Rucaparib (AG-014699,PF-01367338) phosphate

Catalog No.S1098

Molecular Weight(MW): 421.36

Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with K_i of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.

Cited by 35 Publications

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J Hepatol, 2015, 63(5):1164-72

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Clin Cancer Res, 2013, 19(18):5003-15

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Purity & Quality Control

Choose Selective PARP Inhibitors

Biological Activity

Description

Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with K_i of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.

Features

The first PARP inhibitor used in clinical trials combined with temozolomide.

Targets

PARP ^[1]
(Cell-free assay)

1.4 nM(Ki)

In vitro

Rucaparib is a potent inhibitor of purified full-length human PARP-1 and shows higher inhibition of cellular PARP in LoVo and SW620 cells. Besides, Rucaparib binds detectably to eight other PARP domains, including PARP2, 3, 4, 10, 15, 16, TNKS1 and TNKS2. ^[1] ^[2] The radio-sensitization by Rucaparib is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib could target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions. ^[3] Rucaparib inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells. ^[4]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Formulation	Activity Description	PMID
BT-474	MmXVSpVv[3Srb36gRZN{[Xl?	NYTzOpRnOC5zL{GvOVAxNzFyMECgcm0>			NIXnUnRqdmirYnn0d{BRSVKSIHHjeIl3cXS7IHH0JJN1[XK2aX7nJINwdmOncn70doF1cW:wIH;mJFUxOCCwTR?=	MnS4NlUyOjh2NUW=
BT474	MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVu1NFAhdk1?	M3jUUlEx6oDVMUZCpIQ>		NFjWPJNz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6	M4XM[FI2OTJ6NEW1
SKBR3	MlzRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NG\2bZA2ODBibl2=	NWP5co9nOTEkgKOxOeKh\A>?		MUTy[YR2[2W\|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC\|aXfubYZq[2GwdHz5	NX;L[IJEOjVzMki0OVU>
AU565	NHXzUXdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NXzvOJM{PTByIH7N	MXKxNQKBmzF3wrDk		M1jmZZJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk>	M4LRb\|I2OTJ6NEW1
EFM192A	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWK1NFAhdk1?	MlXkNVDjiJNzNdMg[C=>		MVXy[YR2[2W\|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC\|aXfubYZq[2GwdHz5	M3jvZVI2OTJ6NEW1
MDA-MB-231	NXW0ZpVwTnWwY4Tpc44hSXO\|YYm=	MXKxNE8zOC92MDFOwG0>	M2DER\|I1KGh?		MmnYbY5kemWjc3XzJJAuSUuWIHzleoVteyCrbjDhJIRwe2VvZHXw[Y5l\W62IH3hco5meg>?	M3;EPFI1PDJyMUWy
MDA-MB-231	NW\TU3VYS2WubDDWbYFjcWyrdImgRZN{[Xl?	MoPNNE4yNTRyIN88US=>	M4\OS\|I1KGh?		NVXvVlRKUUN3MPMAjV3jiIlzNz63O:Kh\|ryP	M1ThTFI1PDJyMUWy
MDA-MB-231	M3TLR2Fxd3C2b4Ppd{BCe3OjeR?=	M1LvRVExNzJyL{SwJO69VQ>?	M3rVTVI1KGh?		M4rhTYlv\HWlZYOgZZBweHSxc3nzJIRwe2ViZHXw[Y5l\W62bIm=	MXiyOFQzODF3Mh?=
MDA-MB-231	MlThS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NH;t[G0yOC9{MD:0NEDPxE1?	MUGyOEBp		NV[yXmJO[myxY3vzJINmdGxiY4njcIUheHKxZ4Lld5Nqd25iaX6gS\|IwVSCyaHHz[S=>	MViyOFQzODF3Mh?=
H460	NXzYNHpuT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MWK0NFAhdk1?	MV[yOOKhcA>?		MXXpcoNz\WG\|ZYOgZ4VtdHWuYYKgdoFlcW:\|ZX7zbZRqfmm2eR?=	MYWyOFQyOTZzMR?=
