Bevacizumab (Anti-Human VEGF, Humanized Antibody)
(Synonyms: 贝伐珠单抗 (PBS); Anti-Human VEGF, Humanized Antibody (PBS)) 目录号 : GC34216
贝伐单抗Bevacizumab是一种抗VEGF的人源化单克隆抗体。.
Cas No.:216974-75-3
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
-
Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
|
Cell lines |
HHT cell cultures 、HUVEC cell |
|
Preparation Method |
After 24, 48 or 72 h of incubation with 0, 2, 4, 6, 8 or 10 mg/ml Bevacizumab, the expression of VEGF was analyzed in the supernatants of the HHT cell cultures and the HUVECs. |
|
Reaction Conditions |
0, 2, 4, 6, 8 or 10 mg/ml; 24, 48 or 72 h |
|
Applications |
VEGF expression decreased after 24h in cell cultures incubated with bevacizumab concentration levels of 2 and 4 mg/ml but increased again after 48h. |
| Animal experiment [2]: | |
|
Animal models |
NMRI nu/nu nude mice |
|
Preparation Method |
Bevacizumab was used to inhibit tumor cell-derived human VEGF-A and was administered i.p. at doses of 25, 5, and 0.5mg/kg bodyweight every second day for 12 days. A control group with size-matched tumors received human polyclonal immunoglobulin G at a dose of 25 mg/kg. |
|
Dosage form |
25, 5, and 0.5mg/kg; every second day for 12 days; i.p. |
|
Applications |
Bevacizumab significantly inhibited tumor blood vessel growth rate and improved survival rate. |
|
References: [1]Haneen Sadick, Elena SchÄfer, Christel Weiss, et al. An in vitro study on the effect of bevacizumab on endothelial cell proliferation and VEGF concentration level in patients with hereditary hemorrhagic telangiectasia[J].Experimental and Therapeutic Medicine.July 5, 2022.11493. | |
Bevacizumab is a humanized monoclonal antibody against VEGF. It specifically binds to VEGF and blocks its binding to the corresponding receptors on the cell surface, thereby inhibiting angiogenesis[1]. Bevacizumab has high affinity for all VEGF-A isoforms and inhibits its interaction with VEGFR-1 and VEGFR-2[2]. Bevacizumab is a targeted therapy drug called an angiogenesis inhibitor that is used to study and treat many types of cancer [3].
In vitro, In vitro, low-concentration Bevacizumab (2-4 mg/ml) treated intranasal endothelial cells in HHT patients, significantly reducing the expression of VEGF after 24 hours, but it increased again after 48 hours, and exceeding 4 mg/ml would produce cytotoxic effects[4]. Bevacizumab (5-1000 ng/mL) does not cause cell death after treating U87-RFP cells for 48 hours [5].
In vivo, Bevacizumab (5 and 25 mg/kg) treated by intraperitoneal injection in mice with orthotopic glioma significantly inhibited the growth rate of tumor blood vessels and improved the survival rate[5]. Intraperitoneal administration of Bevacizumab (5 mg/kg) can prolong the survival of ovarian cancer model mice[6]. Bevacizumab (5mg/kg) showed strong anti-angiogenic activity in the treatment of osteosarcoma model mice[7].
References:
[1] Minckwitz G V , Eidtmann H , Rezai M ,et al.Neoadjuvant Chemotherapy and Bevacizumab for HER2-Negative Breast Cancer[J].New England Journal of Medicine, 2012.
[2] Tan H, et al. 99mTc-labeled bevacizumab for detecting atherosclerotic plaque linked to plaque neovascularization and monitoring antiangiogenic effects of treatment in ApoE-/-mice. [J]Sci Rep. 2017 Jun 14;7(1):3504.
[3]Pujade-Lauraine.Bevacizumab Combined With Chemotherapy for PlatinumResistant Recurrent Ovarian Cancer: The AURELIA Open-Label Randomized Phase III Trial [J].Journal of Clinical Oncology, 2014.
[4]Haneen Sadick, Elena SchÄfer, Christel Weiss, et al. An in vitro study on the effect of bevacizumab on endothelial cell proliferation and VEGF concentration level in patients with hereditary hemorrhagic telangiectasia[J].Experimental and Therapeutic Medicine.July 5, 2022.11493.
