SU212

SU212 is a podophyllotoxin-derived ENO1 inhibitor and AMPK activator. SU212 can selectively induce oxidative phosphorylation, reduce glycolysis activity and glucose uptake in tumor cells, and directly bind to ENO1 without affecting these pathways in normal cells. SU212 induces apoptosis and promotes ENO1 degradation via proteasomal and autophagic pathways without inhibiting the catalytic activity. SU212 leads to mitotic arrest and apoptosis in TNBC (triple-negative breast cancer) cells by activating AMPK, demonstrating potent anti-tumor activity in vitro. SU212 inhibits tumor growth and metastasis in syngeneic, xenograft, and diabetic mouse models, exhibiting an excellent safety profile. SU212 can be used in research on t TNBC, diabetes, and fatty liver disease[1][2].

Product Specifications

CAS Number

[1262219-89-5]

UNSPSC

12352005

Target

AMPK; Apoptosis; Autophagy; Caspase; Enolase; mTOR

Related Pathways

Apoptosis; Autophagy; Epigenetics; Metabolic Enzyme/Protease; PI3K/Akt/mTOR

Field of Research

Cancer; Metabolic Disease

Smiles

COC1=CC(C2C3=CC4=C(CCC4)C=C3N(C5=C2C(OC5)=O)CCO)=CC(OC)=C1OC

Molecular Formula

C25H27NO6

Molecular Weight

437.48

References & Citations

[1]Tailor D, et al., Malhotra SV. Non-orthosteric inhibition of enolase 1 impedes growth of triple-negative breast cancer. Cell Rep Med. 2025 Nov 18;6 (11) :102451.|[2]Tailor D, et al., Novel Aza-podophyllotoxin derivative induces oxidative phosphorylation and cell death via AMPK activation in triple-negative breast cancer. Br J Cancer. 2021 Feb;124 (3) :604-615.