- Bevacizumab
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- $0.00 / 1G
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2023-02-07
- CAS:216974-75-3
- Min. Order: 1G
- Purity: 98%min
- Supply Ability: 30kg/month
- Bevacizumab
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- $0.00 / 10mg
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2021-09-16
- CAS:216974-75-3
- Min. Order: 1mg
- Purity: 99%
- Supply Ability: 100KG
- Bevacizumab USP/EP/BP
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- $1.10 / 1g
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2021-06-05
- CAS:216974-75-3
- Min. Order: 1g
- Purity: 99.9%
- Supply Ability: 100 Tons Min
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| | Bevacizumab Basic information |
| Product Name: | Bevacizumab | | Synonyms: | BevacizuMab [USAN:INN];Anti-vegf monoclonal antibody;Bevacizumab;Immunoglobulin G1, anti-(human vascular endothelial growth factor) (human-mouse monoclonal rhumab-vegf gamma1-chain), disulfide with human-mouse monoclonal rhumab-vegf light chain, dimer;Rhumab-vegf;Unii-2S9zzm9Q9v;Avastatin;Bevacituzumab | | CAS: | 216974-75-3 | | MF: | C6638H10160N1720O2108S44 | | MW: | 0 | | EINECS: | 200-160-3 | | Product Categories: | | | Mol File: | Mol File | ![Bevacizumab Structure]() |
| | Bevacizumab Chemical Properties |
| storage temp. | Store at -80°C | | solubility | Soluble in DMSO |
| | Bevacizumab Usage And Synthesis |
| Description | Bevacizumab, a humanized IgG1 monoclonal antibody against vascular endothelial
growth factor (VEGF), inhibits tumor angiogenesis and delays disease progression.
It was launched in the US as an intravenous infusion for the treatment of
metastatic colorectal cancer in combination with fluorouracil-based chemotherapy.
Bevacizumab was developed by engineering the VEGF binding residues of the
murine neutralizing antibody A.4.6.1 into the framework of the consensus human
IgG1. Its amino acid sequence is approximately 93% human IgG and 7% murine
antibody and is produced in a CHO cell expression system. Bevacizumab binds
VEGF with high affinity (Kd=0.5 nM) and prevents its interaction with tyrosine
kinase receptors VEGFR1 and VEGFR2 on the surface of endothelial cells, thereby
inhibiting cell proliferation and microvascular growth. In mouse models, administration
of bevacizumab blocked the growth of human tumor xenografts and
reduced the size and number of metastases. The recommended dosage of bevacizumab
is 5 mg/kg administered once every 2 weeks as an intravenous infusion
until disease progression is detected. Based on a population pharmacokinetic analysis
of patients who received 1–20 mg/kg of bevacizumab once every 1–3 weeks, the
estimated half-life was approximately 20 days, and the predicted time to reach
steady state was 100 days. The maximum and minimum steady-state serum concentrations
at 2.5 mg/kg/week dose were 226 and 88 μg/mL, respectively. Clearance
of bevacizumab is low, and varies with body weight, gender and tumor burden. In
patients with colorectal cancer receiving bevacizumab 5–10 mg/kg in combination
with fluorouracil and leucovorin, mean total clearance was 2.79 ml/kg/day. In clinical
studies involving the administration of bevacizumab (5 mg/kg every 2 weeks) or
placebo in addition to bolus-IFL (irinotecan 125 mg/m2 i.v., 5-fluorouracil 500 mg/
m2 i.v., and leucovorin 20 mg/m2 i.v. administered once weekly for four weeks every six weeks), the median overall survival was significantly increased from 15.6 months
in the bolus IFL + placebo arm to 20.3 months in the bolus IFL + bevacizumab
arm. Similar increases were also seen in progression-free survival (6.4 versus 10.6
months), overall response rate (35% versus 45%), and duration of response (7.1
months versus 10.4 months). The most common adverse events in these trials were
hypertension, diarrhea and leucopenia. Other clinically significant adverse events
reported occasionally were gastrointestinal perforations, thromboembolic events,
bleeding and proteinuria. Because wound healing may be impaired by inhibition of
VEGF, bevacizumab therapy is not recommended until 28 days after primary
surgery. | | Originator | Genentech (US) | | Brand name | Avastin | | Clinical Use | Monoclonal antibody:
Treatment of colorectal cancer
Treatment of breast cancer
Treatment of renal cell carcinoma
Treatment of lung cancer
Treatment of ovarian, fallopian tube or peritoneal
cancer | | Enzyme inhibitor | This humanized monoclonal antibody (MW = 149.2 kDa; CAS 216974-75- 3), known by the tradename Avastinò, is an angiogenesis inhibitor that targets vascular endothelial growth factor A (VEGF-A). Because VEGF is the key angiogenic factor in tumors, blocking VEGF signal transduction can lead to tumor growth arrest and inhibition of metastasis. The rationale for Avastin therapy is premised on findings that high VEGF expression correlates with (a) reduced overall survival, (b) disease progression, (c) greater risk of relapse, (d) lymph node involvement, and (e) malignant pleural effusion. By binding directly bind to VEGF-A, Avastin blocks its interaction with endothelial cell VEGF receptors, thereby inhibiting neovascularization and depriving cancer cells of vital nutrients and oxygen. Avastin is approved for: metastatic colorectal cancer (mCRC), when started with the first or second intravenous 5-FU–based chemotherapy for metastatic cancer; advanced-stage nonsquamous, non–small cell lung cancer (NSCLC), when administered in combination with carboplatin and paclitaxel in patients who have not received chemotherapy for their advanced disease; metastatic renal cell cancer (mRCC) when used with interferon-a; and glioblastoma multiforme (GBM) in adult patients whose cancer has progressed after prior treatment. | | target | Angiogenesis is important for tumour growth and metastasis, and is an important target for new biological agents. Bevacizumab is a humanised recombinant antibody that prevents vascular endothelial growth factor (VEGF) receptor binding, and inhibits angiogenesis and tumour growth. | | Drug interactions | Potentially hazardous interactions with other drugs
Bisphosphonates: increased risk of osteonecrosis of
the jaw.
Cytotoxics: avoid with panitumumab.
Vaccines: risk of generalised infections with live
vaccines - avoid. | | Metabolism | Assessment of bevacizumab metabolism in rabbits
following a single IV dose of 125I-bevacizumab indicated
that its metabolic profile was similar to that expected for
a native IgG molecule which does not bind VEGF. The
metabolism and elimination of bevacizumab is similar to
endogenous IgG i.e. primarily via proteolytic catabolism
throughout the body, including endothelial cells, and does
not rely primarily on elimination through the kidneys and
liver. Binding of the IgG to the FcRn receptor results in
protection from cellular metabolism and the long terminal
half-life. |
| | Bevacizumab Preparation Products And Raw materials |
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