SBP-1750 is an orally active ULK inhibitor and an ATG13 degrader. SBP-1750 strongly inhibits ULK1/2 activity, with IC50 values of 8 and 50 nM, respectively. SBP-1750 induces ATG13 degradation, with an EC 50 value of 114 nM. SBP-1750 can inhibit autophagy in cancer cells and induce cell death. SBP-1750 can be used in cancer research, such as for pancreatic cancer [1].
In Vivo, SBP-1750 (40 mg/kg; i.g.; daily; from day 10 to 28) reduces pancreatic tumor size and metastasis in KPC4662 PDAC mice model[1].
In Vitro, SBP-1750 (5 μM; 18 hours) inhibits autophagy in A549 cells[1]. SBP-1750 (48 h) induces ATG13 degradation in A549 ATG13-HiBiT cells with EC50 of 114 nM[1]. SBP-1750 (48 h) inhibits cell viability in KRAS-mutant cancer cells (A549, MiaPaCa2, NCI-H358, PANC-1) with IC50 <50 nM[1].
References:
[1]. Hagan PM, et al. ULK1/2 Inhibitors that Degrade ATG13 Effectively Target KRAS-Mutant Cancers. bioRxiv [Preprint]. 2025 Oct 15:2025.10.14.682402.
In Vivo, SBP-1750 (40 mg/kg; i.g.; daily; from day 10 to 28) reduces pancreatic tumor size and metastasis in KPC4662 PDAC mice model[1].
In Vitro, SBP-1750 (5 μM; 18 hours) inhibits autophagy in A549 cells[1]. SBP-1750 (48 h) induces ATG13 degradation in A549 ATG13-HiBiT cells with EC50 of 114 nM[1]. SBP-1750 (48 h) inhibits cell viability in KRAS-mutant cancer cells (A549, MiaPaCa2, NCI-H358, PANC-1) with IC50 <50 nM[1].
References:
[1]. Hagan PM, et al. ULK1/2 Inhibitors that Degrade ATG13 Effectively Target KRAS-Mutant Cancers. bioRxiv [Preprint]. 2025 Oct 15:2025.10.14.682402.