Rucaparib

Identification

Summary

Rucaparib is an anti-cancer agent used to treat recurrent ovarian, fallopian tube, or peritoneal cancer.

Brand Names

Rubraca

Generic Name

Rucaparib

DrugBank Accession Number

DB12332

Background

Rucaparib is a potent mammalian poly(ADP-ribose) polymerase (PARP) 1, 2 and 3 inhibitor with anticancer properties. PPAR is an enzyme that plays an essential role in DNA repair by activating response pathways and facilitating repair ², and defects in these repair mechanisms have been demonstrated in various malignancies, including cancer. Regulation of repair pathways is critical in promoting necessary cell death. BRCA genes are tumor suppressor genes mediate several cellular process including DNA replication, transcription regulation, cell cycle checkpoints, apoptosis, chromatin structuring and homologous recombination (HR). Homologous recombination deficiency (HRD), along with PPAR inhibition, is a vulnerability that enhances the cell death pathway when the single mutations alone would permit viability. Ovarian cancer commonly possesses defects in DNA repair pathways such as HRD due to BRCA mutations or otherwise.

There are three main types of ovarian cancer: epithelial (90%), germ cell (5%) and sex cord stromal cell (5%). Epithelial ovarian, being the most common, fifth leading cause of cancer-related deaths in women in the United States. Advanced ovarian cancer particularly poses challenges due to reduced therapeutic response rates from standard platinum-based chemotherapy and overall survival rates. Rucaparib has shown to induce cytotoxicity in tumor cell lines with deficiencies in BRCA1/2 and other DNA repair genes ^Label. Of all the BRCA1/2 mutations in ovarian cancer, most are due to germline mutations (18%), and approximately 7% represent somatic mutations acquired within the tumor ⁴.

The indication of rucaparib as an oral monotherapy in patients with deleterious BRCA mutation (germline and/or somatic) associated advanced ovarian cancer was granted accelerated approval in 2016 for selected patients who have previously received greater than two lines of platinum-based therapy. It is currently marketed in the US under the brand name Rubraca that contains rucaparib camsylate as the active ingredient. The identification of patients who are eligible for rucaparib therapy is performed via in vitro diagnostic tests to detect the presence of a deleterious BRCA mutation (germline and/or somatic). The FDA-approved test qualitatively detects sequence alterations in BRCA1 and BRCA2 (BRCA1/2) genes. More information can be found on the FDA Website ⁸.

While rucaparib is indicated for deleterious BRCA mutation (germline and/or somatic)-associated advanced ovarian cancer, there is evidence that its antitumor activity is also clinically effective against ovarian tumors with high homologous recombination deficiency (HRD) loss of heterozygosity (LOH) ⁴.

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Rucaparib (DB12332)

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Weight

Average: 323.371
Monoisotopic: 323.143390375

Chemical Formula

C₁₉H₁₈FN₃O

Synonyms

• Rucaparib

External IDs

• AG-14447

Pharmacology

Indication

Indicated as monotherapy for the treatment of patients with deleterious BRCA mutation (germline and/or somatic) associated advanced ovarian cancer who have been treated with two or more chemotherapies. Select patients for therapy based on an FDA-approved companion diagnostic for rucaparib.

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Associated Conditions

• Advanced Ovarian Cancer

Contraindications & Blackbox Warnings

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Pharmacodynamics

Rucaparib has been shown to decrease tumor growth in mouse xenograft models of human cancer with or without deficiencies in BRCA ^Label.

The effect of multiple doses of rucaparib on QTc interval was evaluated in an open-label single-arm study in 56 patients with solid tumors who were administered continuous doses of rucaparib ranging from 40 mg once daily (0.03 times the approved recommended dosage) to 840 mg twice daily (1.4 times the approved recommended dosage). The mean QTcF increase from baseline (90% confidence interval [CI]) in population pharmacokinetics estimated 95% percentile Cmax (3019 ng/mL) at steady state of 600 mg rucaparib twice daily was 14.9 msec (11.1-18.7 msec) ^Label.

Mechanism of action

Poly (ADP-ribose) polymerase (PARP) enzymes play a role in DNA repair. PPAR-1 is responsible in repairing single stranded breaks (SSBs) in base excision repair (BER). PARP1 also functions in nonhomologous end-joining (NHEJ) regulation, chromatin remodeling and homologous recombination (HR) DNA repair pathways ². When PARP is inhibited, single-strand breaks become double-strand breaks, which are typically repaired via homologous recombination ². Pre-existing homologous recombination deficiency (HRD) may occur through mutations in the BRCA1 or BRCA2 genes, which confers persistant cell repair and growth in cancer cells.