A549	M4HYdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MkHrOFAxKG6P	NYPxbod[OjUEoHi=		NYPFcG9vcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk>	Mly4NlQ1OTF4MUG=
DT40	M{XuO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7				M2rtSGlEPTB;MkGgcm0>	NF\FSmczPDN3NkixNy=>
DU145	NUT1UWVOT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NW\oSW5iUUN3ME2xPEBvVQ>?	NIXBRVczPDN3NkixNy=>
COLO704	MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				MYHJR\|UxRTJwNUKgxtEhOC54NzFOwG0>	MmfyNlM4Ojl2MEK=
OVMANAb	MnXpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				M2nOO2lEPTB;Mj61PEDDuSByLkO4JO69VQ>?	M4XVSlI{PzJ7NECy
OV177	MoqzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				NYPEUFRjUUN3ME2yMlc5KMLzIECuO\|Eh\|ryP	Mlf3NlM4Ojl2MEK=
OAW28	MlL3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				M3LzRmlEPTB;Mz62NUDDuSByLkK4JO69VQ>?	M3zFRlI{PzJ7NECy
OVSAHO	MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				M4rH[WlEPTB;Mz62OEDDuSByLkOzJO69VQ>?	MXGyN\|czQTRyMh?=
OVKATE	M{H0OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7				MWTJR\|UxRTNwNkSgxtEhOS55OTFOwG0>	NWPHOlE1OjN5Mkm0NFI>
OVCAR3	NXLGXWE3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MmrHTWM2OD1\|Lke0JOKyKDBwNECg{txO	MnrjNlM4Ojl2MEK=
PEO14	MmrMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				NUfZW5NiUUN3ME2zMlg1KMLzIECuO\|Yh\|ryP	M1O5SlI{PzJ7NECy
A2780	NHnDR2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=				MmTrTWM2OD1\|Lkm0JOKyKDBwMkWg{txO	Mo\2NlM4Ojl2MEK=
OVTOKO	NVXtN4diT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NITCV2lKSzVyPUSuNVQhyrFiMT61N{DPxE1?	NETpdJUzOzd{OUSwNi=>
KURAMOCHIb	MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				M{XqOmlEPTB;ND6zOEDDuSByLkK5JO69VQ>?	MXKyN\|czQTRyMh?=
TOV21G	MknkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				NEP4[I5KSzVyPUWuNFchyrFiMT6zNEDPxE1?	NV\mSHJUOjN5Mkm0NFI>
OVISE	MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				MXrJR\|UxRTVwNkigxtEhOC5{MzFOwG0>	MUiyN\|czQTRyMh?=
KK	NGW0RmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=				NXfsWGtIUUN3ME22MlE2KMLzIEGuOFIh\|ryP	Mk\iNlM4Ojl2MEK=
RMUGS	NUHyfJh{T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NVXp[ZprUUN3ME23MlA{KMLzIEGuPFMh\|ryP	MmW4NlM4Ojl2MEK=
PEO6	MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				M{KzNGlEPTB;Nz6wOkDDuSByLke0JO69VQ>?	MmOxNlM4Ojl2MEK=
OVCA429	M4rE[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7				NXXhXnJLUUN3ME24MlI6KMLzIEGuOlQh\|ryP	MY[yN\|czQTRyMh?=
OV167	NHmzXlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=				NYfzRm5tUUN3ME24MlM{KMLzIEGuNVgh\|ryP	M1nGc\|I{PzJ7NECy
RMG1	MnLxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				Ml\yTWM2OD17LkOyJOKyKDJwM{[g{txO	M4rIO\|I{PzJ7NECy
OVCAR5	MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				M3\kTmlEPTB;OT61NEDDuSB{LkW5JO69VQ>?	MXqyN\|czQTRyMh?=
EFO21	MmjXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				M1[0TWlEPTB;OT65NkDDuSBzLki3JO69VQ>?	NXPP[lh6OjN5Mkm0NFI>
ES2	NIDFPIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=				M4CxNGlEPTB;MUCuNVIhyrFiMT6yN{DPxE1?	M376[\|I{PzJ7NECy
Tyk-nu	M2fPd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7				NH\ic5BKSzVyPUGwMlIxKMLzIEGuNVIh\|ryP	NHrufVIzOzd{OUSwNi=>
CAOV3	NWXocGY6T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NEfMc3pKSzVyPUGwMlM4KMLzIECuPFch\|ryP	NWTOdFRkOjN5Mkm0NFI>
OV207	M4K5eWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7				NH:3bmpKSzVyPUGyMlI4KMLzIECuN\|Ih\|ryP	NGnneoEzOzd{OUSwNi=>
HEY	MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?				NWDLU2g3UUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?=	NEfTOVkzOzd{OUSwNi=>
DOV13	NWn4Um1jT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MXnJR\|UxRjF3IN88US=>	MXeyN\|czQTRyMh?=
EFO27	NXPMPYNTT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MXLJR\|UxRjF3IN88US=>	Mn;tNlM4Ojl2MEK=
HEY C2	NYDne\|lWT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				Mon5TWM2OD5zNTFOwG0>	MYOyN\|czQTRyMh?=
KOC-7cc	NVK3cJZET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MmX1TWM2OD5zNTFOwG0>	NYHUTWtQOjN5Mkm0NFI>
MCASb	MomxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				MVzJR\|UxRjF3IN88US=>	NGjtXJIzOzd{OUSwNi=>
OAW42	NYfLZXQ2T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NXzUUYs3UUN3ME6xOUDPxE1?	M3XjcVI{PzJ7NECy
OV2008	NVm2T5ViT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NFr1dGtKSzVyPkG1JO69VQ>?	M{nCPVI{PzJ7NECy
OV90	NVrwS4RxT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				NXO1e2ZNUUN3ME6xOUDPxE1?	NGfib\|IzOzd{OUSwNi=>
OVCA420b	MkHWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				MkLaTWM2OD5zNTFOwG0>	NIO4SWQzOzd{OUSwNi=>
OVCA432	NWjMVWkzT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MUHJR\|UxRjF3IN88US=>	NGDaXnMzOzd{OUSwNi=>
PEA2	NYXj[YJiT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=				MknBTWM2OD5zNTFOwG0>	Mn63NlM4Ojl2MEK=
SKOV3	Ml7FS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?				MXPJR\|UxRjF3IN88US=>	M3zzfFI{PzJ7NECy
TOV112D	MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M1PKeFAuOyEQvF2=			MV7JR\|UxRjF3IN88US=>	NGDtRoEzOzd{OUSwNi=>
C4-2	NYD6PHYzT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NE\mXWoxNTNizszN	NUm3N49sOTRiZB?=	MkHQSG1UVw>?	Mmrz[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>?	NVr5NYpCOjN3NkWyOFQ>
PC3	MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M3jvdFAuOyEQvF2=	MUmxOEBl	MWLEUXNQ	MUXk[YNz\WG\|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6	M4DXeFI{PTZ3MkS0
DU145	M{nZfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NWqwcJk4OC1\|IN88US=>	NIrNeXMyPCCm	NGm5Z5FFVVOR	MlXt[IVkemWjc3XzJINwdG:weTDueY1j\XJiZH;z[UBl\XCnbnTlcpRtgQ>?	NXjvZZF2OjN3NkWyOFQ>
VCaP	MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M2i2WVAuOyEQvF2=	NWe5ZWtqOTRiZB?=	M2noTWROW09?	MV\k[YNz\WG\|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6	NGe4OoMzOzV4NUK0OC=>
LNCaP	MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{iyU\|AuOyEQvF2=	MYexOEBl	NYDDUIJ2TE2VTx?=	NF7KToZl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7	NFLYT5YzOzV4NUK0OC=>
MDA-MB-468	M{fLO2NmdGxiVnnhZoltcXS7IFHzd4F6				NE[4TlVKSzVyPUmuO{DPxE1?	M1rtXlIzPjd6MU[x
MDA-MB-231	NEG4SFJE\WyuIG\pZYJqdGm2eTDBd5NigQ>?				M1KzO2lEPTB;MUOg{txO	NIDtWY8zOjZ5OEG2NS=>
Cal-51	M3iyR2NmdGxiVnnhZoltcXS7IFHzd4F6				M1;oO2lEPTB;OD62JO69VQ>?	NHTrPXYzOjZ5OEG2NS=>

