ipatasertib

Ipatasertib (GDC-0068) is a selective, ATP-competitive pan-Akt inhibitor that inhibits Akt1 (IC50:5 nM), Akt2 (IC50:18 nM), and Akt3 (IC50:8 nM). Ipatasertib (GDC-0068) can lead to p53-independent PUMA activation by inhibiting Akt, thereby activating FoxO3a and NF-κB simultaneously, directly binding to the PUMA promoter, upregulating PUMA transcription and Bax-mediated intrinsic mitochondrial apoptosis.

BMS-986034 is a GPR119 agonist.

Ipatasertib-NH2 (GDC-0068-NH2;RG7440-NH2) is a ligand for the target protein AKT used in PROTAC, binding to lenalidomide, a ligand of ubiquitin E3 ligase cereblon (CRBN), via a ten-hydrocarbon linker to form INY-03-041 for AKT degradation[1].

Ipatasertib-NH2 dihydrochloride is a ligand for the target protein AKT in PROTAC [INY-03-041], comprising Ipatasertib-NH2, a ten-hydrocarbon linker, and the CRBN ligand Lenalidomide, which functions as an E3 ubiquitin ligase.

INY-03-041 trihydrochloride, a potent and highly selective PROTAC-based pan-AKT degrader, comprises Ipatasertib, an ATP-competitive AKT inhibitor, conjugated to Lenalidomide. It effectively inhibits AKT1, AKT2, and AKT3 with IC50 values of 2.0, 6.8, and 3.5 nM, respectively [1].