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momordicine-I
- Development stage
- Preclinical
- Lead developer
- Saint Louis University
- Modality
- Small Molecules
- Administration
- Intraperitoneal, Parenteral
01
Overview
Momordicine-I is a bioactive cucurbitane-type triterpene isolated from the bitter melon (*Momordica charantia*). It is currently under investigation for its potential therapeutic application in head and neck cancer (HNC). The compound's mechanism of action involves the comprehensive reprogramming of cancer cell metabolism; it inhibits key pathways including glycolysis and de novo lipogenesis by downregulating the expression of enzymes such as hexokinase 1 (HK1), pyruvate dehydrogenase kinase 3 (PDK3), fatty acid synthase (FASN), and ATP citrate lyase (ACLY). Furthermore, momordicine-I activates the AMPK pathway while simultaneously inhibiting the mTOR and Akt signaling axes, leading to the induction of autophagy and suppression of tumor growth. Preclinical evidence from mouse models suggests that momordicine-I can significantly reduce tumor volume, highlighting its potential as a metabolic-targeted antineoplastic agent.
- Other names
- Momordicine I
02
Targets
AMPK (Adenosine monophosphate–activated protein kinase)STAT3 (Signal Transducer and Activator of Transcription 3)AKT (RAC-alpha serine/threonine-protein kinase)HK1 (Hexokinase type I (mitochondrial))SCD1 (Stearoyl-CoA desaturase 1)NF-κBACC (Acetyl-CoA Carboxylase 1)MET (Mesenchymal-epithelial transition factor receptor)FASN (Fatty acid synthase)SREBP-1 / SREBF1 (SREBP-1)PDK (Pyruvate dehydrogenase kinase isoform 1)ACLY (ATP-citrate synthase)mTOR (Mammalian target of rapamycin kinase)NFE2L2 (Nuclear factor (erythroid-derived 2)-like 2)
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