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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5 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.

    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 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYmwMlEuOTByIH7N MmPONlQwPDhxN{KgbC=> MV;pcohq[mm2czDj[YxtKHC{b3zp[oVz[XSrb36g[I9{\SCmZYDlcoRmdnSueR?= MlHUNlYxPDd4OUe=
BR5FVB1-Akt M33I[2Fxd3C2b4Ppd{BCe3OjeR?= MnX4NE4yNTFyMDDuUS=> MmLqO|IhcA>? MlGybY5lfWOnczDhdI9xfG:|aYO= NWHybpU6OjZyNEe2PVc>
Capan-1 M1nDRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVHJR|UxRTF4LkFihKnDueLCiUWuOQKBkcL3TdMg NWPHVXhvOjV6NkS1PVA>
MIA PaCa-2 Mk[zS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkK4TWM2OD13OD6yN-KBkcLz4pEJPE4y6oDLwsXNxsA> NEG3SIozPTh4NEW5NC=>
RD MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3SzTmlEPTB;OD63JI5O NEfLcnQzPTJ4M{WzPS=>
Rh41 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnW1TWM2OD16LkGgcm0> M2L6[VI2OjZ|NUO5
Rh18 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUjJR|UxRTRwOTDuUS=> NVH4e2pXOjV{NkO1N|k>
Rh30 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH:1RVNKSzVyPUOxMlEhdk1? NV3iPWlnOjV{NkO1N|k>
BT-12 M1TvVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1PSWWlEPTB-4pEJNUwxODBibl2= M1qxZlI2OjZ|NUO5
CHLA-266 MoW4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3PkWmlEPTB-4pEJNUwxODBibl2= NWjqUXlIOjV{NkO1N|k>
TC-71 M3u5XGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrX[YVRUUN3ME2zMlchdk1? NGPCXlczPTJ4M{WzPS=>
CHLA-9 MmW3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mlr2TWM2OD16LkKgcm0> MkKzNlUzPjN3M{m=
CHLA-10 MkSwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXjDRnBOUUN3ME22O{45KG6P Ml7lNlUzPjN3M{m=
CHLA-258 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHjyZXdKSzVyPUSuOkBvVQ>? M3fROlI2OjZ|NUO5
SJ-GBM2 NGHyOGtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIHBR4NKSzVyPUG2MlIhdk1? M1H2O|I2OjZ|NUO5
NB-1643 Mk[3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zZXGlEPTB;MUiuOEBvVQ>? Ml73NlUzPjN3M{m=
NB-EBc1 M3[3OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEn6bZRKSzVyPUK1Mlghdk1? NHLOenozPTJ4M{WzPS=>
CHLA-90 M3TTTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2G2RmlEPTB-4pEJNUwxODBibl2= MWKyOVI3OzV|OR?=
CHLA-136 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUfLOlB6UUN3ME2xOE4zKG6P MYOyOVI3OzV|OR?=
NALM-6 M2T1PWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXeyW5d7UUN3ME20PUBvVQ>? NGTSSW8zPTJ4M{WzPS=>
COG-LL-317 MlLtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NY\odVZiUUN3ME25MlQhdk1? NFG4XWczPTJ4M{WzPS=>
RS4;11 NWP6VFR[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX\JR|UxRTV{Lk[gcm0> NFrtfG0zPTJ4M{WzPS=>
MOLT-4 NYPP[pNXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYXJR|UxRTF4Lk[gcm0> MonXNlUzPjN3M{m=
Kasumi-1 NIXINVlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWC4cIFHUUN3ME23PFYvOiCwTR?= MXSyOVI3OzV|OR?=
Karpas-299 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWfXT5pkUUN3ME23OU44KG6P M3TteVI2OjZ|NUO5
Ramos-RA1 NEL3NoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUDJR|UxRTZ6LkOgcm0> NXXvWpBqOjV{NkO1N|k>
DT40 NF;NXoRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH\MXpZKSzVyPUSgcm0> NGHHcmwzPDN3NkixNy=>
DU145 NEDTRmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYrGW2MzUUN3ME2xNUBvVQ>? NHe1SGMzPDN3NkixNy=>
H209 NVXEeJdlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRTFwNzDuUS=> MmrONlQxPzd|NUC=
H1048 NX[wR|dIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYnMVYhFUUN3ME2yMlIhdk1? NF\ue|czPDB5N{O1NC=>
H524 MkLiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRTNwMTDuUS=> MXSyOFA4PzN3MB?=
H1930 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnvDTWM2OD12LkGgcm0> NYnoU3FOOjRyN{ezOVA>
H69 NVjRZlY4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVjJR|UxRTVwMjDuUS=> M2r0dFI1ODd5M{Ww
H2081 M1PTPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWLJR|UxRTZwMzDuUS=> MWiyOFA4PzN3MB?=
H2107 MlztS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTdwMzDuUS=> NIDHSXgzPDB5N{O1NC=>
H1092 NWiwWFViT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1jQN2lEPTB;OD65JI5O M{\MSlI1ODd5M{Ww
DMS-79 NXSzTIhNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{e3bWlEPTB;OT6zJI5O NUXNc2dqOjRyN{ezOVA>
COR-L279 Ml\jS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVjJR|UxRTF3IH7N MknoNlQxPzd|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