LCL-161 1005342-46-0

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LCL-161, a small molecule second mitochondrial activator of caspase (SMAC) mimetic, potently binds to and inhibits multiple IAPs (i.e. XIAP, c-IAP).

LCL161 binds to inhibitors of apoptosis proteins (IAPs) with high affinity and initiates the destruction of cIAP1 and cIAP2, which further induces apoptosis via caspase activation. LCL161 modestly inhibits the growth of FLT3-ITD-expressing cells when administered alone, with an IC50 ranging from ~0.5 μM (Ba/F3-FLT3-ITD cells) to ~4 μM (MOLM13-luc+ cells). The potency of LCL161 against the D835Y mutant is observed to be considerably higher, with an IC50 of ~50 nM when tested against Ba/F3-D835Y cells. Treatment of MOLM13-luc+ cells with a combination of LCL161 and PKC412 leads to significantly more killing of cells than either agent alone, with Calcusyn combination indices suggestive of synergy. PKC412 and LCL161 induces apoptosis of MOLM13-luc+ cells. The combination of PKC412 and LCL161 leads to a higher induction of apoptosis than either agent alone. LCL161 is able to override stromal-mediated rescue of mutant FLT3-expressing cells through positive combination with PKC412. LCL161 inhibits the growth of Ba/F3.p210 cells with an IC50 of ~100 nM. The combination of LCL161 and the ABL inhibitor, imatinib, is observed to be synergistic against BCR-ABL-expressing cells. LCL161 also has demonstrated activity against drug-resistant cells expressing point mutations in the target proteins. LCL161 at 1000 nM is able to mostly or completely kill Ba/F3-derived cell lines conferring resistance to PKC412, which express FLT3-ITD harboring point mutations in the ATP-binding pocket of FLT3. LCL161 also shows activity at concentrations ranging from 100 to 1000 nM against Ba/F3 cells expressing various imatinib- and nilotinib-resistant BCR-ABL point mutations.

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