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	PAR; PubMed: 27960087 Cancer Cell MCF-7 cells were pretreated ± Rucaparib (15 µM, 2 hr), then ± Rucaparib (15 µM) or two different doses of β-lap (2.0 or 5.0 µM) for 2 hr. Levels of PAR (PARP hyperactivation) formation were assessed with α-tubulin as loading controls. BRCA1; PubMed: 24085845 Proc Natl Acad Sci U S A MCF7 cells, MDA-MB-436 parental cells and resistant clones RR-1, RR-5, and RR-6 were treated with DMSO (−) or 1 µM rucaparib (+) for 24 h, and BRCA1 protein levels were assessed by using BRCA1 N- or C-terminal-specific antibodies by Western blot.	27960087 24085845
Growth inhibition assay	Cell viability; PubMed: 31119062 Adv Wound Care (New Rochelle) The effect of rucaparib on proliferation of keloid fibroblasts. (A) Keloid cell growth following treatment with rucaparib at various concentration (0, 2, 10, 20 μM) was evaluated by MTT assays. Data are expression as mean standard deviation of percent changes of triplicate optical densities. (B) Rucaparib (20 μM) significantly decreased proliferation of keloid fibroblasts. The combination of rucaparib (20 μM) and triamcinolone (50 μM) showed additive suppressive effect on keloid fibroblasts as compared with rucaparib single therapy. Data are expression as mean standard deviation of percent changes of triplicate optical densities. MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide.	31119062
Immunofluorescence	α-tubulin; PubMed: 30589644 J Clin Invest Representative immunofluorescence images of DMSO-, rucaparib- (Ruca-), and Ola-exposed A549-ERCC1(WT/WT) and A549-ERCC1(–/–) cells. Cells were exposed to 15 μM Ruca or 40 μM Ola during 72 hours. White arrows, CCFs; yellow arrows, micronuclei. Scale bar: 20 μm. PAR; PubMed: 27515310 BMC Cancer Cells were treated with 20 mM hydrogen peroxide (H2O2) in order to stimulate PARP-1 activity in the presence or absence of the PARP-1 inhibitors rucaparib and olaparib. Poly(ADP-ribose) (PAR) chain synthesis was detected using an anti-PAR monoclonal Alexa Fluor 488-conjugated antibody (green). The nucleus was visualised using the nuclear counterstain DAPI (blue). Representative images obtained from the analysis of anti-PAR staining of SK-N-BE(2c) cells are shown. γH2AX; PubMed: 23565244 PLoS One γH2AX foci was determined by immunofluoresecence microscopy at 24 h following combined treatment with radiation and rucaparib in PC3 and LNCaP cells. 53BP1; PubMed: 23565244 PLoS One 53BP1 foci was determined by immunofluoresecence microscopy at 24 h following combined treatment with radiation and rucaparib in PC3 and LNCaP cells.	30589644 27515310 23565244

In vivo

Rucaparib is not toxic but significantly enhances temozolomide-induced TGD in the DNA repair protein-competent D384Med xenografts. Pharmacokinetics studies also show that Rucaparib is detected in the brain tissue, which indicates that Rucaparib has potential in intra-cranial malignancy therapy. ^[4] Rucaparib significantly potentiates the cytotoxicity of topotecan and temozolomide in NB-1691, SH-SY-5Y, and SKNBE (2c) cells. Rucaparib enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts. ^[5]

Protocol

Kinase Assay:^[1]	+ Expand K_i Determination: Inhibition of human full-length recombinant PARP-1 by [³²P]NAD⁺ incorporation is measured. The [³²P]ADP-ribose incorporated into acid insoluble material is quantified using a PhosphorImager. K_i is calculated by nonlinear regression analysis.
Cell Research:^[4]	+ Expand Cell lines: D425Med, D283Med and D384Med cells Concentrations: 0.4 μM Incubation Time: 3 or 5 days Method: Medulloblastoma cell lines are seeded in 96-well plates at a density of 1 × 10³, 3 × 10³ and 3 × 10³, respectively. At 24 hours (D384Med) or 48 hours (D283Med and D425Med) after seeding, the cells are exposed to various concentrations of temozolomide in the presence or absence of 0.4 μM Rucaparib. After 3 days (D425Med and D384Med) or 5 days (D283Med) of culture, cell viability is evaluated by a XTT cell proliferation kit assay. Cell growth is expressed as a percentage in relation to DMSO or 0.4 μM Rucaparib-alone controls. The concentration of temozolomide, alone or in combination with Rucaparib that inhibited growth by 50% (GI50) is calculated. The potentiation factor 50 (PF50) is defined as the ratio of the GI50 of temozolomide in the presence of Rucaparib to the GI50 of temozolomide alone. (Only for Reference)
Animal Research:^[4]	+ Expand Animal Models: CD-1 nude mice bearing established D283Med xenografts Formulation: Normal saline Dosages: 1 mg/kg Administration: One or four daily by i.p. (Only for Reference)

References

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Solubility (25°C)

In vitro	DMSO	84 mg/mL (199.35 mM)
	Water	Insoluble
	Ethanol	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 2% DMSO+30% PEG 300+2% Tween 80+ddH2O For best results, use promptly after mixing.	10mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information Download Rucaparib (AG-014699,PF-01367338) phosphate SDF

Molecular Weight	421.36
Formula	C₁₉H₁₈FN₃O.H₃PO₄
CAS No.	459868-92-9
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	N/A

Bio Calculators

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

Serial Dilutions
Concertration (start):
Dilution-folds:

Computed Result

C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
C3=C2/X	C3:	LOG(C3):
C4=C3/X	C4:	LOG(C4):
C5=C4/X	C5:	LOG(C5):
C6=C5/X	C6:	LOG(C6):
C7=C6/X	C7:	LOG(C7):
C8=C7/X	C8:	LOG(C8):

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on )

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT03954366	Recruiting	Drug: Rucaparib\|Drug: Rosuvastatin\|Drug: Oral Contraceptives	Neoplasms	Clovis Oncology Inc.	May 8 2019	Phase 1
NCT03824704	Recruiting	Drug: Rucaparib\|Drug: Nivolumab	Epithelial Ovarian Cancer\|Fallopian Tube Cancer\|Primary Peritoneal Carcinoma\|High Grade Serous Carcinoma\|Endometrioid Adenocarcinoma	Clovis Oncology Inc.\|Bristol-Myers Squibb\|Foundation Medicine	May 15 2019	Phase 2
NCT03413995	Recruiting	Drug: Rucaparib	Prostate Cancer Metastatic	Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins\|Clovis Oncology Inc.	September 10 2018	Phase 2
NCT03572478	Recruiting	Drug: Rucaparib\|Drug: Nivolumab	Prostate Cancer\|Endometrial Cancer	University of Chicago\|Bristol-Myers Squibb\|Clovis Oncology Inc.	August 14 2018	Phase 1\|Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

PARP Signaling Pathway Map

PARP Inhibitors with Unique Features

Selective PARP Inhibitors

AG-14361 : PARP1-selective, K_i<5 nM.
Selective PARP Inhibitors

UPF 1069 : PARP2-selective, IC50=0.3 μM.
Most Potent PARP Inhibitor

MK-4827 (Niraparib) : PARP1, IC50=3.8 nM; PARP2, IC50=2.1 nM.
PARP Inhibitor in Clinical Trial

Iniparib (BSI-201) : Phase III for solid tumors.
Newest PARP Inhibitor

PJ34 HCl ^New : PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.

Related PARP Products

G007-LK ^New

G007-LK is a potent and selective tankyrase inhibitor with IC50 of 46 nM and 25 nM for TNKS1/2, respectively.
NU1025 ^New

NU1025 is a potent PARP inhibitor with IC50 of 400 nM.
SCR7 ^New

SCR7 is a specific DNA Ligase IV inhibitor, which blocks nonhomologous end-joining (NHEJ). It increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.
Olaparib (AZD2281, Ku-0059436)

Olaparib (AZD2281, KU0059436) is a selective inhibitor of PARP1/2 with IC50 of 5 nM/1 nM in cell-free assays, 300-times less effective against tankyrase-1.

Features:A potent PARP inhibitor (currently in late stage clinical trials).
Veliparib (ABT-888)

Veliparib (ABT-888) is a potent inhibitor of PARP1 and PARP2 with K_i of 5.2 nM and 2.9 nM in cell-free assays, respectively. It is inactive to SIRT2. Phase 3.

Features:Increases the efficacy of common cancer therapies such as radiation and alkylating agents.
Talazoparib (BMN 673)

Talazoparib (BMN 673) is a novel PARP inhibitor with IC50 of 0.57 nM for PARP1 in a cell-free assay. It is also a potent inhibitor of PARP-2, but does not inhibit PARG and is highly sensitive to PTEN mutation. Phase 3.

Features:Most potent and selective PARPi reported thus far.
Iniparib (BSI-201)

Iniparib (BSI-201) is a PARP1 inhibitor with demonstrated effectiveness in triple-negative breast cancer (TNBC). Phase 3.
PJ34 HCl

PJ34 HCl is the hydrochloride salt of PJ34, which is a PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.

Features:Water-soluble PARP1/2 inhibitor with >10,000-fold potentcy vs. 3-aminobenzamide (prototypical PARP inhibitor). Potential uses in cardiovascular diseases (stroke, cerebral ischemia, & myocardial ischemia).
AG-14361

AG14361 is a potent inhibitor of PARP1 with K_i of <5 nM in a cell-free assay. It is at least 1000-fold more potent than the benzamides.

Features:The 1st high-potency PARP-1 inhibitor with the specificity & in vivo activity to enhance chemotherapy and radiation therapy of human cancers.
A-966492

A-966492 is a novel and potent inhibitor of PARP1 and PARP2 with K_i of 1 nM and 1.5 nM, respectively.

Features:A promising, structurally diverse benzimidazole analogue that is being further characterized preclinically.

Choose Your Country or Region

By Signaling Pathways

By product type

Rucaparib (AG-014699,PF-01367338) phosphate

Cited by 35 Publications

Purity & Quality Control

Choose Selective PARP Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Rucaparib (AG-014699,PF-01367338) phosphate SDF

Bio Calculators

Molarity Calculator

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

Dilution Calculator

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

Instructions to calculate molar mass (molecular weight) of a chemical compound:

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on )

Tech Support

PARP Signaling Pathway Map

PARP Inhibitors with Unique Features

Related PARP Products

Choose Your Country or Region

By Signaling Pathways

By product type

Rucaparib (AG-014699,PF-01367338) phosphate

Cited by 35 Publications

Purity & Quality Control

Choose Selective PARP Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Rucaparib (AG-014699,PF-01367338) phosphate SDF

Bio Calculators

Molarity Calculator

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

Dilution Calculator

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

Instructions to calculate molar mass (molecular weight) of a chemical compound:

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on )

Tech Support

PARP Signaling Pathway Map

PARP Inhibitors with Unique Features

Related PARP Products

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)