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Telaglenastat

CB-839

Glutaminase inhibitor

Evidence Score

60

clinical trial
Mechanism of Action

Selective, orally bioavailable inhibitor of glutaminase (GLS). Blocks the conversion of glutamine to glutamate, cutting off the primary anaplerotic fuel source for SDH-deficient cells with disrupted TCA cycles.

Pathway Connections
Glutamine Dependency

With the TCA cycle disrupted at Complex II, SDH-deficient cells become addicted to glutamine for anaplerosis and lipid synthesis via reductive carboxylation.

Upstream event:

TCA cycle disruption at succinate → fumarate step

Downstream effects:

Glutaminase (GLS) upregulationReductive carboxylation for lipid synthesisα-KG production via glutaminolysisMetabolic vulnerability
Molecular Targets

GLS

Glutaminase (kidney isoform)

metabolic

Converts glutamine to glutamate for TCA anaplerosis. SDH-deficient cells are glutamine-addicted. Target of telaglenastat (CB-839).

UniProt: O94925

Quick Facts
Not FDA Approved
ChEMBL IDCHEMBL3707341
PubChem CID71577426
Evidence

Evidence from PubMed, OpenTargets, and ChEMBL will appear here once external data integration is enabled.

Coming in Phase 3

For research exploration only — not medical advice. Consult your doctor before acting on any information.

AI Analysis

Have Claude analyze this drug's repurposing potential for SDH-deficient diseases.