MK-2048

MK-2048 potently inhibits the growth of HTLV-1-infected cell lines and ATL-derived cell lines^[1].
MK-2048 induces apoptosis in HTLV-1-infected cell lines through activation of the PERK-eIF2a-ATF4 UPR pathway and upregulation of pro-apoptotic markers CHOP and cleaved PARP^[1].
MK-2048 upregulates the PERK-mediated UPR pathway in HTLV-1-infected cell lines and ATL-derived cell lines, leading to activation of pro-apoptotic signaling^[1].
MK-2048 (4 h pre-incubation) potently inhibits cell-free HTLV-1 infection of 293T cells with an EC₅₀ of 1 nM, with no associated cell toxicity^[2].
MK-2048 (0.25-1 nM; 6 days) significantly inhibits cell-to-cell HTLV-1 infection of B5Luc cells at concentrations similar to those active in cell-free infection assays^[2].
MK-2048 (1-10 nM; 10 days) dose-dependently reduces HTLV-1 integration and total viral DNA levels in Jurkat cells, with complete inhibition of integration at concentrations ≥2 nM^[2].
MK-2048 (4 h) inhibits HTLV-1 infection of 293T cells at the stage of viral integration, without affecting reverse transcription^[2].
MK-2048 (0.0256 nM-2 μM; 72 h) inhibits wild-type NL4-3 HIV-1 replication in PM1 cells with an EC₅₀ of 0.0019 μM^[3].

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