Endostatin

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Endostatin monomer, basic amino acid residues shown in red 1KOE
Endostatin monomer, basic amino acid residues shown in red 1KOE

Endostatin is a naturally-occurring 20-kDa C-terminal fragment derived from type XVIII collagen. It is reported to serve as an anti-angiogenic agent, similar to angiostatin and thrombospondin

Endostatin is a angiogenesis inhibitor. Endostatin is a broad spectrum angiogenesis inhibitor and may interfere with the pro-angiogenic action of growth factors such as basic fibroblast growth factor (bFGF/FGF-2) and vascular endothelial growth factor (VEGF).[1]

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[edit] Research

Endostatin is currently being studied as part of cancer research.

[edit] Phase I

In a Phase I clinical trial of Endostatin of the 19 patients treated, 12 were switched out of the trial by their physicians due to continued progression of their disease.[2]

Two patients continued to be treated, and the remaining patients withdrew on their own.

The trial, designed primarily to demonstrate safety, indeed showed that the drug was safe and well-tolerated.

[edit] Phase II

In a Phase II clinical trial of Endostatin forty two patients with pancreatic endocrine tumors or carcinoid tumors were treated.[3] Of the 40 patients which could be evaluated for a radiologic response, none experienced partial response to therapy, as defined by World Health Organization criteria.

The conclusion from the trial was that "Treatment with Endostatin did not result in significant tumor regression in patients with advanced neuroendocrine tumors."

[edit] References

  1. ^ Folkman, J. (2006). "Antiangiogenesis in cancer therapy--endostatin and its mechanisms of action.". Exp. Cell. Res. 312: 594–607. doi:10.1016/j.yexcr.2005.11.015. 
  2. ^ Dana-Farber Cancer Institute (November 2000). "Boston hospitals report early results of Endostatin clinical trial". Press release. Retrieved on 2006-07-12.
  3. ^ Kulke M H et al (2006). "Phase II study of recombinant human endostatin in patients with advanced neuroendocrine tumors". J. Clin. Oncol. 24: 3555–3561. doi:10.1200/JCO.2006.05.6762. 

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