Rucaparib is an inhibitor of PARP-1, PARP-2, and PARP-3. Via an inhibitory effect on the PARP enzymatic activity, rucaparib decreases the formation of PARP-DNA complexes resulting in DNA damage, apoptosis, and cell death ^Label. It is proposed that PARP inhibition specifically targets tumor cells with preexisting HRD, such as those cells possessing mutations in the BRCA1 or BRCA2 genes ⁴. Rucaparib induces synthetic lethality by disrupting ingle- and double-strand repair pathways leading to tumor cell death. It is also suggested that PARP inhibition can lead to trapping of PARP-1 enzyme on damaged DNA, effectively preventing continuation of the DNA repair process; defective BRCA1 recruitment to damaged DNA; and activation of alternative DNA repair such as error-prone nonhomologous end joining (NHEJ) or alternative end joining pathways leading to mutations or chromosomal changes and ultimately cell death ⁴.

Target	Actions	Organism
APoly [ADP-ribose] polymerase 1	antagonist	Humans
APoly [ADP-ribose] polymerase 2	antagonist	Humans
APoly [ADP-ribose] polymerase 3	antagonist	Humans

Absorption

Rucaparib demonstrates a linear pharmacokinetic properties over a dose range from 240 to 840 mg twice daily with time-independence and dose-proportionality. The mean steady-state rucaparib Cmax was 1940 ng/mL (54% coefficient of variation [CV]) and AUC0-12h was 16900 h⋅ng/mL (54% CV) at the approved recommended dosage. The time to reach the steady-state peak plasma concentration (Tmax) was 1.9 hours at the recommended dosage. The mean absolute bioavailability of rucaparib immediate-release tablet was 36% with a range from 30% to 45%. Following a high-fat meal, the Cmax was increased by 20% and AUC 0-24h was increased by 38%, and T max was delayed by 2.5 hours, as compared to dosing under fasted conditions ^Label.

Volume of distribution

Following a single intravenous dose of 12mg to 40mg rucaparib, the steady-state volume of distribution was 113L to 262L ^Label.

Protein binding

In vitro, the protein binding of rucaparib was 70% in human plasma at therapeutic concentrations. Rucaparib preferentially distributed to red blood cells with a blood-to-plasma concentration ratio of 1.83 ^Label.

Metabolism

According to in vitro studies, rucaparib is primarily metabolized by CYP2D6 and to a lesser extent by CYP1A2 and CYP3A4 ^Label.

Route of elimination

Fecal excretion was the major route of elimination, accounting for ≥ 79% of the total dose.

Half-life

Following a single oral dose of 600mg rucaparib, the mean terminal half life (t1/2) was 17-19 hours ^Label.

Clearance

Following continuous 600mg rucaparib administration orally twice daily, the apparent clearance ranges from 15.3 to 79.2 L/hour. The clearance ranged from 13.9 to 18.4 L/hour, following a single intravenous dose of rucaparib 12 mg to 40 mg ^Label.

Adverse Effects

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Toxicity

According to a bacterial reverse mutation (Ames) test, rucaparib has shown to be mutagenic. It was also clastogenic in an in vitro chromosomal aberration assay in cultured human lymphocytes. Rucaparib has a genotoxic potential. Based on its mechanism of action and findings from animal studies, rucaparib can cause fetal harm when administered to a pregnant woman. Female patients of reproductive potential should be advised to use effective contraception during treatment and for 6 months following the last dose of rucaparib ^Label.

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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Abacavir	The metabolism of Abacavir can be decreased when combined with Rucaparib.
Abametapir	The serum concentration of Rucaparib can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Rucaparib can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be increased when it is combined with Rucaparib.
Abiraterone	The serum concentration of Rucaparib can be increased when it is combined with Abiraterone.
Acalabrutinib	The metabolism of Acalabrutinib can be decreased when combined with Rucaparib.
Acamprosate	The excretion of Acamprosate can be decreased when combined with Rucaparib.
Acebutolol	The metabolism of Acebutolol can be decreased when combined with Rucaparib.
Acenocoumarol	The serum concentration of Acenocoumarol can be increased when it is combined with Rucaparib.
Acetaminophen	The metabolism of Acetaminophen can be decreased when combined with Rucaparib.

