Bevacizumab
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- | < | + | <StructureSection load='' size='350' side='right' scene='Bevacizumab/Ba/1' caption='Model Bevacizumab, also known as Avastin (PDB code [[1igt]])'> |
+ | __TOC__ | ||
+ | |||
===Better Known as: Avastin=== | ===Better Known as: Avastin=== | ||
* Marketed By: Genentech & Roche<br /> | * Marketed By: Genentech & Roche<br /> | ||
* Major Indication: Colorectal [[Cancer]]<br /> | * Major Indication: Colorectal [[Cancer]]<br /> | ||
- | * Drug Class: [[ | + | * Drug Class: [[Vascular Endothelial Growth Factor]] Inhibitor - [[Monoclonal Antibody]] |
- | * Date of FDA Approval (Patent Expiration): 2004 ( | + | * Date of FDA Approval (Patent Expiration): 2004 (2019) |
- | * 2009 Sales: $4.8 Billion | + | * 2009 Sales: $4.8 Billion |
* Importance: It is one of the best selling [[cancer]] treatments in history. Despite being effective against colorectal cancer, post-approval studies after accelerated approval revealed that Avastin was ineffective in treating breast cancer. Many question the $90,000/year bill to take Avastin when it extends life on average only 10 months. | * Importance: It is one of the best selling [[cancer]] treatments in history. Despite being effective against colorectal cancer, post-approval studies after accelerated approval revealed that Avastin was ineffective in treating breast cancer. Many question the $90,000/year bill to take Avastin when it extends life on average only 10 months. | ||
- | * | + | * See [[Pharmaceutical Drugs]] for more information about other drugs and disorders |
===Mechanism of Action=== | ===Mechanism of Action=== | ||
+ | [[Vascular Endothelial Growth Factor]] (VEGF) is a signal protein often over-expressed in cancerous cells. It is responsible for activating [[Vascular Endothelial Growth Factor Receptors]] (VEGFRs) to accelerate angiogenesis and vasculogenesis. Accelerated angiogenesis creates the overly developed blood vessel system common to all tumors, providing oxygen and nutrients to the prodigal tumors. Bevacizumab binds to VEGF, preventing it from interacting with VEGFR, thus halting accelerated angiogenesis in tumors, preventing the cancer from growing rapidly.<ref>PMID:11815711</ref> | ||
===Pharmacokinetics=== | ===Pharmacokinetics=== | ||
{| class="wikitable" border="1" width="30%" style="text-align:center" | {| class="wikitable" border="1" width="30%" style="text-align:center" | ||
|- | |- | ||
- | ! colspan="2" align="center"| VEGF Inhibitor [[ | + | ! colspan="2" align="center"| VEGF Inhibitor [[Pharmacokinetics]]<ref>PMID:17093010</ref> |
|- | |- | ||
! Parameter | ! Parameter | ||
! [[Bevacizumab]] | ! [[Bevacizumab]] | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Tmax|T<sub>max</sub>]] (hr) |
! 5.17 | ! 5.17 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Cmax|C<sub>max</sub>]] (ng/ml) |
! 284000 | ! 284000 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Bioavailability_.28F.29|Bioavailability]] (%) |
! 100 | ! 100 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Half_Life_.28T1.2F2.29|T<sub>1/2</sub>]] (days) |
! 20 | ! 20 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Area_Under_the_Curve_.28AUC.29|AUC]] (ug/ml/hr) |
! 97488 | ! 97488 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Inhibitory_Concentration_.28IC50.29|IC<sub>50</sub>]] (nM) |
! .9 | ! .9 | ||
|- | |- | ||
- | ! [[ | + | ! [[Pharmacokinetics#Clearance_.28Cl.29|Clearance]] (L/h) |
! .0096 | ! .0096 | ||
|- | |- | ||
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! 10 | ! 10 | ||
|} | |} | ||
- | + | </StructureSection> | |
- | + | ||
===References=== | ===References=== | ||
<references/> | <references/> | ||
__NOEDITSECTION__ | __NOEDITSECTION__ | ||
__NOTOC__ | __NOTOC__ |
Current revision
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References
- ↑ Ferrara N, Gerber HP. The role of vascular endothelial growth factor in angiogenesis. Acta Haematol. 2001;106(4):148-56. PMID:11815711
- ↑ Garnier-Viougeat N, Rixe O, Paintaud G, Ternant D, Degenne D, Mouawad R, Deray G, Izzedine H. Pharmacokinetics of bevacizumab in haemodialysis. Nephrol Dial Transplant. 2007 Mar;22(3):975. Epub 2006 Nov 8. PMID:17093010 doi:10.1093/ndt/gfl664
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David Canner, Michal Harel, Joel L. Sussman, Alexander Berchansky