PT2399 is a potent and selective HIF-2α antagonist, which directly binds to HIF-2α PAS B domain. PT2399 displays potent antitumor activity in vivo.

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

DMSO : ≥ 200 mg/mL (476.96 mM)

HIF-2α

PT2399 can bind directly to the HIF-2α PAS B domain, and cripple HIF-2α’s ability to bind to Aryl hydrocarbon receptor nuclear translocator (ARNT).PT2399 (20 μM) causes off-target toxicity because it inhibits the proliferation of HIF-2α −/− 786-O cells and other cancer cell lines with undetectable HIF-2α. PT2399 (0.2–2 μM; 0-21 days) inhibits 786-O cells soft agar growth.PT2399 represses various HIF target genes in 786-O VHL−/− ccRCC cells, does not suppress HIF-1α-specific targets such as BNIP3.Cell Viability AssayCell Line:786-O cellsConcentration:0 μM, 0.2 μM, 2 μMIncubation Time:0-21 daysResult:Inhibited 786-O cell soft agar growth at 0.2–2 μM.

PT2399 inhibits tumor cell proliferation 3.5 fold in renal cell carcinoma (RCC) bearing mice.PT2399 reduces tumor cell density and increases fibrosis in RCC bearing mice.PT2399 (100 mg/kg; oral gavage; every 12 hours) is more active than sunitinib, and inhibits tumor growth in several sunitinib-resistant tumors in RCC bearing mice .PT2399 directly inhibits HIF-2α causes tumor regression in preclinical models of primary and metastatic pVHL-defective ccRCC in an on-target fashion.Animal Model:Mice with RCC tumorgraftDosage:100 mg/kgAdministration:Oral gavage; every 12 hoursResult:More active than sunitinib, and inhibited tumor growth in several sunitinib-resistant tumors.