mtor-independent

RU-SKI 43 is a potent and selective hedgehog acyltransferase (Hhat) inhibitor with an IC50 of 850 nM. It exhibits anticancer activity and is a potential treatment for lung adenocarcinomas. RU-SKI 43 reduces Gli-1 activation through smoothening-independent non-canonical signaling and inhibits Akt and mTOR pathway activity.

SMER28 is a small-molecule enhancer (SMER) of autophagy, inducing autophagy independently of rapamycin in mammalian cells via an mTOR-independent mechanism and prevented the accumulation of amyloid beta peptide.

EGFR-IN-79 (compound 21), an EGFR inhibitor, exhibits antitumor activity through ROS-independent apoptosis and EGFR/AKT/mTOR-mediated autophagy. It effectively induces cell death in proliferating and quiescent zones of EJ28 spheroids and demonstrates a safety profile in zebrafish-based models [1].

SMER18 is a small molecule enhancer of rapamycin, functioning as an mTOR-independent autophagy inducer.

TFEB activator 1 (Curcumin analog compound C1) is an activator of transcription factor EB (TFEB) with promise for the prevention or treatment of Alzheimer's disease.

Cucurbitacin D, a triterpenoid isolated from Ecballium elaterium (L.), exhibits anticancer and antitumor activity, inhibits glucose uptake and lactate production in metastatic PrC, and induces inflammasome activation independent of ERK1 2 activation. Cucurbitacin D, a novel inflammasome activator in macrophages, inhibits HepG2 cell proliferation and induces apoptosis by modulating the JAK STAT3, PI3K Akt mTOR and MAPK signaling pathways, and can be used in the study of cervical cancer, leukemia, and prostate cancer.

BRD5631 is an autophagy enhancer that operates through an mTOR-independent pathway. It influences several cellular disease phenotypes associated with autophagy, such as protein aggregation, cell survival, bacterial replication, and inflammatory cytokine production. BRD5631 can serve as a valuable tool for studying the role of autophagy in cellular homeostasis and disease. [1].

Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, exhibits potent antiproliferative activity, induces autophagosome accumulation via an mTOR-independent mechanism, and triggers apoptosis. Furthermore, it inhibits VEGFA VEGFR2 expression, effectively suppressing tumor growth in glioblastoma xenografts [1] [2].

8-Aminoadenosine (8-NH2-Ado) is an RNA-directed nucleoside analogue that effectively diminishes cellular ATP levels and impedes mRNA synthesis. It also obstructs Akt mTOR signaling, inducing autophagy and apoptosis in a p53-independent manner. Its significant antitumor activity underscores its therapeutic potential.