Talazoparib (BMN 673)

Catalog No.S7048 Synonyms: LT-673

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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6 Customer Reviews

  • DNA damage persists on withdrawal of PARPi in RNASEH2AKO cells. Wild-type and RNASEH2AKO HeLa cells were treated with talazoparib and released into fresh medium for the indicated times before being processed for γ-H2AX immunofluorescence and propidium iodide (PI) staining. The γ-H2AX immunofluorescence (pseudocolor plots) and cell cycle (histograms) FACS profiles shown are representative of three biologically independent experiments.

    Nature, 2018, 559(7713):285-289. Talazoparib (BMN 673) purchased from Selleck.

    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.

    Clin Cancer Res, 2017, 23(14):3711-3720. Talazoparib (BMN 673) purchased from Selleck.

  • Western blot assessment of effects on PAR, PARP, and dsDNA breaks mediated by IMMU-132 plus PARPi in TNBC tumor lines. Cells were plated overnight in 6-well plates before the addition of chemotherapeutics. After a 24-hour incubation, cells were harvested and cell lysates resolved and transferred for Western analysis as described in Materials and Methods. PAR and FL-PARP levels were determined on the same gel. Assessment of dsDNA breaks (p-H2A.X) was calculated as ratios relative to untreated control (Unt) normalized to b-actin protein loading control (Dp-H2A.X). B, HCC1806 cells exposed to rucaparib (Ruc) and IMMU-132 or to (C) talazoparib (Tala) and IMMU-132.

    Clin Cancer Res, 2017, 23(13):3405-3415. Talazoparib (BMN 673) purchased from Selleck.

    PARP inhibition prevents adhesion to and migration of monocytes across BMVEC monolayers preserving the barrier. Primary human monocytes were treated for 24 h with PARPi (AIQ, olaparib, EB47, talazoparib), calcein-labeled, washed, and then added to BMVEC monolayers (untreated or treated for 24 h with TNFα). Treatments were removed prior to the addition of monocytes. Adhesion to (a) and migration of (b) monocytes across blood-brain barrier models were measured and are presented as fold difference compared to TNFα-only control (mean ± SEM) for each treatment from at least quadruplicate determinations, which was assigned a value of 1 (7600 relative fluorescent units for adhesion or equivalent to 37 migrated cells). *P < 0.05, **P < 0.01 indicate significance vs. non-treated. TEER, an indicator of barrier integrity, was continuously measured in BMVEC monolayers treated with or without TNFα following the addition of primary human monocytes that had been treated with PARPi.

    J Neuroinflammation, 2016, 13(1):254.. Talazoparib (BMN 673) purchased from Selleck.

  • BT-549 cells reconstituted with Vet, WT, 336* or PTEN WT HP1aKD were treated with BMN673. Relative cell viability was determined by MTT assay. The results were presented as mean of 3 independent experiments. Error bars indicate s.d.

    Cell Cycle, 2015, 14(14): 2323-32. Talazoparib (BMN 673) purchased from Selleck.

    We treated the FA defective and control lung cancer cell lines H1299D2-down/H1299E and A549D2 down/A549E with BMN673 (0.5 µM). MTT assay was used for the cell viability analysis and an averaged absorbance was recorded 24, 48 and 72 h post treatment.

    Front Oncol, 2014, 4: 368. Talazoparib (BMN 673) purchased from Selleck.

