Talazoparib (BMN 673)

For research use only. Not for use in humans.

Catalog No.S7048 Synonyms: LT-673

79 publications

Talazoparib (BMN 673) Chemical Structure

Molecular Weight(MW): 380.35

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.

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Selleck's Talazoparib (BMN 673) has been cited by 79 publications

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Biological Activity

Description 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.
PARP1 [1]
(Cell-free assay)
0.57 nM
In vitro

BMN-673 selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability and eventually leads to apoptosis. BMN 673 selectively kills cancer cells with BRCA-1 or BRCA-2 mutations. BMN 673 demonstrates single-agent cytotoxicityin BRCA-1 mutant (MX-1, IC50 = 0.3 nM) and BRCA-2 mutant cells (Capan-1, IC50 = 5 nM). In contrast, in MRC-5 normal human fibroblastand other tumor cell lines with wild-type BRCA-1 and BRCA-2 genes, IC50 of BMN 673 ranges between 90 nM and 1.9 μM. [1] In cultured human cancer cells, BMN 673 also significantly enhances the cytotoxic efficacy of both Temozolomide and SN-38. Off-target molecular screening did not identify significant non-specific activity for this class of PARP inhibitors. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BR5FVB1-Akt MoSzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXuwMlEuOTByIH7N MnPtNlQwPDhxN{KgbC=> MX3pcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36g[I9{\SCmZYDlcoRmdnSueR?= M1zJWlI3ODR5Nkm3
BR5FVB1-Akt NUfIbGpISXCxcITvd4l{KEG|c3H5 NVPFZm4{OC5zLUGwNEBvVQ>? NE\jRZM4OiCq MkD2bY5lfWOnczDhdI9xfG:|aYO= MkLkNlYxPDd4OUe=
Capan-1 Mk\3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4\KdmlEPTB;MU[uNQKBkcLz4pEJOU416oDLwsXNxsA> NEfFR2EzPTh4NEW5NC=>
MIA PaCa-2 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2rF[WlEPTB;NUiuNlPjiIoEsfMAjVgvOeLCidM1UeKh NGfMOHQzPTh4NEW5NC=>
RD MmTvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHvibG9KSzVyPUiuO{BvVQ>? NHnTclEzPTJ4M{WzPS=>
Rh41 NXfRPGtpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkHKTWM2OD16LkGgcm0> MVeyOVI3OzV|OR?=
Rh18 M{f3WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1H2SWlEPTB;ND65JI5O NEO0cYEzPTJ4M{WzPS=>
Rh30 M4\1Xmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1zmN2lEPTB;M{GuNUBvVQ>? NEfifm8zPTJ4M{WzPS=>
BT-12 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\QeoY1UUN3ME9ihKkyNDByMDDuUS=> M32ycFI2OjZ|NUO5
CHLA-266 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1S1eGlEPTB-4pEJNUwxODBibl2= MYmyOVI3OzV|OR?=
TC-71 MoS2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIH3ZXhKSzVyPUOuO{BvVQ>? Mlr2NlUzPjN3M{m=
CHLA-9 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWTJRmVIUUN3ME24MlIhdk1? NGHETIgzPTJ4M{WzPS=>
CHLA-10 M3\4cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYHJR|UxRTZ5Lkigcm0> NV\ucm5JOjV{NkO1N|k>
CHLA-258 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYj5OoFvUUN3ME20MlYhdk1? NXj6V3dFOjV{NkO1N|k>
SJ-GBM2 NV3IfWZLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXzaelY{UUN3ME2xOk4zKG6P MlPMNlUzPjN3M{m=
NB-1643 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1rQVWlEPTB;MUiuOEBvVQ>? NI\temIzPTJ4M{WzPS=>
NB-EBc1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYLJR|UxRTJ3Lkigcm0> NUXZOoR[OjV{NkO1N|k>
CHLA-136 NV;jSW9bT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DPXmlEPTB;MUSuNkBvVQ>? NETQbowzPTJ4M{WzPS=>
COG-LL-317 NHfoe2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFvSTGhKSzVyPUmuOEBvVQ>? MoW5NlUzPjN3M{m=
RS4;11 NFjHSVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkOwTWM2OD13Mj62JI5O MmLuNlUzPjN3M{m=
MOLT-4 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFnEVopKSzVyPUG2MlYhdk1? MmnnNlUzPjN3M{m=
Kasumi-1 M4nUOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYLJR|UxRTd6Nj6yJI5O Mne2NlUzPjN3M{m=
Karpas-299 MoDXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUHLeoRyUUN3ME23OU44KG6P MVmyOVI3OzV|OR?=
Ramos-RA1 NYHUXlhlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPrUoF[UUN3ME22PE4{KG6P M{fjU|I2OjZ|NUO5
DT40 M1HPWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnvvTWM2OD12IH7N MUiyOFM2PjhzMx?=
DU145 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYXSe5NxUUN3ME2xNUBvVQ>? NFvlc5EzPDN3NkixNy=>
H209 M{[4PGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGr0[JVKSzVyPUGuO{BvVQ>? M{TzblI1ODd5M{Ww
H1048 NYPHXVJST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWP0O2lTUUN3ME2yMlIhdk1? MnLMNlQxPzd|NUC=
H524 NWnLWmRqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnHzTWM2OD1|LkGgcm0> NXLTNIlDOjRyN{ezOVA>
H69 M4\nOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlvUTWM2OD13LkKgcm0> NVGzdmJmOjRyN{ezOVA>
H2081 NWnkTXB1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4DY[WlEPTB;Nj6zJI5O MYSyOFA4PzN3MB?=
H2107 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV\TVoZUUUN3ME23MlMhdk1? NHzkd5YzPDB5N{O1NC=>
H1092 NUf6fYRnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn;1TWM2OD16Lkmgcm0> NYqyclZbOjRyN{ezOVA>
DMS-79 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{\5SGlEPTB;OT6zJI5O MX:yOFA4PzN3MB?=
H446 M2\yTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHrrcWZKSzVyPUGzJI5O NGjkfnEzPDB5N{O1NC=>
COR-L279 NH;lNW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MonSTWM2OD1zNTDuUS=> MnrwNlQxPzd|NUC=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
cleaved-PARP / cleaved-caspase3 / γ-H2AX; 