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Food Interactions

• Exercise caution with grapefruit products. Rucaparib is primarily metabolized through CYP2D6 but is also metabolized by CYP3A4 and CYP1A2. Grapefruit inhibits CYP3A4 metabolism, which may increase rucaparib serum levels.
• Exercise caution with St. John's Wort. Rucaparib is primarily metabolized through CYP2D6 but is also metabolized by CYP3A4 and CYP1A2. St. John's Wort induces CYP3A4 metabolism, which may reduce rucaparib serum levels.
• Take with or without food. High-fat meals may increase the bioavailability and delay the Tmax of rucaparib.

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Rucaparib camsylate	41AX9SJ8KO	1859053-21-6	INBJJAFXHQQSRW-STOWLHSFSA-N
Rucaparib phosphate	H3M9955244	459868-92-9	FCCGJTKEKXUBFZ-UHFFFAOYSA-N

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Rubraca	Tablet, film coated	200 mg/1	Oral	Clovis Oncology, Inc.	2016-12-19	Not applicable
Rubraca	Tablet, film coated	300 mg/1	Oral	Clovis Oncology, Inc.	2016-12-19	Not applicable
Rubraca	Tablet, film coated	250 mg/1	Oral	Clovis Oncology, Inc.	2017-05-01	Not applicable
Rubraca	Tablet, film coated	200 mg	Oral	Clovis Oncology Ireland Limited	2020-12-16	Not applicable
Rubraca	Tablet, film coated	250 mg	Oral	Clovis Oncology Ireland Limited	2020-12-16	Not applicable
Rubraca	Tablet, film coated	300 mg	Oral	Clovis Oncology Ireland Limited	2020-12-16	Not applicable

Categories

ATC Codes

L01XX55 — Rucaparib

• L01XX — Other antineoplastic agents
• L01X — OTHER ANTINEOPLASTIC AGENTS
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• BCRP/ABCG2 Inhibitors
• BCRP/ABCG2 Substrates
• Cytochrome P-450 CYP1A2 Inducers
• Cytochrome P-450 CYP1A2 Inducers (moderate)
• Cytochrome P-450 CYP1A2 Inhibitors
• Cytochrome P-450 CYP1A2 Inhibitors (weak)
• Cytochrome P-450 CYP1A2 Substrates
• Cytochrome P-450 CYP1A2 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 CYP2C19 Inhibitors
• Cytochrome P-450 CYP2C19 Inhibitors (weak)
• Cytochrome P-450 CYP2C8 Inhibitors
• Cytochrome P-450 CYP2C8 Inhibitors (weak)
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2D6 Inhibitors
• Cytochrome P-450 CYP2D6 Inhibitors (moderate)
• Cytochrome P-450 CYP2D6 Substrates
• Cytochrome P-450 CYP2D6 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 CYP3A Inhibitors
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inhibitors
• Cytochrome P-450 CYP3A4 Inhibitors (weak)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A4 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 CYP3A5 Inhibitors
• Cytochrome P-450 CYP3A5 Inhibitors (strength unknown)
• Cytochrome P-450 CYP3A7 Inhibitors
• Cytochrome P-450 CYP3A7 Inhibitors (strength unknown)
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Enzyme Inhibitors
• Heterocyclic Compounds, Fused-Ring
• MATE 1 Inhibitors
• MATE 2 Inhibitors
• MATE inhibitors
• Narrow Therapeutic Index Drugs
• OAT1/SLC22A6 inhibitors
• OAT3/SLC22A8 Inhibitors
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B3 inhibitors
• OCT1 inhibitors
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• P-glycoprotein substrates with a Narrow Therapeutic Index
• Poly(ADP-ribose) Polymerase Inhibitors
• UGT1A1 Inhibitors

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as 2-phenylindoles. These are indoles substituted at the 2-position with a phenyl group.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Indoles and derivatives

