and the concentration of niraparib in the mother liquor was determined by HPLC. Any solid separated by filtration was evaluated by XRPD to determine whether the form of the material had changed. For those samples with a solubility greater than 30 mg / ml, the solution was observed after the first addition of 30 mg of solid. The solubility assessment of these samples was repeated (samples prepared in triplicate) using the following procedure: The appropriate salt (30 mg) was weighed into a vial and water or buffer solution (1 mL) was added. The sample was shaken at 37 °C for 24 hours. After 1 hour and after about 17 hours, the salt was added again to the mandelate samples (except those samples in the pH 1 buffer solution), resulting in approximately 50 - 60 mg of solid. For the mandelate pH 1 samples, when observing a two-phase system, the material was reloaded until saturation was reached. The samples were analyzed as described above. The solubility of niraparib salts is shown in Table 8 below. In each case, the reported solubility values are the average of triplicate measurements based on the concentration of niraparib free base in the solution. Table 8: The data in Table 8 indicate that camphorates, mandelates, and camphorsulfonates have greater solubility than tosylates, especially in low pH media. Mandelates exhibit particularly high solubility at various pH values, which is an advantageous property (and unexpected if it lacks hygroscopicity). The teachings of all patents, published applications, and references cited herein are incorporated by reference in their entirety. Although the present invention has been specifically shown and described with reference to exemplary embodiments thereof, those skilled in the art will understand that various changes in form and detail may be made therein without departing from the spirit and scope of the invention as covered by the appended claims. Figure 1 shows an exemplary XRPD pattern of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) tosylate monohydrate used in Example 10. Figure 2 shows the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1. Figure 3 shows an exemplary XRPD pattern of the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1. Figure 4 shows an exemplary XRPD pattern of the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1 after storage at 40 °C and 75% relative humidity for 24 hours. Figure 5 shows an exemplary differential scanning calorimetry thermogram of the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1. Figure 6 shows an exemplary thermogravimetric vapor sorption thermogram of the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1. Figure 7 shows visible light microscopic images of the (1 R,3 S)-(+)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1 (top: non-polarized; bottom: polarized). Figure 8 shows an exemplary FT-IR spectrum of the (1 S,3 R)-(-)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) in crystalline form 1. Figure 9 shows the illustrative XRPD pattern of crystalline Form 1 of (1 S,3 R)-(−)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 10 shows the illustrative XRPD pattern of crystalline Form 1 of (1 S,3 R)-(−)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) after storage at 40 °C and 75% relative humidity for 24 hours. Figure 11 shows the illustrative differential scanning calorimetry thermogram of crystalline Form 1 of (1 S,3 R)-(−)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 12 shows the illustrative scanning gravimetric vapor sorption thermogram of crystalline Form 1 of (1 S,3 R)-(−)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 13 shows the visible light microscopic images of crystalline Form 1 of (1 S,3 R)-(−)-camphorate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (upper figure: non-polarized; lower figure: polarized). Figure 14 shows the illustrative FT-IR spectrum of crystalline Form 1 of ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 15 shows the illustrative XRPD pattern of crystalline Form 1 of ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 16 shows the illustrative XRPD pattern of crystalline Form 1 of ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) after storage at 40 °C and 75% relative humidity for 24 hours. Figure 17 shows the structure of the ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) as determined by single crystal X-ray crystallography. Figure 18 shows an exemplary differential scanning calorimetry thermogram of crystalline form 1 of the ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 19 shows an exemplary dynamic vapor sorption thermogram of crystalline form 1 of the ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 20 shows visible light microscopic images (upper figure: non-polarized; lower figure: polarized) of crystalline form 1 of the ( R)-(−)-mandelate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 21 shows an exemplary FT-IR spectrum of crystalline form 1 of the (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 22 shows an exemplary XRPD pattern of crystalline form 1 of the (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 23 shows an exemplary XRPD pattern of crystalline form 1 of the (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) after storage at 40 °C and 75% relative humidity for 24 hours. Figure 24 shows an exemplary differential scanning calorimetry thermogram of crystalline form 1 of the (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 25 shows an exemplary gravimetric vapor sorption thermogram of crystalline form 1 of the (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib). Figure 26 shows the visible light microscopic images of crystalline Form 1 of (1 S)-(+)-camphorsulfonate of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (niraparib) (upper figure: non-polarized light; lower figure: polarized light).

Claims

1. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide salt, wherein the salt is selected from: 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide camphorate; 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide amygdalinate; and 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide camphor sulfonate.

2. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1R,3S)-(+)-camphorate.

3. A crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1R,3S)-(+)-camphorate.

4. The crystalline form as described in claim 3, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 6.5, 11.7, 13.4, 14.1, 14.5, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6, 22.3, 22.8, 24.0, 24.5, 26.9, and 27.6 degrees 2θ.

5. The crystalline form as described in claim 3, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 11.7, 13.4, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6, 22.8 and 24.0 degrees 2θ.

6. The crystalline form as described in claim 3, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 13.4, 15.2, 16.2, 17.5, 18.0, 20.0, 20.4, 21.6, and 24.0 degrees 2θ.

7. The crystalline form of any one of claims 3 to 6, wherein, The crystalline form is characterized substantially according to the X-ray powder diffraction (XRPD) pattern in Figure 3.

8. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S,3R)-(-)-camphorate.

9. A crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S,3R)-(-)-camphorate.

10. The crystal form as described in claim 9, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 6.5, 11.6, 13.4, 14.0, 14.5, 15.1, 16.2, 17.4, 18.9, 19.9, 20.2, 20.3, 21.5, 21.9, 22.2, 22.3, 23.9, 24.4, and 26.9 degrees 2θ.

11. The crystal form as described in claim 9, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 11.6, 13.4, 15.1, 16.2, 17.4, 19.9, 20.2, 20.3, 22.2, 22.3, 24.4, and 26.9 degrees 2θ.

12. The crystal form as described in claim 9, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 11.6, 15.1, 16.2, 17.4, 19.9, 20.2, 20.3, 22.3, and 24.4 degrees 2θ.

13. The crystalline form of any of claims 9 to 12, characterized in that it is substantially in accordance with the X-ray powder diffraction (XRPD) pattern of Figure 9.

14. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (R)-(-)-amymidine.

15. A crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (R)-(-)-amymidine.

16. The crystalline form as described in claim 15, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 4.3, 8.4, 8.6, 8.7, 12.4, 13.7, 14.1, 16.1, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 27.7, 28.0, and 28.7 degrees 2θ.

17. The crystalline form as described in claim 15, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 8.4, 8.6, 8.7, 13.7, 14.1, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 27.7, 28.0, and 28.7 degrees 2θ.

18. The crystalline form as described in claim 15, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 8.6, 8.7, 13.7, 16.4, 17.4, 18.4, 18.5, 21.5, 25.1, 27.3, 27.6, 28.0, and 28.7 degrees 2θ.

19. The crystalline form of any one of claims 15 to 18, wherein, The crystal is characterized substantially according to the X-ray powder diffraction (XRPD) pattern in Figure 15.

20. A 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S)-(+)-camphor sulfonate.

21. A crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S)-(+)-camphor sulfonate.

22. The crystalline form as claimed in claim 21, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 6.7, 9.5, 11.1, 13.5, 14.3, 16.0, 16.4, 16.7, 16.9, 17.6, 20.3, 22.8, 23.7, 24.3, 24.6, 25.0, 25.2, 25.8, and 26.8 degrees 2θ.

23. The crystalline form as claimed in claim 21, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 11.1, 13.5, 16.0, 16.4, 16.7, 17.6, 20.3, 23.7, 24.3, 24.6, 25.0, 25.2, and 25.8 degrees 2θ.

24. The crystalline form as described in claim 21, wherein, The crystal form is characterized by X-ray powder diffraction (XRPD) patterns with at least three diffraction angles selected from the following groups when measured using Cu K radiation: approximately 11.1, 13.5, 16.0, 16.4, 16.7, 17.6, 20.3, 23.7, 24.3 and 24.6 degrees 2θ.

25. The crystalline form of any of claims 21 to 24, characterized in that it is substantially in accordance with the X-ray powder diffraction (XRPD) pattern of Figure 22.

26. A pharmaceutical composition comprising crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1R,3S)-(+)-camphorate of any one of claims 3 to 7, and at least one pharmaceutically acceptable excipient.

27. The pharmaceutical composition as claimed in claim 26, wherein, This pharmaceutical composition is suitable for oral administration.

28. A pharmaceutical composition comprising crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S,3R)-(-)-camphorate of any one of claims 9 to 13, and at least one pharmaceutically acceptable excipient.

29. The pharmaceutical composition as claimed in claim 28, wherein, This pharmaceutical composition is suitable for oral administration.

30. A pharmaceutical composition comprising crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (R)-(-)-amymidine salt of any one of claims 15 to 19, and at least one pharmaceutically acceptable excipient.

31. The pharmaceutical composition as claimed in claim 30, wherein, This pharmaceutical composition is suitable for oral administration.

32. A pharmaceutical composition comprising crystalline form of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-methamide (nirapanib) (1S)-(+)-camphor sulfonate of any one of claims 21 to 25, and at least one pharmaceutically acceptable excipient.

33. The pharmaceutical composition as claimed in claim 32, wherein, This pharmaceutical composition is suitable for oral administration.

34. The compound of any one of claims 1, 2, 8, 14 and 20, the crystalline form of any one of claims 3 to 7, 9 to 13, 15 to 19 and 21 to 25, or the pharmaceutical composition of any one of claims 26 to 33, which is used in a therapeutic manner.

35. Use of a compound of any one of claims 1, 2, 8, 14 and 20, a crystalline form of any one of claims 3 to 7, 9 to 13, 15 to 19 and 21 to 25, or a pharmaceutical composition of any one of claims 26 to 33, for the manufacture of a pharmaceutical preparation.

36. Use of a compound of any one of claims 1, 2, 8, 14 and 20, a crystalline form of any one of claims 3 to 7, 9 to 13, 15 to 19 and 21 to 25, or a pharmaceutical composition of any one of claims 26 to 33 in the preparation of a medicament for the treatment of cancer, stroke, autoimmune diabetes, neurological disorders, inflammatory diseases, metabolic diseases, or cardiovascular diseases in humans in need.

37. As used in claim 36, wherein, This drug is used to treat cancer.

38. As used in request item 37, wherein, This cancer is associated with BRCA1 and / or BRCA2 mutations.

39. As used in claim 37 or 38, wherein, This cancer is associated with mutations in ATM, ATR, BAP1, BARD1, BLM, BRIP1, MRE11A, NBN, PALB2, RAD51, RAD51B, RAD51C, RAD51D, RAD52, RAD54L, or XRCC2, or any combination thereof.

40. As in the use of claim 37 or 38, wherein, The cancer could be epithelial ovarian cancer, fallopian tube cancer, or primary peritoneal cancer.

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