Bevacizumab 100mg/4ml solution for infusion vials
Requires a prescription from a doctor or prescriber
Cytotoxic drugs
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Bevacizumab
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Bevacizumab
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9 branded products available
MHRA licensed products
View all licensed products for Bevacizumab on the MHRA register
Abevmy 100mg/4ml concentrate for solution for infusion vials
Alymsys 100mg/4ml concentrate for solution for infusion vials
Avastin 100mg/4ml solution for infusion vials
Aybintio 100mg/4ml solution for infusion vials
Bevqolva 100mg/4ml concentrate for solution for infusion vials
Oyavas 100mg/4ml concentrate for solution for infusion vials
Vegzelma 100mg/4ml concentrate for solution for infusion vials
Versavo 100mg/4ml concentrate for solution for infusion vials
Zirabev 100mg/4ml solution for infusion vials
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Bevacizumab
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(15)
Bevacizumab gamma for treating wet age-related macular degeneration (TA1022)
Atezolizumab with bevacizumab for treating advanced or unresectable hepatocellular carcinoma (TA666)
Bevacizumab (originator and biosimilars) with fluoropyrimidine-based chemotherapy for metastatic colorectal cancer (TA1136)
Bevacizumab in combination with capecitabine for the first-line treatment of metastatic breast cancer (TA263)
Bevacizumab in combination with a taxane for the first-line treatment of metastatic breast cancer (TA214)
Bevacizumab in combination with paclitaxel and carboplatin for first-line treatment of advanced ovarian cancer (TA284)
Trifluridine–tipiracil with bevacizumab for treating metastatic colorectal cancer after 2 systemic treatments (TA1008)
Bevacizumab in combination with gemcitabine and carboplatin for treating the first recurrence of platinum-sensitive advanced ovarian cancer (TA285)
Olaparib with bevacizumab for maintenance treatment of advanced high-grade epithelial ovarian, fallopian tube or primary peritoneal cancer (TA946)
Pembrolizumab plus chemotherapy with or without bevacizumab for persistent, recurrent or metastatic cervical cancer (TA939)
Cetuximab, bevacizumab and panitumumab for the treatment of metastatic colorectal cancer after first-line chemotherapy (TA242)
Bevacizumab (first-line), sorafenib (first- and second-line), sunitinib (second-line) and temsirolimus (first-line) for the treatment of advanced and/or metastatic renal cell carcinoma (TA178)
Ovarian cancer: recognition and initial management (CG122)
Bevacizumab for the treatment of non-small-cell lung cancer (terminated appraisal) (TA148)
Bevacizumab for treating EGFR mutation-positive non-small-cell lung cancer (terminated appraisal) (TA436)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & product information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
20 days
Mechanism
Transcription of the VEGF protein is induced by 'hypoxia inducible factor' (HIF) in a hypoxic environment.
Food interactions
None known
Human targets
9 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1mg/k
[A40006][A192981][A19126]…
Half-life
20 days
[L12648][A192921]
Protein binding
97%
[A192939]
Volume of distribution
3.29 L
[A192939]
Metabolism
[A192948]…
Elimination
[A40006]…
Clearance
0.207 L
[A192939]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
In 2004, bevacizumab (Avastin) gained FDA approval for specific types of cancer, and became the first antiangiogenic agent introduced to the market.[A193272][A193275] It is a humanized monoclonal IgG antibody, and inhibits angiogenesis by binding and neutralizing VEGF-A.[A192888][A192939] Bevacizumab is generally indicated for use in combination with different chemotherapy regimens which are specific to the type, severity, and stage of cancer.[L12648] Bevacizumab was approved by Health Canada on March 24, 2010 and by the European Commission on April 21, 2021.[L45793][L43130] There are several biosimilars of bevacizumab, such as bevacizumab-awwb, bevacizumab-maly, bevacizumab-adcd, and bevacizumab-tnjn.
Interestingly, researchers have identified higher VEGF expression in patients with COVID-19, which may contribute to lung pathologies including acute respiratory syndrome (ARDS) and acute lung injury (ALI).[L12699] As such, bevacizumab is being investigated for the treatment of lung complications associated with severe cases of COVID-19.[L12699]
Avzivi® (bevacizumab), a biosimilar of Avastin®, was approved by the EMA in July 2024 to treat several types of cancer, including colorectal, breast, lung, kidney, ovarian, and cervical cancer.[L53088]
[L12648][L39233][L41514][L43130][L43302][L49826]
Interestingly, bevacizumab is currently under investigation for the treatment of COVID-19 complications including acute respiratory distress syndrome (ARDS) and acute lung injury (ALI).