PubMed: 29158830     

Western Blot data testing protein expression after treatment with Olaparib, Niraparib, and Talazoparib on Brca1-deficient cell line in W0069 cells.

pKAP1 / pChk2 / pChk1; 

PubMed: 28947502     

Western blot images (representative from 3 independent experiments) showing the impact of a 24 hour pre-treatment with TAL ± TMZ on DNA damage signaling in U251 (MGMT-low) and T98G (MGMT-high) cells. 


PubMed: 28167507     

MDA-MDA-MB-231 and BT549 cells were treated with 10 μM olaparib or 10 nM talazoparib for 24 hours, and subjected to immunoblotting with the indicated antibodies. PD-L1 knockout (K/O) cells were included as a negative control. 


PubMed: 30472087     

Western blot analysis of the DNA damage sensors ATM, p-ATM (Ser1981), CHK1, p-CHK1 (Ser317), CHK2 and p-CHK2 (Thr68) in MV4-11 and HL-60 cells. GAPDH served as a loading control.

29158830 28947502 28167507 30472087
Growth inhibition assay
Cell viability; 

PubMed: 29158830     

Measured dose response curve and IC50 of Talazoparib in W780 and W0069 cells.

cleaved PARP / 53BP1; 

PubMed: 28958991     

Cleaved-PARP and 53BP1 expression. Representative images with 10× objective from high-content imaging of control cells in the left column, and cells treated with veliparib, olaparib, and talazoparib in three right columns. 53BP1 expression is seen in: A, HCC1143; B, MDAMB231; and C, HCC1806. Blue represents nuclear staining and pink foci represent 53BP1 foci. Cleaved-PARP expression is seen in D, HCC1143 and E, HCC1806. Blue represents nuclear staining and green represents cleaved-PARP expression.


PubMed: 30621214     

(A) MCF7 and (B) MCF7-T cells were treated with either 100 nM tamoxifen (Tamox) or 1 nM talazoparib (Talaz) for 72 h, alone and in combination. 24 h post treatment RAD51 foci formation assay was performed. Scale bar: 20 µm.

28958991 30621214
In vivo In rat pharmacokinetic studies, BMN 673 displays >50% oralbioavailability and pharmacokinetic properties that enable singledaily dosing. In MX-1 xenograft tumor model studies, daily oral dosingof BMN 673 significantly enhances the antitumor effects ofcytotoxic therapies in a dose-dependent manner. [2]


Animal Research:


- Collapse
  • Animal Models: MX-1 model (BRCA-1 deficient)
  • Formulation: --
  • Dosages: 0.33 mg/kg/day, once daily
  • Administration: Oral
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 38 mg/mL warmed (99.9 mM)
Water Insoluble
Ethanol Insoluble

* 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

Molecular Weight 380.35


CAS No. 1207456-01-6
Storage powder
in solvent
Synonyms LT-673

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03974217 Recruiting Drug: Talazoparib Leukemia Dana-Farber Cancer Institute|Pfizer August 1 2019 Phase 1
NCT03901469 Recruiting Drug: ZEN003694|Drug: Talazoparib Triple Negative Breast Cancer Zenith Epigenetics|Pfizer June 26 2019 Phase 2
NCT03911973 Recruiting Drug: Gedatolisib|Drug: Talazoparib TNBC - Triple-Negative Breast Cancer Kari Wisinski|Pfizer|Big Ten Cancer Research Consortium April 17 2019 Phase 1|Phase 2
NCT03875313 Recruiting Drug: CB-839|Drug: Talazoparib Solid Tumor|Clear Cell Renal Cell Carcinoma|TNBC - Triple-Negative Breast Cancer|Colorectal Cancer|CRC|RCC|ccRCC Calithera Biosciences Inc March 22 2019 Phase 1|Phase 2
NCT03672773 Recruiting Drug: Talazoparib|Drug: Temozolomide Recurrent Extensive Stage Small Cell Lung Carcinoma|Refractory Extensive Stage Small Cell Lung Carcinoma Jonsson Comprehensive Cancer Center|Translational Research in Oncology|National Cancer Institute (NCI) October 31 2018 Phase 2

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Frequently Asked Questions

  • Question 1:

    Which solvent do you recommend to dilute the inhibitor for in vivo study in mice?

  • Answer:

    BMN673 (S7048) can be dissolved in vehicle (10% DMAc, 6% Solutol, and 84% PBS) according to the paper: http://clincancerres.aacrjournals.org/content/19/18/5003.full. Quote from Method and Material section "Xenograft experiments: BMN 673 (various doses as indicated), or vehicle (10% DMAc, 6% Solutol, and 84% PBS) was administered by oral gavage"

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID