brca1

BRCA1-IN-2 is a cell membrane-crossing BRCA1 protein-protein interaction (PPI) inhibitor with antitumor activity that acts by disrupting the interaction of BRCA1 (BRCT)2 with proteins.

BRCA1-IN-1 is a novel small-molecule-like inhibitor of BRCA1 with an IC50 of 0.53 μM and a Ki of 0.71 μM.

Rucaparib (PF-01367338) is a PARP protein inhibitor (PARP-1 Ki=1.4 nM) and hexose hexose-6-phosphate dehydrogenase (H6PD) inhibitor with oral activity. Rucaparib exhibits antitumor activity, with activity against desmoplasia-resistant prostate cancer (CRPC).

Rucaparib monocamsylate (Rucaparib Camsylate) is a PARP inhibitor (PARP1,Ki of 1.4 nM). Rucaparib Camsylate also displays binding affinity to eight other PARP domains.

Rucaparib Phosphate (PF-01367338 phosphate) is an inhibitor of PARP (Ki: 1.4 nM for PARP1) that is used in clinical therapy to sensitize cancer cells to chemotherapy.

Talazoparib (LT-673) is a new-type PARP inhibitor (IC50: 0.58 nM), It similarly binds to PARP1/2 (Kis: 1.2/0.85 nM).

Bractoppin is a drug-like inhibitor of phosphopeptide recognition by the human BRCA1 tandem (t)BRCT domain (IC50 = 0.074 μM), which selectively inhibits substrate binding with nanomolar potency in vitro. Structure-activity exploration suggests that Bractoppin engages BRCA1 tBRCT residues recognizing pSer in the consensus motif, pSer-Pro-Thr-Phe, plus an abutting hydrophobic pocket that is distinct in structurally related BRCT domains, conferring selectivity.

The Anti-BRCA1 Antibody (BR64) is a mouse IgG1, κ chimeric antibody that specifically targets human BRCA1. The recommended isotype control for the Anti-BRCA1 Antibody (BR64) is the Mouse IgG1 kappa, Isotype Control.

Carboplatin (JM-8) is a cisplatin derivative, a DNA synthesis inhibitor. Carboplatin binds to DNA, inhibits replication and transcription, and induces cell death. Carboplatin has antitumor activity.

D-I03 is a selective RAD52 inhibitor with a Kd of 25.8 µM. D-I03 inhibits RAD52-dependent single-strand annealing (SSA) and D-loop formation, with IC₅₀ values of 5 µM and 8 µM, respectively. D-I03 exerts significant growth inhibition on BRCA1/2-deficient cancer cells but has no effect on RAD51. D-I03 can be used in combination therapy studies for tumors with DNA damage repair defects.

AB25583 is a potent inhibitor of the Polθ helicase domain (Polθ-hel). It blocks MMEJ repair, leading to DNA damage accumulation and synthetic lethality in BRCA1/2-deficient cancer cells.

PARP1-IN-30 is a specific and effective PARP1 inhibitor with cytotoxic properties. It precisely inhibits PARP1 in tumor cells lacking breast cancer 1 protein (BRCA1) or BRCA2. PARP1-IN-30 holds potential for use in cancer research.

(rac)-Talazoparib ((rac)-BMN-673) (Compound 47) is an orally active inhibitor of PARP1/2, with Ki values of 1.2 nM and 0.87 nM, respectively. It inhibits cellular PARylation at an EC50 of 2.51 nM. This compound leads to the accumulation of DNA damage and suppresses the proliferation of BRCA1/2-mutated MX-1 and Capan-1 cells, with IC50 values of 0.3 nM and 5 nM, respectively. Additionally, (rac)-Talazoparib exhibits antitumor activity in mouse models.

Octamethylcyclotetrasiloxane promotes the growth of MCF-10A and MCF-10F cells under non-adherent conditions. It induces DNA damage upon prolonged high concentration exposure and inhibits the expression of DNA repair protein BRCA1. Additionally, octamethylcyclotetrasiloxane exhibits inherent estrogenic activity.

