Talazoparib (BMN 673)
Catalog No.S7048 Synonyms: LT-673
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.
Cited by 7 Publications
4 Customer Reviews
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
|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.|
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.  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. 
|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. |
|In vitro||DMSO||38 mg/mL warmed (99.9 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03426254||Enrolling by invitation||Advanced or Recurrent Solid Tumors|Breast Neoplasm||Center Trials & Treatment|BioGene Pharmaceutical||February 8 2018||Phase 1|
|NCT02997163||Recruiting||Advanced Solid Tumors||Pfizer|Medivation Inc.||February 8 2017||Phase 1|
|NCT02921919||Recruiting||Cancer||Pfizer|Medivation Inc.||November 8 2016||Phase 2|
|NCT03377556||Recruiting||ATM Gene Mutation|ATR Gene Mutation|BARD1 Gene Mutation|BRCA1 Gene Mutation|BRCA2 Gene Mutation|BRIP1 Gene Mutation|CHEK1 Gene Mutation|CHEK2 Gene Mutation|FANCA Gene Mutation|FANCC Gene Mutation|FANCD2 Gene Mutation|FANCF Gene Mutation|FANCM Gene Mutation|NBN Gene Mutation|PALB2 Gene Mutation|RAD51 Gene Mutation|RAD51B Gene Mutation|RAD54L Gene Mutation|Recurrent Squamous Cell Lung Carcinoma|RPA1 Gene Mutation|Stage IV Squamous Cell Lung Carcinoma AJCC v7||Southwest Oncology Group|National Cancer Institute (NCI)||February 7 2017||Phase 2|
|NCT03077607||Completed||Advanced Solid Tumors||Pfizer|Medivation Inc.||November 7 2016||Phase 1|
|NCT03148795||Recruiting||Prostate Cancer||Pfizer|Medivation Inc.||July 4 2017||Phase 2|
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Frequently Asked Questions
Which solvent do you recommend to dilute the inhibitor for in vivo study in mice?
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"