HPA-12

HPA-12 (60-100 μM; 48 h) reduces the viability and proliferation of FLT3^ITD+ MV4-11 and Molm13 acute myeloid leukemia (AML) cell lines in a dose-dependent manner, but exerts no effect on FLT3^-WT AML cell lines after 48 h of treatment^[1].
Treatment with HPA-12 (100 μM; 48 h) induces apoptosis in FLT3^ITD+-type Molm13 AML cells^[1].
HPA-12 (2.5 μM; 30 min) inhibits CERT-mediated intracellular trafficking of fluorescent ceramide analogs in HeLa cells and prevents the accumulation of such analogs in the perinuclear Golgi region^[2].
HPA-12 (0.1-2.5 μM; 2-5 h) potently and concentration-dependently inhibits de novo SM synthesis in CHO cells, exerts weak effects on Cer and GlcCer synthesis, and has no impact on the synthesis of phosphatidylethanolamine or phosphatidylserine^[3].
HPA-12 (2.5 μM; 48 h) reduces the content of SM by approximately 30% in CHO cells, while increasing the content of glycosphingolipids, without altering the content of total phospholipids or Cer, nor inhibiting the synthesis of PC (1 μM HPA-12; 4 h)^[3].
HPA-12 (20 μM; 10 min-1 h) is not an in vitro inhibitor of SM synthase or other key enzymes involved in de novo sphingolipid synthesis^[3].
(1R,3R)-HPA-12 (1 μM; 15 min pre-treatment + 30 min exposure) primarily inhibits the ATP-dependent pathway of ceramide transport from the endoplasmic reticulum to sphingomyelin (SM) synthesis sites in CHO cells^[3].
(1R,3R)-HPA-12 (2.5 μM; 0-120 min) does not inhibit the trafficking of GPI-anchored or transmembrane glycoproteins from the endoplasmic reticulum (ER) to the Golgi apparatus in CHO cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.