B20 4

Manufactured by Genentech

Sourced in United States

The B20-4.1.1 is a laboratory equipment designed for scientific research and analysis. It is a compact and versatile instrument that serves as a core function for various applications. The specific details and intended use of this product are not available at this time.

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Lab products found in correlation

Bevacizumab, by Genentech (1 mentions) Cediranib, by AstraZeneca (1 mentions) Decalcifying solution lite, by Merck Group (1 mentions) Ab46154, by Abcam (1 mentions) Rabbit anti mouse polyclonal antibodies, by Abcam (1 mentions) Cd31 ab28364, by Abcam (1 mentions) Complete freund s adjuvant cfa, by Merck Group (1 mentions) Rs102895, by Merck Group (1 mentions)

Spelling variants of this product

Anti-VEGF antibody (B20-4.1.1) (3 citations)

13 protocols using b20 4

Modeling Liver Metastasis in Mice

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To model liver metastasis in the host with intact systemic immunity, the spleen of a C57BL/6 or Ccr2^−/− mouse was split in two sections and 1 × 10⁵ SL4 cells were injected into the distal caudal sector, which was then resected³⁰. The other hemi-spleen remained in place. Tumor burden was assessed by measuring Gaussia luciferase (Gluc) activity in the blood from GUc-transduced SL4 tumorbearing mice³⁰. After the development of macroscopic liver metastases (~7 d post-injection), mice were randomly assigned to treatment groups of various combinations of the following treatments as indicated and treatment was initiated: anti-VEGF therapy (B20–4.1.1, 5 mg kg⁻¹, 2 × weekly, generous gift from Genentech); ICB (anti-PD-1 100 μg + CTLA-4 200 μg, 2 × weekly); and anti-murine EGFR D1D4J -MMP14-SIINFEKL-APEC (1.67 mg kg⁻¹, 2 × weekly for 2 weeks), with adoptive transfer of 10⁶ ex vivo expanded OT-I CD8+ T cells at one time. Mice were euthanized at the designated time points for sample collection or when they become moribund. Survival was estimated by Kaplan-Meier curves and compared using the log-rank test.

Millar D.G., Ramjiawan R.R., Kawaguchi K., Gupta N., Chen J., Zhang S., Nojiri T., Ho W.W., Aoki S., Jung K., Chen I., Shi F., Heather J.M., Shigeta K., Morton L.T., Sepulveda S., Wan L., Joseph R., Minogue E., Khatri A., Bardia A., Ellisen L.W., Corcoran R.B., Hata A.N., Pai S.I., Jain R.K., Fukumura D., Duda D.G, & Cobbold M. (2020). Antibody-mediated delivery of viral epitopes to tumors harnesses CMV-specific T cells for cancer therapy. Nature biotechnology, 38(4), 420-425.

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Anti-VEGF, Neutrophil Depletion, and Chemotherapy Protocol

Cited 1 time

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The anti-VEGF monoclonal antibody B20.4-1.1 (Genentech) was administered by intraperitoneal injection twice a week at 5 or 1 mg/kg. For neutrophil depletion, an anti-Ly6G antibody (clone RB6-8C5) was administered intraperitoneally every 2 days at a dose of 5 mg/kg. PEG-HAse (see the Supplementary Materials and Methods) was administered intravenously twice a week or 24 hours before administration of chemotherapy at a dose of 4.5 mg/kg (43 (link)). 5-FU chemotherapy was administered intravenously twice a week at a dose of 50 mg/kg.

Rahbari N.N., Kedrin D., Incio J., Liu H., Ho W.W., Nia H.T., Edrich C.M., Jung K., Daubriac J., Chen I., Heishi T., Martin J.D., Huang Y., Maimon N., Reissfelder C., Weitz J., Boucher Y., Clark J.W., Grodzinsky A.J., Duda D.G., Jain R.K, & Fukumura D. (2016). Anti-VEGF therapy induces ECM remodeling and mechanical barriers to therapy in colorectal cancer liver metastases. Science translational medicine, 8(360), 360ra135.

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Targeting VEGF-A with Anti-VEGF mAb

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Bevacizumab (Genentech/Roche) is a humanized mAb (monoclonal antibody) that inhibits VEGF-A. Anti-VEGF antibody B20-4.1.1 (Genentech), heretofore referred to as B20-4.1.1, is a cross-species reactive, function-blocking mAb targeting both human and murine VEGF-A.

Jiang X., Engelbach J.A., Yuan L., Cates J., Gao F., Drzymala R.E., Hallahan D.E., Rich K.M., Schmidt R.E., Ackerman J.J, & Garbow J.R. (2014). Anti-VEGF antibodies mitigate the development of radiation necrosis in mouse brain. Clinical cancer research : an official journal of the American Association for Cancer Research, 20(10), 2695-2702.

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Combination Therapies for Treating NCI-N87-TR Tumors

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To evaluate the efficacy of different combination therapies, 1 × 10⁶ NCI‐N87‐TR cells were injected into the right flank of nude mice. Tumor measurement and grouping method were performed as previously described at 2.11. The mice were randomly divided into seven experimental groups (6‐8 mice for each group): PBS; trastuzumab; trastuzumab + BPTES; trastuzumab + BPTES + celecoxib; trastuzumab + BPTES + B20‐4.1.1; trastuzumab + B20‐4.1.1 + celecoxib; trastuzumab + BPTES + celecoxib + B20‐4.1.1. The following 3‐week treatments were given as one or as a combination of the following: PBS, trastuzumab and BPTES are the same with 2.11; celecoxib (HY‐14398, MedChemExpress, Princeton, NJ, USA), 80 mg/kg, intragastrical administration, every other day; B20‐4.1.1 (Genentech, South San Francisco, CA, USA), 5 mg/kg, intraperitoneal injection, twice a week. Tumor volumes and weights were measured and recorded, and the mice were euthanized by cervical dislocation at the end of treatment.

Hu X., Ma Z., Xu B., Li S., Yao Z., Liang B., Wang J., Liao W., Lin L., Wang C., Zheng S., Wu Q., Huang Q., Yu L., Wang F, & Shi M. (2023). Glutamine metabolic microenvironment drives M2 macrophage polarization to mediate trastuzumab resistance in HER2‐positive gastric cancer. Cancer Communications, 43(8), 909-937.

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Anti-VEGF Impacts Achilles Tendon Vascularity

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This prospective study was performed in accordance with the University of Pennsylvania Institutional Animal Care and Use Committee. 32 male Sprague Dawley rats (450–550g) underwent bilateral Achilles tendon incisional injury, followed by bilateral intratendinous injection with either saline (control), 50 μg (low), 250 μg (mid), or 500 μg (high) murine-compatible anti-VEGF antibody (B20.4–1-1, Genentech, San Francisco, CA, USA) on days 4–6 post-injury. Color Doppler ultrasound and photoacoustic imaging was performed on days 7 and 14 post-injury and compared to the saline control group. Pre-injury ultrasound was not evaluated due to the hypovascularity of healthy tendon tissue preventing any detection of vascular signal. Animals were sacrificed at either day 7 or 14 for histological analysis (n=8 tendons/group).

Riggin C.N., Schultz S.M., Sehgal C.M, & Soslowsky L.J. (2019). Ultrasound Evaluation of Anti-VEGF Induced Changes in Vascular Response Following Tendon Injury. Ultrasound in medicine & biology, 45(7), 1841-1849.

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Evaluating Cediranib and B20-4.1.1 in Tumor-Bearing Mice

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Tumor-bearing mice were randomized prior to MRI into control and treatment cohorts as follows:

SF188^luci.

MRI prior to and after 48 h treatment with 6 mg/kg cediranib (AZD2171, AstraZeneca) (n = 6) or vehicle (1% polysorbate-80 in water) (n = 5) daily. 3 oral doses were given over 48 h: i) following recovery from anesthesia for pre-treatment imaging, ii) 24 h later, iii) a further 24 h later immediately prior to post-treatment imaging.

MDA-MB-231 LM2–4i.

MRI prior to and after 48 h treatment with either 6 mg/kg cediranib (n = 6) or vehicle (n = 5), as described above.

ii.

MRI prior to and 48 h after a single intraperitoneal 10 mg/kg dose of B20-4.1.1 (Genentech) (n = 7) or an isotype-matched control antibody (anti-Ragweed:1428) (n = 6).

Treatment and imaging regimens are depicted in Supplementary Figure S1 with cohort sizes, time from tumor implantation to study start, and mean pre-treatment tumor volume.

Boult J.K., Box G., Vinci M., Perryman L., Eccles S.A., Jones C, & Robinson S.P. (2017). Evaluation of the Response of Intracranial Xenografts to VEGF Signaling Inhibition Using Multiparametric MRI. Neoplasia (New York, N.Y.), 19(9), 684-694.

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Evaluating Angiogenesis Inhibition in Mice

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All experiments were conducted in compliance with the guidelines of Tohoku University. The Institutional Animal Care and Use Committee at Tohoku University approved the experimental protocol. Ten to fourteen-week-old female eNOS^+/+; PAR2^+/+, eNOS^+/+; PAR2^−/−, eNOS^−/−; PAR2^+/+, or eNOS^−/−; PAR2^−/− mice with C57BL/6J genetic background^{7 (link)} were used. eNOS^−/− or eNOS^−/−; PAR2^−/− mice were obtained by mating male and female eNOS^+/−; PAR2^+/− mice. Thereafter, eNOS^−/− or eNOS^−/−; PAR2^−/− littermate colony was individually maintained. These mice were injected with B20–4.1.1 (5 mg/kg), a mouse anti-VEGF Ab, on day 0 and 4^{54 (link)}. The samples were collected on day 7. B20-4.1.1 was kindly provided by Genentech Inc. for research use (South San Francisco, CA, USA). Control groups received a vehicle. Our preliminary observations demonstrated that IgG isotype does not show apparent kidney injury in our experimental condition (data not shown).

Oe Y., Fushima T., Sato E., Sekimoto A., Kisu K., Sato H., Sugawara J., Ito S, & Takahashi N. (2019). Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury. Scientific Reports, 9, 2986.

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Gamma Knife Radiation Necrosis Therapy

Cited 2 times

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All experiments were approved by the Washington University Animal Studies Committee and were performed on six-to-eight week old female BALB/c mice (Harlan/Envigo, Indianapolis, IN, USA). A single-fraction, 50-Gy dose of radiation (50% isodose) from the Leksell Gamma Knife^TM Perfexion^TM (Elekta, Stockholm, Sweden) was focused on the cortex of the left hemisphere (n = 24). As has been shown previously [18 (link)–20 (link)], this large, single-fraction dose of radiation reproducibly and robustly generates, in all irradiated mice, radiation necrosis whose histology recapitulates all of the features of clinical RN. At this dose, moderate focal RN can be observed at approximately 8 weeks post irradiation (PIR) on both anatomic MRI and histology [20 (link)]. B20-4.1.1, a murine antibody that recognizes VEGF, and GP120:9239, a murine antibody of the same isotype that targets the HIV capsid protein, were obtained from Genentech (South San Francisco, CA, USA). At week 8 PIR, mice were randomly divided into two groups: (i) an anti-VEGF group, treated with B20-4.1.1 and (ii) an isotype-control group, treated with GP120:9239. Each antibody was administrated intraperitoneally at 10 mg/kg twice weekly until week 12 PIR. To minimize the acute effect of blocking VEGF activity on permeability and therefore contrast-agent extravasation, all MRI scans were performed two days following a treatment.

Duan C., Perez-Torres C.J., Yuan L., Engelbach J.A., Beeman S.C., Tsien C.I., Rich K.M., Schmidt R.E., Ackerman J.J, & Garbow J.R. (2017). Can anti-Vascular Endothelial Growth Factor Antibody Reverse Radiation Necrosis? A Preclinical Investigation. Journal of neuro-oncology, 133(1), 9-16.

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VEGFA Neutralizing Antibody Efficacy

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Animals were administered 5 mg/kg B20-4.1.1 (Genentech) VEGFA neutralizing antibody or antibody isotype control by intravenous injection 6 h before termination of the experiment.

Harney A.S., Arwert E.N., Entenberg D., Wang Y., Guo P., Qian B.Z., Oktay M.H., Pollard J.W., Jones J.G, & Condeelis J.S. (2015). Real-time imaging reveals local, transient vascular permeability and tumor cell intravasation stimulated by Tie2Hi macrophage-derived VEGFA. Cancer discovery, 5(9), 932-943.

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AAV Gene Therapy Delivery Protocols

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Subretinal injections and intravitreous injections (1 μL each) were performed with a 35-gauge Exmire microsyringe (Ito Corporation). The VEGF neutralizing antibody B20-4.1.1 or an equivalent mass of isotype antibody, both provided by Genentech, were delivered by intravitreous injection (0.5 to 1 μg). One microliter of 10¹¹ viral genomes (vg)/mL (or 10⁸ vg/μL) of AAV-OptiDicer, or AAV2-CMV-null were delivered by subretinal injection. Separately, AAV2-hRPE(0.8)-iCre-WPRE was delivered at by intravitreous injection at 10¹⁰ genome copies in 1 μL.

Wright C.B., Uehara H., Kim Y., Yasuma T., Yasuma R., Hirahara S., Makin R.D., Apicella I., Pereira F., Nagasaka Y., Narendran S., Fukuda S., Albuquerque R., Fowler B.J., Bastos-Carvalho A., Georgel P., Hatada I., Chang B., Kerur N., Ambati B.K., Ambati J, & Gelfand B.D. (2020). Chronic Dicer1 deficiency promotes atrophic and neovascular outer retinal pathologies in mice. Proceedings of the National Academy of Sciences of the United States of America, 117(5), 2579-2587.

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