SBI-0206965

inhibits ULK1 kinase; structure in first source

Networked: 6 relevant articles (0 outcomes, 0 trials/studies)

1.	Neoplasms (Cancer) 07/16/2015 - "SBI-0206965 greatly synergized with mechanistic target of rapamycin (mTOR) inhibitors to kill tumor cells, providing a strong rationale for their combined use in the clinic." 10/01/2018 - "The combination of two separate antiautophagy agents, SBI-0206965 and chloroquine, plus cabozantinib increased apoptosis in vitro Cabozantinib demonstrated significant antitumor activity, reduction in tumor vascularity, increased autophagy, and altered cell metabolism compared with regorafenib. "
2.	Atherosclerosis 02/01/2020 - "The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells."
3.	Neuroblastoma 11/01/2018 - "Here we demonstrate that targeted inhibition of an essential autophagy kinase, unc-51 like autophagy kinase 1 (ULK1), with a recently developed small-molecule inhibitor of ULK1, SBI-0206965, significantly reduces cell growth and promotes apoptosis in SK-N-AS, SH-SY5Y, and SK-N-DZ neuroblastoma cell lines. "
4.	Glioblastoma (Glioblastoma Multiforme) 10/01/2022 - "Brain pharmacokinetics and metabolism of the AMP-activated protein kinase selective inhibitor SBI-0206965, an investigational agent for the treatment of glioblastoma."
5.	Renal Cell Carcinoma (Grawitz Tumor) 08/01/2018 - "Overexpression of ULK1 Represents a Potential Diagnostic Marker for Clear Cell Renal Carcinoma and the Antitumor Effects of SBI-0206965."

1.	AMP-Activated Protein Kinases
2.	Sirolimus (Rapamycin)
3.	Phosphotransferases (Kinase)
4.	Chloroquine (Aralen)
5.	MTOR Inhibitors
6.	regorafenib
7.	cabozantinib