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fruquintinib

FruzaqlaVEGFR kinase inhibitor

Fruzaqla (fruquintinib) is an oral kinase inhibitor from Takeda that selectively blocks VEGF receptors 1, 2 and 3. By cutting off tumour blood vessel formation it is used in metastatic colorectal cancer that has progressed through standard therapies.

This page is based on FDA prescribing information and the EMA medicine record for fruquintinib, cross-checked with DailyMed and MedlinePlus; the mechanism is explained in plain language, and analogies are used only where they stay accurate.

How it works

Explains what the medicine does in the body, not dosing, side effects, or safety.

An analogy

A growing tumour sends out construction permits, VEGF signals, to build private supply roads of new blood vessels. Fruquintinib blocks the three permit offices, VEGFR-1, 2 and 3, so the road crews never get orders. The tumour's supply network stalls and its growth slows.

In simple terms

Cancers need new blood vessels to grow and spread, and they build them by sending VEGF signals to vessel cells. Fruquintinib blocks the receptors that receive those signals, so new vessels cannot form properly. Deprived of blood supply, the tumour grows more slowly. This approach is used after chemotherapy and other targeted treatments have stopped working.

In depth

Fruquintinib is an oral, highly selective small-molecule inhibitor of VEGFR-1, VEGFR-2 and VEGFR-3 tyrosine kinases. It inhibits VEGF-induced receptor phosphorylation, suppressing endothelial cell migration, proliferation and survival, and thereby tumour angiogenesis. Its selectivity limits off-target kinase effects, and trials in heavily pretreated metastatic colorectal cancer demonstrated improved overall survival versus placebo.

See it in motion

A schematic animation of the mechanism — simplified for clarity, not drawn to scale.

How VEGFR inhibitors block vessel growth

VEGF receptor kinasefruquintinibTumor blood-vessel growth
  1. VEGF docks the VEGF receptor on blood-vessel lining cells, flipping on its internal kinase.
  2. The drug is a small-molecule inhibitor that blocks these receptor kinases.
  3. With the kinase blocked, the growth signal cannot pass into the cell.
  4. New vessel sprouting toward the tumor slows and the tumor's blood supply weakens.
How fruquintinib works

Target: Vascular endothelial growth factor receptors 1, 2 and 3 (VEGFR-1/2/3)

Receptors on blood vessel cells that drive new vessel growth feeding tumours; blocking all three starves the cancer of its expanding blood supply.

Approved uses

Approved uses differ by country and change over time. Always follow your local prescribing information.

Approved uses in United States

FDA
  • Treatment of adults with metastatic colorectal cancer previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti-VEGF therapy, and, if RAS wild-type and medically appropriate, an anti-EGFR therapy

Approved uses in European Union

EMA
  • As monotherapy, for adults with metastatic colorectal cancer previously treated with available standard therapies, including fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapies, anti-VEGF agents and anti-EGFR agents, who have progressed on or are intolerant to trifluridine/tipiracil or regorafenib

Official sources

The statements on this page trace back to these records.

  1. DailyMed: Fruzaqla (fruquintinib) label

    DailyMed, U.S. National Library of Medicine

  2. MedlinePlus: fruquintinib

    MedlinePlus, U.S. National Library of Medicine

This page explains how the medicine works — it isn’t the patient leaflet. For anything that applies to you, read the leaflet that came with your medicine or ask your pharmacist.

MedUnfold provides educational content and is not medical advice. Always follow your local prescribing information and healthcare professional.