VEGF

Selection of molecular targeted drugs

1.    Donft choose drug whose end is ending with mab (Bevacizumab)

~mab  monoclonal antibody with large molecule that cannot enter into malignant and endothelial cells

2.    Let's choose drug whose end is ending with ib.

~ib  inhibitory with small molecule that works in the cells

 

Vascular endothelial growth factor (VEGF) is a signalling protein that promotes the growth of new blood vessels. One of the main functions of VEGF is to form new blood vessels as a baby grows and develops in the womb. Solid tumors require an increased blood supply if they are to continue growing beyond a certain size and tumors that express VEGF are able to continue growing because they can develop this enhanced blood supply, a process referred to as angiogenesis. Cancers that express VEGF are therefore able to grow and spread (metastasize) to other organs and regions of the body.

When targeting VEGF for cancer treatment, we must change our thought. VEGF is the name given by a human to the last, does not mean that there is no other protein that promotes angiogenesis. VEGF has seven types of VEGF (A-E), PIGF 1 - 2, and its receptors are VEGFR 1 - 3. VEGF is a ball, receptors are gloves and it will be easy to understand. VEGF is not the only factor that promotes angiogenesis. There are many such factors as FGF, PDGF, COX-2. Angiogenesis is caused by many factors, and inhibitors of VEGF inhibit angiogenesis, but its probability is very low. Tumor ascites fluids contain activity that rapidly increases microvascular permeability, which is induced by microvascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF). As a potent permeability factor, VPF/VEGF promotes extravasation of plasma fibrinogen, leading to fibrin deposition which alters the tumor extracellular matrix. This matrix promotes the ingrowth of macrophages, fibroblasts, and endothelial cells. Bevacizumab (vastin) is a drug having angiogenesis inhibitory effect. Avastin interferes with the binding of VEGF-A and VEGFR-2 and exerts its efficacy. Since other routes are not inhibited, the effect cannot be expected much. It is impossible to treat pleural effusion and ascites with Avastin that inhibits VEGF. To eradicate pleural effusion and ascites, drugs that suppress the production of VEGF, not suppress the function of VEGF. In order to control ascites, drugs that inhibit the production of VEGF must be selected. Drugs that inhibit the function of VEGF cannot be expected to be effective. Furthermore, drugs acting simultaneously on the matrix are more effective.

 Oral treatment of thalidomide or sulindac alone inhibited tumour growth by 55% and 35% respectively. When given together, the growth of the V2 carcinoma was inhibited by 75%. Our results indicated that oral antiangiogenic combination therapy with thalidomide and sulindac may be a useful non-toxic treatment for cancer. At present, the combination of thalidomide and COX-2 inhibitor celecoxib is very effective.

 

Donft choose drug whose end is ending with mab (Bevacizumab)

Let's choose drug whose end is ending with ib (Solafenib).