Raptinal, a agent that directly activates caspase-3, initiates intrinsic pathway caspase-dependent apoptosis. Raptinal is able to rapidly induce cancer cell death by directly activating the effector caspase-3, bypassing the activation of initiator caspase-8 and caspase-9[2].In Vitro: H. pylori?infection-induced apoptosis resistance in gastric epithelial cells triggered by Raptinal.?
Treatment with 10?μM of Raptinal for 2?h induces the cleavage of pro-caspase-3 into it’s active form in human gastric cancer cell lines AGS, MKN28, MKN45.
Raptinal initiates intrinsic pathway caspase-dependent apoptosis within minutes in multiple cell lines. Raptinal induces death against various cancer and non-cancerous cell lines with 24 hour IC50?values between 0.7-3.4 μM, indicating activity across a wide variety of cell lines[2].In Vivo: Raptinal is an unusually rapid inducer of caspase-dependent apoptosis in multiple cell lines and?in vivo?systems.
Raptinal (20 mg/kg; administered intraperitoneally; once daily for 3 consecutive days for B16-F10 and 4 consecutive days for 4T1 models) exerts anticancer activity?in vivo[2].
C57BL/6 mice are administered intravenous Raptinal across a range of dosages as a one-time injection. When administered intravenously at a dosage of 37.5 mg/kg, the peak plasma concentration and elimination half-life of Raptinal are 54.4±0.9 μg/mL and 92.1±5.8 minutes, respectively. Single-dose intravenous Raptinal is well tolerated across a wide dose range (15-60 mg/kg) and does not cause hematologic toxicity as assessed 7 days post-administration[2].