Calphostin C

Calphostin C is a highly selective PKC inhibitor (IC₅₀=0.05 μM) and tumor apoptosis inducer. Calphostin C competitively binds to PKC and inhibits PKC-mediated phosphorylation signal transduction. Calphostin C restores Na+/K+ ATPase activity in the sciatic nerve of diabetic mice and improves neuropathy. Calphostin C can be used in the study of anti-tumor and diabetic complications^[1][2][3]. IC50 & Target:protein kinase C^[1] In Vitro:Calphostin C blocks the binding of [³H]PDBu to PKC and inhibits its activation process with IC₅₀=0.03 μM^[1].
Calphostin C (5 μM; 10 min-6 h) induces apoptosis in NALM-6 leukemia cells^[2].
Calphostin C (2 μM; 24 h) is metabolized to inactive Calphostin B by esterases, and Calphostin B is not toxic to NALM-6 cells^[2]. In Vivo:Calphostin C (40 mg/kg; i.p.; single dose) has a maximum plasma concentration of 2.9 μM and an elimination half-life of 91.3 minutes in CD-1 mice, and showed no toxicity^[2].
Calphostin C (1 μg/kg and 10 μg/kg; i.p.; single dose) restores the sciatic nerve Na+/K+ ATPase activity to normal levels in a streptozotocin (STZ)-induced diabetic mouse model^[3].
Calphostin C (50 μg/mL; continuous administration by mini-osmotic pump; 0.5 μL per day; 2 weeks) restores the sciatic nerve Na+/K+ ATPase activity to normal levels in diabetic mice without affecting blood glucose levels^[3].