RBN-2397

In Vitro

RBN-2397 (0.0001-100 μM; 24 hours) inhibits cells proliferation with an IC50 value of 20 nM in NCI-H1373 lung cancer cells[2]. RBN-2397 (0.4 nM-1 μM; 24 hours) shows a restoration of type I IFN response by an increase in STAT1 phosphorylation as a dose-dependent manner in NCI-H1373 human lung cancer cells[2]. RBN-2397 (0.0001-1 μM; 24 hours) inhibits cell MARylation in a cell biochemial assay with an EC50 value of 1 nM[2]. Cell Proliferation Assay[2] Cell Line: NCI-H1373 lung cancer cells Concentration: 0.0001 μM; 0.001 μM; 0.001 μM; 0.1 μM; 1 μM; 10 μM; 100 μM Incubation Time: 24 hours Result: Blocked cell proliferation. Western Blot Analysis[2] Cell Line: NCI-H1373 lung cancer cells Concentration: 0.4 nM-1 μM Incubation Time: 24 hours Result: Increased p-STAT1 protein expression.

In Vivo

RBN-2397 (oral administration; 3-100 mg/kg; once daily; 24-32 days) induces tumor-specific adaptive immune memory in CT26 syngeneic model with durable complete responses in CT26 tumor-bearing BALB/c mice[2]. RBN-2397 (oral administration; 3-100 mg/kg; once daily; 32 days) causes complete regressions at the dose 100 mg/kg and exerts a dose-dependent effects on tumor growth at dose levels of ≥30 mg/kg[2]. The half-life (t1/2) of RBN-2397 in vivo is 325 mins[2]. Animal Model: CB17 SCID mice with NCI-H1373 xenografts[2] Dosage: 3 mg/kg, 10mg/kg, 30 mg/kg, 100 mg/kg Administration: Oral administration; once daily; 24-32 days Result: Decreased tumor volume and exerted anti-tumor effects.

References & source

[1]. RBN-2397-Inhibiting PARP7, a Key monoPARP Cancer Dependency

[2]. Melissa Vasbinder, et al. RBN-2397: A First-in-Class PARP7 Inhibitor Targeting a Newly Discovered Cancer Vulnerability in Stress-Signaling Pathways.

DC Chemicals original product information