Pulrodemstat (CC-90011) is a potent, selective, reversible and orally active inhibitor oflysine specific demethylase-1 (LSD1)with anIC₅₀of 0.25 nM. Pulrodemstat is less enzymatic inhibition against LSD2, MOA-A, andMAO-B. Pulrodemstat induces acute myeloid leukemia (AML) and small cell lungcancer(SCLC) cells differentiation and has potent anticancer activity^[1].

IC50: 0.25 nM (LSD1)^[1]

Pulrodemstat (CC-90011, Compound 11) shows potent induction of on-target cellular differentiation marker CD11b in THP-1 cell line with an EC₅₀of 7 nM, antiproliferative activity in AML kasumi-1 cells with an EC₅₀of 2 nM^[1].
Suppression of GRP is observed with treatment of Pulrodemstat (4 days) in a dose-dependent manner and at pharmacologically useful concentrations (EC₅₀=3 nM, H209 and 4 nM, H1417). Pulrodemstat (12 days) treatment of SCLC cells results in potent antiproliferative activity (EC₅₀=6 nM, H1417) that correlated with GRP suppression^[1].

Pulrodemstat (CC-90011; 5 mg/kg; oral administration; daily; for 30 days; for 30 days) treatment inhibits tumor growth in patient-derived xenograft SCLC models^[1].
Pulrodemstat (once a day; for 4 days) treatment results in robust downregulation of GRP mRNA levels at 2.5 mg/kg and maximum suppression of GRP at 5 mg/kg in a SCLC human tumor xenograft (H1417) mice^[1].
After i.v. administration, Pulrodemstat (Compound 11; 5 mg/kg) has systemic clearance of 32.4 mL/min/kg, elimination half-life of 2 h, and a high volume of distribution of 7.5 L/kg. Pulrodemstat (Compound 11; 5 mg/kg) is readily absorbed after oral administration with an AUC_0-24hof 1.8 μM·h, C/sub>maxof 0.36 μM, and oral bioavailability of 32%^[1].

451.47

C₂₄H₂₃F₂N₅O₂

1821307-10-1

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.