Vitaxin

Vitaxin (MEDI-523): An Angiogenesis Inhibitor

Vitaxin (MEDI-523) is a humanized monoclonal antibody designed to target the vascular integrin alpha-v beta-3, playing a significant role in angiogenesis inhibition. With implications for the treatment of various cancers, Vitaxin's development and clinical investigation have underscored its potential therapeutic utility, as well as its safety profile.

Background

Classification: Humanized monoclonal antibody.
Target: Vascular integrin alpha-v beta-3.

Mechanism of Action

Vitaxin functions as an antagonist to the vascular integrin alpha-v beta-3. This integrin is central to the process of angiogenesis, or the formation of new blood vessels, which is a crucial process for the growth and survival of tumors^[1].

Therapeutic Applications

Cancer Treatment: Due to its inhibitory effects on angiogenesis, Vitaxin has been investigated as a therapeutic agent in the management of several cancers. The ability to curtail blood vessel formation can deprive tumors of necessary nutrients, leading to their stagnation or regression.
Rheumatoid Arthritis: In 2002, researchers began exploring the potential of Vitaxin in treating rheumatoid arthritis, a chronic inflammatory condition that can benefit from angiogenesis inhibition^[2].

Developmental Lineage

Origin: Vitaxin is derived from the mouse antibody LM609.
Successor: Vitaxin served as the developmental precursor for Etaracizumab (MEDI-522), which also targets the same integrin.

Clinical Assessment

Safety Profile: Clinical studies have demonstrated that Vitaxin is well-tolerated and safe for human administration^[3].
Efficacy: While safe, its therapeutic efficacy for advanced cancers appears to be limited. Further studies are necessary to determine the best applications and patient populations for Vitaxin treatment^[4].

Conclusion

Vitaxin, as an angiogenesis inhibitor, embodies the potential of targeted therapies in the realm of oncology and other diseases. Its safety profile encourages further investigation into its therapeutic applications, while its developmental lineage has spurred the creation of subsequent compounds, broadening the scope of this class of drugs.

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↑ Brooks PC, et al. Integrin alpha v beta 3 antagonists promote tumor regression by inducing apoptosis of angiogenic blood vessels. Cell. 1994;79(7):1157-1164.
↑ Feldmann M, Maini RN. Lasker Clinical Medical Research Award. TNF defined as a therapeutic target for rheumatoid arthritis and other autoimmune diseases. Nat Med. 2003;9(10):1245-1250.
↑ Dechantsreiter MA, et al. N-Methylated cyclic RGD peptides as highly active and selective alpha(V)beta(3) integrin antagonists. J Med Chem. 1999;42(16):3033-3040.
↑ Gutheil JC, et al. Targeted antiangiogenic therapy for cancer using Vitaxin: a humanized monoclonal antibody to the integrin alphavbeta3. Clin Cancer Res. 2000;6(8):3056-3061.

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[1] Brooks PC, et al. Integrin alpha v beta 3 antagonists promote tumor regression by inducing apoptosis of angiogenic blood vessels. Cell. 1994;79(7):1157-1164.

[2] Feldmann M, Maini RN. Lasker Clinical Medical Research Award. TNF defined as a therapeutic target for rheumatoid arthritis and other autoimmune diseases. Nat Med. 2003;9(10):1245-1250.

[3] Dechantsreiter MA, et al. N-Methylated cyclic RGD peptides as highly active and selective alpha(V)beta(3) integrin antagonists. J Med Chem. 1999;42(16):3033-3040.

[4] Gutheil JC, et al. Targeted antiangiogenic therapy for cancer using Vitaxin: a humanized monoclonal antibody to the integrin alphavbeta3. Clin Cancer Res. 2000;6(8):3056-3061.

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