[L12699]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 481 interactions
[A192960][A192963]
Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications.
[A192960]
Cancer cells promote tumor angiogenesis by releasing VEGF, resulting in the creation of an immature and disorganized vascular network.[A192894][A192897] The hypoxic microenvironment promoted by cancer cells favors the survival of more aggressive tumor cells, and gives rise to a challenging environment for immune cells to respond appropriately.[A192897][A192900][A192903] As a result, VEGF has become a well-known target for anti-cancer drugs like bevacizumab.[A192837] Bevacizumab is a mAb that exerts its effects by binding and inactivating serum VEGF.[A192939] When bound to the mAb, VEGF is unable to interact with its cell surface receptors, and proangiogenic signalling is inhibited.[A192939] This prevents formation of new blood vessels, decreases tumor vasculature, and reduces tumor blood supply.[A192939][L12648]
There is also evidence to suggest that VEGF is upregulated in COVID-19 patients, hence, bevacizumab is being investigated for the treatment of associated complications.[L12699] Higher levels of VEGF may contribute to pulmonary edema, leading to acute respiratory distress syndrome (ARDS) and acute lung injury (ALI).[L12699] Researchers are hopeful that by inhibiting VEGF, bevacizumab may effectively treat ARDS and ALI - both common features of severe COVID-19 cases.[L12699]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A40006][A192981][A19126]
Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously.
[A40006][A19126]
In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows[A192975]:
Geometric mean Cmax = 17.38 ug/mL
Geometric mean AUCinf = 5,358 ugxh/mL
Geometric mean Tmax = 2.50 hrs
[L12648][A192921]
[A192939]
[A192939]
[A192948]
Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver.
[A192948][A40006]
Target-mediated clearance is a result of specific interactions between the mAb and its target antigen.
[A192948]
Once bound, the antibody-antigen complex may be cleared via lysosomal degradation.
[A192948][A40006]
Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance.
[A192948]
[A40006]
Catabolism or excretion are the primary processes of elimination.
[A40006]
[A192939]
The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively.
[A192939]
Males tend to clear bevacizumab at a faster rate than females (26% faster on average).
[A192939]
Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate.
[A192939]
Proteins and enzymes this drug interacts with in the body
PMID:35455969
Involved in protecting cells from hypoxia-mediated cell death (By similarity)
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:34155115 PMID:6249812 PMID:6776418
The classical complement pathway is initiated by the C1Q subcomplex of the C1 complex, which specifically binds IgG or IgM immunoglobulins complexed with antigens, forming antigen-antibody complexes on the surface of pathogens: C1QA, together with C1QB and C1QC, specifically recognizes and binds the Fc regions of IgG or IgM via its C1q domain .
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:6776418
Immunoglobulin-binding activates the proenzyme C1R, which cleaves C1S, initiating the proteolytic cascade of the complement system .
PMID:29449492
The C1Q subcomplex is activated by a hexamer of IgG complexed with antigens, while it is activated by a pentameric IgM .
PMID:19706439 PMID:24626930 PMID:29449492
The C1Q subcomplex also recognizes and binds phosphatidylserine exposed on the surface of cells undergoing programmed cell death, possibly promoting activation of the complement system PMID:18250442
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:34155115 PMID:6249812 PMID:6776418
The classical complement pathway is initiated by the C1Q subcomplex of the C1 complex, which specifically binds IgG or IgM immunoglobulins complexed with antigens, forming antigen-antibody complexes on the surface of pathogens: C1QA, together with C1QB and C1QC, specifically recognizes and binds the Fc regions of IgG or IgM via its C1q domain .
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:6776418
Immunoglobulin-binding activates the proenzyme C1R, which cleaves C1S, initiating the proteolytic cascade of the complement system .
PMID:29449492
The C1Q subcomplex is activated by a hexamer of IgG complexed with antigens, while it is activated by a pentameric IgM .
PMID:19706439 PMID:24626930 PMID:29449492
The C1Q subcomplex also recognizes and binds phosphatidylserine exposed on the surface of cells undergoing programmed cell death, possibly promoting activation of the complement system PMID:18250442
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:34155115 PMID:6249812 PMID:6776418
The classical complement pathway is initiated by the C1Q subcomplex of the C1 complex, which specifically binds IgG or IgM immunoglobulins complexed with antigens, forming antigen-antibody complexes on the surface of pathogens: C1QA, together with C1QB and C1QC, specifically recognizes and binds the Fc regions of IgG or IgM via its C1q domain .
PMID:12847249 PMID:19006321 PMID:24626930 PMID:29449492 PMID:3258649 PMID:6776418
Immunoglobulin-binding activates the proenzyme C1R, which cleaves C1S, initiating the proteolytic cascade of the complement system .
PMID:29449492
The C1Q subcomplex is activated by a hexamer of IgG complexed with antigens, while it is activated by a pentameric IgM .
PMID:19706439 PMID:24626930 PMID:29449492
The C1Q subcomplex also recognizes and binds phosphatidylserine exposed on the surface of cells undergoing programmed cell death, possibly promoting activation of the complement system PMID:18250442
PMID:11711607 PMID:21768335 PMID:22023369 PMID:24412922 PMID:25786175 PMID:25816339 PMID:28652325 PMID:8609432 PMID:9242542
Mediates IgG effector functions on natural killer (NK) cells.
Binds antigen-IgG complexes generated upon infection and triggers NK cell-dependent cytokine production and degranulation to limit viral load and propagation. Involved in the generation of memory-like adaptive NK cells capable to produce high amounts of IFNG and to efficiently eliminate virus-infected cells via ADCC .
PMID:24412922 PMID:25786175
Regulates NK cell survival and proliferation, in particular by preventing NK cell progenitor apoptosis .
PMID:29967280 PMID:9916693
Fc-binding subunit that associates with CD247 and/or FCER1G adapters to form functional signaling complexes. Following the engagement of antigen-IgG complexes, triggers phosphorylation of immunoreceptor tyrosine-based activation motif (ITAM)-containing adapters with subsequent activation of phosphatidylinositol 3-kinase signaling and sustained elevation of intracellular calcium that ultimately drive NK cell activation.
The ITAM-dependent signaling coupled to receptor phosphorylation by PKC mediates robust intracellular calcium flux that leads to production of pro-inflammatory cytokines, whereas in the absence of receptor phosphorylation it mainly activates phosphatidylinositol 3-kinase signaling leading to cell degranulation .
PMID:1825220 PMID:23024279 PMID:2532305
Costimulates NK cells and trigger lysis of target cells independently of IgG binding .
PMID:10318937 PMID:23006327
Mediates the antitumor activities of therapeutic antibodies. Upon ligation on monocytes triggers TNFA-dependent ADCC of IgG-coated tumor cells .
PMID:27670158
Mediates enhanced ADCC in response to afucosylated IgGs PMID:34485821
ATC L01FG01
ATC S01LA08
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Bevacizumab
Additional database identifiers
Drugs Product Database (DPD)
16200
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12680
GenAtlas
VEGF
GeneCards
VEGFA
GenBank Gene Database
M32977
GenBank Protein Database
181971
UniProt Accession
VEGFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1241
GenAtlas
C1QA
GeneCards
C1QA
GenBank Gene Database
AF135157
GenBank Protein Database
4894854
UniProt Accession
C1QA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1242
GenAtlas
C1QB
GeneCards
C1QB
GenBank Gene Database
X03084
GenBank Protein Database
573114
UniProt Accession
C1QB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1245
GenAtlas
C1QC
GeneCards
C1QC
GenBank Gene Database
AF087892
GenBank Protein Database
33150626
UniProt Accession
C1QC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3619
GenAtlas
FCGR3A
GeneCards
FCGR3A
GenBank Gene Database
X52645
GenBank Protein Database
31324
Guide to Pharmacology
3017
UniProt Accession
FCG3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3613
GenAtlas
FCGR1A
GeneCards
FCGR1A
GenBank Gene Database
X14356
GenBank Protein Database
31332
UniProt Accession
FCGR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3616
GenAtlas
FCGR2A
GeneCards
FCGR2A
GenBank Gene Database
M31932
GenBank Protein Database
182474
UniProt Accession
FCG2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3618
GenAtlas
FCGR2B
GeneCards
FCGR2B
GenBank Gene Database
U87560
GenBank Protein Database
4099445
UniProt Accession
FCG2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15626
GenAtlas
FCGR2C
GeneCards
FCGR2C
GenBank Gene Database
X17652
GenBank Protein Database
32074
UniProt Accession
FCG2C_HUMAN
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
All patents expired, 2 expired
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: