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Sunitinib

Sutent

Multi-kinase inhibitor (VEGFR/PDGFR/KIT)

Evidence Score

75

established
Mechanism of Action

Inhibits multiple receptor tyrosine kinases including VEGFR1/2/3, PDGFR-α/β, KIT, FLT3, and RET. Blocks angiogenesis and has direct anti-tumor effects. Used as standard therapy in advanced GIST and has shown activity in SDH-deficient GIST and paraganglioma.

Pathway Connections
VEGF Signaling

Downstream of HIF activation, VEGF/VEGFR2 signaling drives tumor angiogenesis — the formation of new blood vessels that supply the tumor with oxygen and nutrients.

Upstream event:

HIF-mediated VEGFA transcriptional activation

Downstream effects:

Tumor angiogenesisVascular permeabilityEndothelial cell proliferationTumor blood supply
mTOR / PI3K / AKT

Metabolic reprogramming from SDH loss activates the PI3K/AKT/mTOR signaling axis, promoting cell growth, proliferation, and survival. Multiple upstream inputs converge on mTOR.

Upstream event:

HIF-mediated growth factor signaling + metabolic stress + AMPK dysregulation

Downstream effects:

Cell growth and proliferationProtein synthesisMetabolic reprogrammingSurvival signaling
Molecular Targets

KDR

VEGF receptor 2 (VEGFR2)

downstream

Primary VEGF receptor on endothelial cells. Target of sunitinib, regorafenib, and other multi-kinase inhibitors.

UniProt: P35968

KIT

KIT proto-oncogene receptor tyrosine kinase

downstream

Primary oncogene in most GISTs, but SDH-deficient GISTs typically have wild-type KIT. Some residual KIT signaling may persist.

UniProt: P10721

Quick Facts
FDA Approved

Approved Indications

  • Advanced GIST (after imatinib failure)
  • Advanced renal cell carcinoma
  • Pancreatic neuroendocrine tumors
ChEMBL IDCHEMBL535
PubChem CID5329102
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.