[5]Von Baumgarten L , Brucker D , Tirniceru A ,et al. Bevacizumab Has Differential and Dose-Dependent Effects on Glioma Blood Vessels and Tumor Cells[J].Clinical Cancer Research, 2011, 17(19):6192-205.
[6]Mabuchi S , Terai Y , Morishige K ,et al.Maintenance treatment with bevacizumab prolongs survival in an in vivo ovarian cancer model.[J]Clinical Cancer Research , 2008, 14(23):7781-9.
[7]Zhao Z X , Li X , Liu W D , et al. Inhibition of Growth and Metastasis of Tumor in Nude Mice after Intraperitoneal Injection of Bevacizumab[J]. Orthopaedic Sugery. 2016.234-240.
贝伐单抗Bevacizumab是一种抗VEGF的人源化单克隆抗体,通过与VEGF特异性结合,阻断其与细胞表面相应的受体结合,进而抑制血管生成[1]。贝伐单抗对所有VEGF-A异构体具有高亲和力,并抑制其与VEGFR-1和VEGFR-2的相互作用[2]。贝伐单抗是一种靶向治疗药物,称为血管生成抑制剂,可用于研究和治疗多种类型的癌症[3]。
在体外,贝伐单抗(2-4 mg/ml)低浓度水平处理HHT患者鼻内内皮细胞,24h后显著降低了VEGF的表达,但在48h后再次升高,且超过4 mg/ml会产生细胞毒性作用[4]。贝伐单抗(5- 1000 ng/mL)处理U87-RFP细胞48h后,不会引起细胞死亡[5]。
在体内,贝伐单抗(5和25 mg/kg)通过腹腔注射治疗原位胶质瘤小鼠,显著抑制了肿瘤血管生长速率,提高了存活率[5]。贝伐单抗(5mg/kg)腹膜给药可以延长卵巢癌模型小鼠的生存期[6]。贝伐单抗(5mg/kg)治疗骨肉瘤模型小鼠,表现出较强的抗血管生成活性[7]。
| Cas No. | 216974-75-3 | SDF | |
| 别名 | 贝伐珠单抗 (PBS); Anti-Human VEGF, Humanized Antibody (PBS) | ||
| Canonical SMILES | [Bevacizumab] | ||
| 分子式 | 分子量 | 146542.45 | |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -80°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 0.0068 mL | 0.0341 mL | 0.0682 mL |
| 5 mM | 0.0014 mL | 0.0068 mL | 0.0136 mL |
| 10 mM | 0.0007 mL | 0.0034 mL | 0.0068 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Comparing The Efficacy Of An Anti-Human VEGF-A Neutralizing Antibody Versus Bevacizumab On A Laser-Induced Choroidal Neovascularization (CNV) Rhesus Monkey Model
Drug Des Devel Ther 2019 Nov 4;13:3813-3821.PMID:31806932DOI:10.2147/DDDT.S219350.
Purpose: To evaluate the efficacy of a therapy on improving characteristics of laser-induced choroidal neovascularization (CNV) via single intravitreal injection of a humanized anti-human VEGF monoclonal antibody (PRO-169) versus Bevacizumab in a rhesus monkey model. Methods: To induce experimental CNV, small high-energy laser spots were used to treat several areas, around the macula in the retinas of monkeys at Day -21. Eighteen rhesus monkeys were used for CNV induction. The efficacy endpoints were fluorescein leakage by FFA and retinal thickness by OCT. FFA examinations were performed 19 days after induction. Appropriate animals were enrolled for treatment and randomly divided into 3 groups: Bevacizumab (n=5, 7 eyes), PRO-169 (n=5, 7 eyes), and vehicle controls (n=4, 7 eyes). Results: In 25 of 36 (69.4%) eyes, CNV lesions were identified. The average percent change of retinal thickness in the eyes of Bevacizumab group was -159.3±62.2% and -154.0±45.1% (p<0.01 vs Vehicle) at Day 14 and Day 28, respectively; in the eyes of PRO-169 group it was -131.6±68.7% and -131.5±63.8% (p<0.01 vs Vehicle), respectively. The average percent change of leakage area in the eyes of Bevacizumab group was -75.3±49.4% and -78.0±42.6% (p<0.01 vs Vehicle) at Day 14 and Day 28, respectively; in the eyes of PRO-169 group it was -82.0±19.3% and -81.4±21.0% (p<0.01 vs Vehicle), respectively. There were no abnormalities found in behavior, skin and hair, excretion and overall eye appearance before and after treatment in all groups. Conclusion: After photocoagulation, the eyes enrolled in this studio showed CNV related characteristics including increased retinal thickness, and fluorescein leakage at laser spots. PRO-169 (1.25 mg per eye) can reduce the retinal thickness and fluorescein leakage area after treatment for 14 and 28 days in this rhesus monkeys model, without toxic effect or adverse events. These findings suggested that PRO-169 can inhibit CNV.
Genetic delivery of the murine equivalent of Bevacizumab (avastin), an anti-vascular endothelial growth factor monoclonal antibody, to suppress growth of human tumors in immunodeficient mice
Hum Gene Ther 2008 Mar;19(3):300-10.PMID:18324912DOI:10.1089/hum.2007.109.
Vascular endothelial growth factor (VEGF) produced by tumor cells plays a central role in stimulating angiogenesis required for solid tumor growth. VEGF-specific antibodies inhibit tumor cell line growth in animal models and a humanized monoclonal anti-VEGF antibody (Bevacizumab [Avastin]) is approved as a treatment for metastatic cancer. We hypothesized that administration of an adenoviral (Ad) vector expressing the murine monoclonal antibody equivalent of Bevacizumab would suppress human tumor growth in vivo. The Ad vector (AdalphaVEGF) encodes the light chain and heavy chain cDNAs of monoclonal antibody A.4.6.1, a murine antibody that specifically recognizes human VEGF with the same antigen-binding site as Bevacizumab. AdalphaVEGF efficacy in vivo was evaluated with A-673 rhabdomyosarcoma and DU 145 prostate carcinoma cells in human tumor cell xenografts in SCID mice. For both tumor models, AdalphaVEGF directed the expression of high anti-human VEGF IgG antibody titers in vivo, the numbers of mitotic nuclei and blood vessels in the tumor were significantly decreased (p < 0.05), tumor growth was suppressed (p < 0.05), and there was increased survival (p < 0.005). Thus, AdalphaVEGF, encoding a murine monoclonal antibody that is the equivalent of Bevacizumab, effectively suppresses the growth of human tumors, suggesting gene therapy as an alternative to Bevacizumab monoclonal antibody therapy.
AAVrh.10-mediated genetic delivery of Bevacizumab to the pleura to provide local anti-VEGF to suppress growth of metastatic lung tumors
Gene Ther 2010 Aug;17(8):1042-51.PMID:20596059DOI:10.1038/gt.2010.87.
Vascular endothelial growth factor (VEGF) produced by tumor cells has a central role in stimulating angiogenesis required for tumor growth. Humanized monoclonal anti-VEGF antibody (Bevacizumab, Avastin), approved as a treatment for non-squamous, non-small cell lung cancer, requires administration every 3 weeks. We hypothesized that an intrapleural administration of an adeno-associated virus (AAV) vector expressing an anti-VEGF-A antibody equivalent of Bevacizumab would result in sustained anti-VEGF-A localized expression within the lung and suppress metastatic tumor growth. The AAV vector AAVrh.10alphaVEGF encodes the light chain and heavy chain complementary DNAs of monoclonal antibody A.4.6.1, a murine antibody that specifically recognizes human VEGF-A with the same antigen-binding site as Bevacizumab. A metastatic lung tumor model was established in severe combined immunodeficient mice by intravenous administration of human DU145 prostate carcinoma cells. Intrapleural administration of AAVrh.10alphaVEGF directed long-term expression of the anti-human VEGF-A antibody in lung, as shown by sustained, high-level anti-human VEGF titers in lung epithelial lining fluid for 40 weeks, which was the duration of the study. In the AAVrh.10alphaVEGF-treated animals, tumor growth was significantly suppressed (P<0.05), the numbers of blood vessels and mitotic nuclei in the tumor was decreased (P<0.05) and there was increased survival (P<0.05). Thus, intrapleural administration of an AAVrh.10 vector, encoding the murine monoclonal antibody equivalent of Bevacizumab, effectively suppresses the growth of metastatic lung tumors, suggesting AAV-mediated gene transfer to the pleura to deliver Bevacizumab locally to the lung as a novel alternative platform to conventional monoclonal antibody therapy.
Interaction between Bevacizumab and murine VEGF-A: a reassessment
Invest Ophthalmol Vis Sci 2008 Feb;49(2):522-7.PMID:18234994DOI:10.1167/iovs.07-1175.
Purpose: Bevacizumab is a humanized anti-human VEGF-A monoclonal antibody (mAb) approved by the United States Food and Drug Administration for cancer therapy and used off label to treat neovascular age-related macular degeneration. Earlier studies characterized Bevacizumab as species specific and lacking the ability to neutralize murine (m) VEGF-A. However, a recent study reported that Bevacizumab is a potent inhibitor of hemangiogenesis and lymphangiogenesis in murine models. The authors sought to reassess the interaction between Bevacizumab and mVEGF-A. Methods: The authors performed Western blot analysis, plasmon resonance by BIAcore, and endothelial cell proliferation assays to characterize the interaction between Bevacizumab and mVEGF-A. They also tested whether Bevacizumab had any effects in two in vivo murine models, laser-induced choroidal neovascularization (CNV) and melanoma growth. Results: Western blot detected a very weak interaction, but BIAcore detected no measurable interaction between mVEGF and Bevacizumab. Bevacizumab failed to inhibit mVEGF-stimulated endothelial cell proliferation. In addition, Bevacizumab was indistinguishable from the control antibody in the CNV and tumor models, whereas a cross-reactive anti-VEGF-A mAb had dramatic inhibitory effects. Conclusions: Bevacizumab has an extremely weak interaction with mVEGF-A, which fails to result in immunoneutralization as assessed by several bioassays.
Genetic delivery of Bevacizumab to suppress vascular endothelial growth factor-induced high-permeability pulmonary edema
Hum Gene Ther 2009 Jun;20(6):598-610.PMID:19254174DOI:10.1089/hum.2008.169.
High-permeability pulmonary edema causing acute respiratory distress syndrome is associated with high mortality. Using a model of intratracheal adenovirus (Ad)-mediated overexpression of human vascular endothelial growth factor (VEGF)-A(165) in mouse lung to induce alveolar permeability and consequent pulmonary edema, we hypothesized that systemic administration of a second adenoviral vector expressing an anti-VEGF antibody (AdalphaVEGFAb) would protect the lung from pulmonary edema. Pulmonary edema was induced in mice by intratracheal administration of AdVEGFA165. To evaluate anti-VEGF antibody therapy, the mice were treated intravenously with AdalphaVEGFAb, an adenoviral vector encoding the light and heavy chains of an anti-human VEGF antibody with the Bevacizumab (Avastin) antigen-binding site. Lung VEGF-A(165) and phosphorylated VEGF receptor (VEGFR)-2 levels, histology, lung wet-to-dry weight ratios, and bronchoalveolar lavage fluid (BALF) levels of total protein were assessed. Administration of AdalphaVEGFAb to mice decreased AdVEGFA165-induced levels of human VEGF-A(165) and phosphorylated VEGFR-2 in the lung. Histological analysis of AdalphaVEGFAb-treated mice demonstrated a reduction of edema fluid in the lung tissue that correlated with a reduction of lung wet-to-dry ratios and BALF total protein levels. Importantly, administration of AdalphaVEGFAb 48 hr after induction of pulmonary edema with AdVEGFA165 was effective in suppressing pulmonary edema. Administration of an adenoviral vector encoding an anti-VEGF antibody that is the equivalent of Bevacizumab effectively suppresses VEGF-A(165)-induced high-permeability pulmonary edema, suggesting that anti-VEGF antibody therapy may represent a novel therapy for high-permeability pulmonary edema.