D-G23 is a selective RAD52 inhibitor. It disrupts RAD52-mediated DNA repair pathways and suppresses the growth of cancer cells deficient in BRCA1 and BRCA2. D-G23 shows promise for research into homologous recombination-related cancers caused by BRCA1/2 mutations, such as hereditary breast and ovarian cancers.

PARP-1/Proteasome-IN-1 (compound 42i) is a dual inhibitor of PARP-1 and the proteasome, demonstrating significant inhibitory effects on breast cancer. By downregulating the expression of BRCA1 and RAD51, it impairs homologous recombination repair and induces apoptosis (cellular death).

Dicycloplatin is an inducer of DNA damage. It activates doubly phosphorylated checkpoint kinase 2 (CHK2), breast cancer 1 (BRCA1), and triply phosphorylated p53 to induce DNA damage. Dicycloplatin can cause cell cycle arrest, inhibit proliferation, and trigger apoptosis in prostate cancer PC3 cells and lung cancer NCI/H446 cells. It is applicable for research in the field of cancer.

EXO1-IN-1 (Compound F684) is a potent and selective inhibitor of exonuclease 1 (EXO1) with an IC50 of 15.7 μM. It inhibits DNA end resection, promotes the accumulation of DNA double-strand breaks, and induces S-phase polyadenylation, thereby disrupting DNA repair pathways in homologous recombination-deficient (HRD) cancer cells. This selectivity effectively targets and kills tumor cells with homologous recombination gene defects, such as BRCA1/2 mutations. EXO1-IN-1 holds promise for researching cancers with homologous recombination deficiencies, including BRCA-related tumors.

PARP1-IN-39 is an inhibitor of PARP1, with an IC50 value of 0.22 nM. In human breast cancer cells, its IC50 is 1.57 nM. PARP1-IN-39 is applicable for studying cancers associated with DNA repair deficiencies, such as breast, ovarian, pancreatic, and prostate cancers, particularly those with BRCA1/2 mutations.

Theophylline-platinum(IV) prodrug-1 is a PARP-1 inhibitor. It enhances DNA damage, ROS generation, mitochondrial dysfunction, apoptosis, and S-phase arrest in SKOV3-BRCA1-KD cells while reducing invasion and metastasis. Additionally, it exhibits strong antitumor activity in SKOV3-BRCA1-KD xenograft tumor models. This compound is used for ovarian cancer research.

DD-CIP2 is a DNA damage inducer that triggers significant DNA damage, cell cycle arrest, and apoptosis by modulating DNA damage response pathways. It demonstrates notable antitumor efficacy without apparent toxicity at well-tolerated doses in vivo. Its exceptional cytotoxicity against a range of cancer cell lines from hematological and solid tumors is independent of their BRCA1/2 status. DD-CIP2 can be utilized in research on small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).

DN1679 is a potent, selective, and orally active CRBN-dependent dual degrader of CDK12/13 PROTAC. It exhibits DC50 values for CDK12/13 at 8.8/9.8 nM in MDA-MB-231 cells, 5.1/6.4 nM in MDA-MB-157 cells, and 17.2/15.8 nM in MDA-MB-468 cells. DN1679 downregulates mRNA levels of DNA damage response genes such as ATM, ATR, BRCA1, and RAD51. When used in combination with Olaparib, DN1679 shows a significant synergistic anti-tumor effect. It is applicable in research on triple-negative breast cancer.

Phosphoramide mustard cyclohexanamine is the active metabolite of cyclophosphamide, an alkylating agent that cross-links DNA strands, organizes cell division and causes cell death, and has antitumor activity.

LCS-1 is a selective superoxide dismutase 1 (SOD1) inhibitor and pyridazin-3-one derivative that displays trypanocidal activity at high concentrations.LCS-1 inhibits superoxide dismutase 1 inducing ROS-dependent death and degrading PARP and BRCA1 in glioma cells.