Sub Class

Indoles

Direct Parent

2-phenylindoles

Alternative Parents

Phenylpyrroles / Benzazepines / 3-alkylindoles / Phenylmethylamines / Benzylamines / Aralkylamines / Azepines / Aryl fluorides / Heteroaromatic compounds / Secondary carboxylic acid amides / Amino acids and derivatives / Lactams / Azacyclic compounds / Dialkylamines / Organopnictogen compounds / Organic oxides / Organofluorides / Hydrocarbon derivatives / Organooxygen compounds

show 9 more

Substituents

2-phenylindole / 2-phenylpyrrole / 3-alkylindole / Amine / Amino acid or derivatives / Aralkylamine / Aromatic heteropolycyclic compound / Aryl fluoride / Aryl halide / Azacycle / Azepine / Benzazepine / Benzenoid / Benzylamine / Carboxamide group / Carboxylic acid derivative / Heteroaromatic compound / Hydrocarbon derivative / Lactam / Monocyclic benzene moiety / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organofluoride / Organohalogen compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Phenylmethylamine / Pyrrole / Secondary aliphatic amine / Secondary amine / Secondary carboxylic acid amide / Substituted pyrrole

show 24 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

Not Available

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

8237F3U7EH

CAS number

283173-50-2

InChI Key

HMABYWSNWIZPAG-UHFFFAOYSA-N

InChI

InChI=1S/C19H18FN3O/c1-21-10-11-2-4-12(5-3-11)18-14-6-7-22-19(24)15-8-13(20)9-16(23-18)17(14)15/h2-5,8-9,21,23H,6-7,10H2,1H3,(H,22,24)

IUPAC Name

6-fluoro-2-{4-[(methylamino)methyl]phenyl}-3,10-diazatricyclo[6.4.1.0^{4,13}]trideca-1,4,6,8(13)-tetraen-9-one

SMILES

CNCC1=CC=C(C=C1)C1=C2CCNC(=O)C3=C2C(N1)=CC(F)=C3

References

General References

1. Nile DL, Rae C, Hyndman IJ, Gaze MN, Mairs RJ: An evaluation in vitro of PARP-1 inhibitors, rucaparib and olaparib, as radiosensitisers for the treatment of neuroblastoma. BMC Cancer. 2016 Aug 11;16:621. doi: 10.1186/s12885-016-2656-8. [Article]
2. Jenner ZB, Sood AK, Coleman RL: Evaluation of rucaparib and companion diagnostics in the PARP inhibitor landscape for recurrent ovarian cancer therapy. Future Oncol. 2016 Jun;12(12):1439-56. doi: 10.2217/fon-2016-0002. Epub 2016 Apr 18. [Article]
3. Drew Y, Ledermann J, Hall G, Rea D, Glasspool R, Highley M, Jayson G, Sludden J, Murray J, Jamieson D, Halford S, Acton G, Backholer Z, Mangano R, Boddy A, Curtin N, Plummer R: Phase 2 multicentre trial investigating intermittent and continuous dosing schedules of the poly(ADP-ribose) polymerase inhibitor rucaparib in germline BRCA mutation carriers with advanced ovarian and breast cancer. Br J Cancer. 2016 Mar 29;114(7):723-30. doi: 10.1038/bjc.2016.41. Epub 2016 Mar 22. [Article]
4. Dockery LE, Gunderson CC, Moore KN: Rucaparib: the past, present, and future of a newly approved PARP inhibitor for ovarian cancer. Onco Targets Ther. 2017 Jun 19;10:3029-3037. doi: 10.2147/OTT.S114714. eCollection 2017. [Article]
5. CENTER FOR DRUG EVALUATION AND RESEARCH [Link]
6. Daily med. [Link]
7. FDA Label [Link]
8. FDA List of Cleared or Approved Companion Diagnostic Devices (In Vitro and Imaging Tools) [Link]

External Links

KEGG Drug

D10079

PubChem Compound

9931954

PubChem Substance

347828593

ChemSpider

8107584

BindingDB

50446130

RxNav

1862579

ChEBI

134689

ChEMBL

CHEMBL1173055

ZINC

ZINC000000025958

PharmGKB

PA166163418

PDBe Ligand

RPB

Wikipedia

Rucaparib

PDB Entries

4bjc / 4rv6 / 6vkk

FDA label

Download (344 KB)

Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
3	Active Not Recruiting	Treatment	Complete Response / Fallopian Tubes Cancer / FIGO Stage III-IV / Newly Diagnosed / Ovarian Cancer (Epithelial) / Partial Response / Primary Peritoneal	1
3	Active Not Recruiting	Treatment	Fallopian Tubes Cancer / Malignant Peritoneal Neoplasm / Ovarian Cancer	1
3	Active Not Recruiting	Treatment	Fallopian Tubes Cancer / Malignant Peritoneal Neoplasm / Ovarian Cancer / Ovarian Cancer (Epithelial)	1
3	Enrolling by Invitation	Treatment	Fallopian Tubes Cancer / Malignant Peritoneal Neoplasm / Metastatic Castration Resistant Prostate Cancer (CRPC) / Other Solid Tumors / Ovarian Cancer / Ovarian Cancer (Epithelial)	1
3	Recruiting	Treatment	Castration-Resistant Prostate Carcinoma / Metastatic Prostate Adenocarcinoma / Stage IV Prostate Cancer AJCC v8 / Stage IVA Prostate Cancer AJCC v8 / Stage IVB Prostate Cancer AJCC v8	1
3	Recruiting	Treatment	Clear Cell Carcinoma / Fallopian Tubes Cancer / Ovarian Cancer / Primary Peritoneal Cancer	1
3	Recruiting	Treatment	Metastatic Castration Resistant Prostate Cancer (CRPC)	1
2	Active Not Recruiting	Treatment	Advanced Gastric Cancer	1
2	Active Not Recruiting	Treatment	Cervical Cancers / Endometrial Cancer	1
2	Active Not Recruiting	Treatment	Endometrial Cancer / Uterine Carcinosarcoma	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral	200 MG
Tablet, film coated	Oral	200 mg/1
Tablet, film coated	Oral	250 mg/1
Tablet, film coated	Oral	250 MG
Tablet, film coated	Oral	300 mg/1
Tablet, film coated	Oral	300 MG

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US8859562	No	2014-10-14	2031-08-04
US8143241	No	2012-03-27	2027-08-12
US6495541	No	2002-12-17	2020-01-10
US8754072	No	2014-06-17	2031-02-10
US9045487	No	2015-06-02	2031-02-10
US8071579	No	2011-12-06	2027-08-12
US7531530	No	2009-05-12	2024-07-23
US7351701	No	2008-04-01	2024-07-23
US9861638	No	2018-01-09	2031-02-10
US9987285	No	2018-06-05	2035-08-17
US10130636	No	2018-11-20	2035-08-17
US10278974	No	2019-05-07	2031-02-10

Properties

State

Solid

Experimental Properties

Property	Value	Source
water solubility	1 mg/mL	FDA Label

Predicted Properties

Property	Value	Source
Water Solubility	0.0114 mg/mL	ALOGPS
logP	2.39	ALOGPS
logP	2.45	ChemAxon
logS	-4.4	ALOGPS
pKa (Strongest Acidic)	13.16	ChemAxon
pKa (Strongest Basic)	9.32	ChemAxon
Physiological Charge	1	ChemAxon
Hydrogen Acceptor Count	2	ChemAxon
Hydrogen Donor Count	3	ChemAxon
Polar Surface Area	56.92 Å2	ChemAxon
Rotatable Bond Count	3	ChemAxon
Refractivity	92.91 m3·mol-1	ChemAxon
Polarizability	35.19 Å3	ChemAxon
Number of Rings	4	ChemAxon
Bioavailability	1	ChemAxon
Rule of Five	Yes	ChemAxon
Ghose Filter	Yes	ChemAxon
Veber's Rule	No	ChemAxon
MDDR-like Rule	No	ChemAxon

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	Not Available

Targets

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insights and accelerate drug research.

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Details1. Poly [ADP-ribose] polymerase 1

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Antagonist

General Function

Zinc ion binding

Specific Function

Involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism. This ...

Gene Name

PARP1

Uniprot ID

P09874

Uniprot Name

Poly [ADP-ribose] polymerase 1

Molecular Weight

113082.945 Da

Details2. Poly [ADP-ribose] polymerase 2

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Antagonist

General Function

Nad+ adp-ribosyltransferase activity

Specific Function

Involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism. This ...

Gene Name

PARP2

Uniprot ID

Q9UGN5

Uniprot Name

Poly [ADP-ribose] polymerase 2

Molecular Weight

66205.31 Da

Details3. Poly [ADP-ribose] polymerase 3

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Antagonist

General Function

Nad+ adp-ribosyltransferase activity

Specific Function

Involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism. This ...

Gene Name

PARP3

Uniprot ID

Q9Y6F1

Uniprot Name

Poly [ADP-ribose] polymerase 3

Molecular Weight

60069.7 Da

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Drug created on October 20, 2016 21:59 / Updated on October 07, 2021 12:09