Purity & Quality Control

Choose Selective PARP Inhibitors

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 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{mxfFAvOS1zMECgcm0> NV7W[HlLOjRxNEivO|IhcA>? NVPabGVHcW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9vKGSxc3Wg[IVx\W6mZX70cJk> M3\HXFI3ODR5Nkm3
BR5FVB1-Akt MUPBdI9xfG:|aYOgRZN{[Xl? M2DBVVAvOS1zMECgcm0> MWq3NkBp Ml;vbY5lfWOnczDhdI9xfG:|aYO= MWCyOlA1PzZ7Nx?=
Capan-1 NGT6eIpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXry[GZ{UUN3ME2xOk4x6oDLwsJihKk2NjUkgJpCuW3DqA>? M{HWWVI2QDZ2NUmw
MIA PaCa-2 MnjFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFn1NY9KSzVyPUW4MlI{6oDLwsJihKk5NjIkgJpCuW3DqA>? MnTJNlU5PjR3OUC=
RD M{PvTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mm\JTWM2OD16Lkegcm0> MYqyOVI3OzV|OR?=
Rh41 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFTpVHhKSzVyPUiuNUBvVQ>? M4m2T|I2OjZ|NUO5
Rh18 NEX0b2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1HFdGlEPTB;ND65JI5O MoK2NlUzPjN3M{m=
Rh30 NXXtOVA1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWroOZVrUUN3ME2zNU4yKG6P MlvNNlUzPjN3M{m=
BT-12 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3nq[mlEPTB-4pEJNUwxODBibl2= MmCzNlUzPjN3M{m=
CHLA-266 MnTxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlrQTWM2OD8kgJmxMFAxOCCwTR?= NXXLPFFtOjV{NkO1N|k>
TC-71 MoC1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmK2TWM2OD1|Lkegcm0> M1rEd|I2OjZ|NUO5
CHLA-9 M{\zR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{W0Z2lEPTB;OD6yJI5O MYWyOVI3OzV|OR?=
CHLA-10 M4i2cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mnm2TWM2OD14Nz64JI5O MoDFNlUzPjN3M{m=
CHLA-258 MnLnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWTyU2FEUUN3ME20MlYhdk1? MnXtNlUzPjN3M{m=
SJ-GBM2 M3nITmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXziXGNJUUN3ME2xOk4zKG6P MoLkNlUzPjN3M{m=
NB-1643 NUnhVZJMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWrJR|UxRTF6LkSgcm0> M4K0TlI2OjZ|NUO5
NB-EBc1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVy3SFdMUUN3ME2yOU45KG6P M3KzSFI2OjZ|NUO5
CHLA-90 M2fiOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXXJR|UxRuLCiUGsNFAxKG6P MVeyOVI3OzV|OR?=
CHLA-136 M2DLN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4nrPWlEPTB;MUSuNkBvVQ>? NGPac28zPTJ4M{WzPS=>
COG-LL-317 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX2xZ3RnUUN3ME25MlQhdk1? NVznXGI6OjV{NkO1N|k>
RS4;11 M4jNcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWj1THd2UUN3ME21Nk43KG6P NEfMSGozPTJ4M{WzPS=>
MOLT-4 MkG4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NE[xVIVKSzVyPUG2MlYhdk1? M3i2RlI2OjZ|NUO5
CCRF-CEM M1;V[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEXTVW9KSzVyPU[5O{4{KG6P NFXRNngzPTJ4M{WzPS=>
Kasumi-1 NEPJV2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVfJR|UxRTd6Nj6yJI5O NFziNHQzPTJ4M{WzPS=>
Karpas-299 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MonaTWM2OD15NT63JI5O NYPU[GhrOjV{NkO1N|k>
Ramos-RA1 MnPwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYTJR|UxRTZ6LkOgcm0> NGi2R4gzPTJ4M{WzPS=>
DT40 M{f0Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTRibl2= MXyyOFM2PjhzMx?=
DU145 M3XjSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV7zfXNsUUN3ME2xNUBvVQ>? NHfLN|UzPDN3NkixNy=>
H209 NXL0c|JLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYG5XZR{UUN3ME2xMlchdk1? M3n5SlI1ODd5M{Ww
H1048 Ml\US5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmDaTWM2OD1{LkKgcm0> MkPZNlQxPzd|NUC=
H524 NHS4OWpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3\MWWlEPTB;Mz6xJI5O NWjrSZVsOjRyN{ezOVA>
H1930 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVm4fnFQUUN3ME20MlEhdk1? M4DXdFI1ODd5M{Ww
H69 NEe4XphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX;yRpZSUUN3ME21MlIhdk1? MnjBNlQxPzd|NUC=
H2081 NIn6b|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mo[zTWM2OD14LkOgcm0> MmjvNlQxPzd|NUC=
H2107 MnWzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWfJR|UxRTdwMzDuUS=> M4PRXlI1ODd5M{Ww
H1092 MkO5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRThwOTDuUS=> MmDHNlQxPzd|NUC=
H446 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRTF|IH7N NFq4[IQzPDB5N{O1NC=>
COR-L279 Mn;XS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVvJR|UxRTF3IH7N Mme1NlQxPzd|NUC=

... Click to View More Cell Line Experimental Data

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:


+ Expand
  • 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 Conditions Sponsor/Collaborators Start Date Phases
NCT03672773 Not yet recruiting 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) November 1 2018 Phase 2
NCT03637491 Recruiting Pancreatic Cancer|Non-Small Cell Lung Cancer|Cancer Pfizer|Array BioPharma August 15 2018 Phase 2
NCT03499353 Recruiting Early Breast Cancer Pfizer August 27 2018 Phase 2
NCT03642132 Recruiting Ovarian Cancer Pfizer July 19 2018 Phase 3
NCT03565991 Recruiting Locally Advanced or Metastatic Solid Tumors|Genes BRCA 1 Pfizer June 18 2018 Phase 2
NCT03426254 Enrolling by invitation Advanced or Recurrent Solid Tumors|Breast Neoplasm Center Trials & Treatment|BioGene Pharmaceutical February 8 2018 Phase 1

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.

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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"

PARP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID