General Information of the Drug (ID: ferrodrug0190)
Name
Niraparib
Synonyms
Niraparib; 1038915-60-4; MK-4827; (S)-2-(4-(piperidin-3-yl)phenyl)-2H-indazole-7-carboxamide; MK4827; Niraparib [USAN]; 2-{4-[(3s)-piperidin-3-yl]phenyl}-2h-indazole-7-carboxamide; MK 4827; HMC2H89N35; 2-[4-[(3S)-piperidin-3-yl]phenyl]indazole-7-carboxamide; CHEMBL1094636; Niraparib (USAN); ZL-2306; JNJ-64091742; (S)-2-(4-(piperidin-3-yl)phenyl)-2H-indazole-7-carboxamide;MK-4827; Niraparib [USAN:INN]; 2-{4-[(3S)-piperidin-3-yl]phenyl}indazole-7-carboxamide; UNII-HMC2H89N35; MK 4827 (Base); 3JD; Zejula (TN); NIRAPARIB [INN]; NIRAPARIB [MI]; MK-4827(Niraparib); NIRAPARIB [WHO-DD]; GTPL8275; SCHEMBL1421875; AMY4192; DTXSID50146129; EX-A290; CHEBI:176844; MK-4827 (PARP-1); BDBM50316226; MFCD17779309; NSC754355; NSC800020; s2741; AKOS016004869; BCP9000940; CCG-267709; compound 56 [PMID 19873981]; CS-0780; DB11793; MK-4827/MK4827; NSC-754355; NSC-800020; NCGC00346435-01; NCGC00346435-04; AC-28447; AS-35248; HY-10619; BCP0726000077; D10140; EN300-7364833; A857972; Q25326660; 2-[4-(3S)-3-Piperidinylphenyl]-2H-indazole-7-carboxamide; 2H-Indazole-7-carboxamide, 2-[4-(3S)-3-piperidinylphenyl]; 2H-INDAZOLE-7-CARBOXAMIDE, 2-(4-(3S)-3-PIPERIDINYLPHENYL)-; 2H-Indazole-7-carboxamide, 2-[4-(3S)-3-piperidinylphenyl]-; 2-[4-(3S)-3-Piperidinylphenyl]-2H-indazole-7-carboxamide; Niraparib; Zejula; MK-4827

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Structure
Formula
C19H20N4O
IUPAC Name
2-[4-[(3S)-piperidin-3-yl]phenyl]indazole-7-carboxamide
Canonical SMILES
C1CC(CNC1)C2=CC=C(C=C2)N3C=C4C=CC=C(C4=N3)C(=O)N
InChI
InChI=1S/C19H20N4O/c20-19(24)17-5-1-3-15-12-23(22-18(15)17)16-8-6-13(7-9-16)14-4-2-10-21-11-14/h1,3,5-9,12,14,21H,2,4,10-11H2,(H2,20,24)/t14-/m1/s1
InChIKey
PCHKPVIQAHNQLW-CQSZACIVSA-N
PubChem CID
24958200
Full List of Ferroptosis Target Related to This Drug
Cystine/glutamate transporter (SLC7A11)
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Suppressor
Responsed Disease Colorectal cancer ICD-11: 2B91
Responsed Regulator Cyclic GMP-AMP synthase (CGAS) Driver
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cytosolic DNA-sensing pathway hsa04623
Cell Process Cell ferroptosis
In Vitro Model HT29 cells Colon cancer Mus musculus CVCL_A8EZ
CT26 cells Colon adenocarcinoma Mus musculus CVCL_7254
MC-38 cells Colon adenocarcinoma Homo sapiens CVCL_B288
In Vivo Model
Six-week-old male BALB/c athymic nude mice were purchased from the Experimental Animal Center of Peking (Beijing, China). Stable cells (5 x 106) were seeded into the right flanks of the mice. After the xenografts had grown to 200 mm3, saline as a vehicle or sorafenib (30 mg/kg) was administered by gavage every day, and the mice were euthanized by the cervical dislocation method five weeks later. Before sacrifice, the tumor sizes and body weights were measured twice per week. The tumor volume (V) was calculated as follows: (L x W2)/2 (length, L, and width, W). The xenografts were excised and further assessed.

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Response regulation Niraparib, a widely used PARPi, augmented cGAS-mediated ferroptosis and immune activation. In colorectal cancer models, cGAS signaling exerts tumor control via ATF3SLC7A11GPX4-mediated ferroptosis and IFNCD8 T cell-mediated antitumor immune response.
References
Ref 1 PARPi treatment enhances radiotherapy-induced ferroptosis and antitumor immune responses via the cGAS signaling pathway in colorectal cancer. Cancer Lett. 2022 Dec 1;550:215919. doi: 10.1016/j.canlet.2022.215919. Epub 2022 Sep 16.