Drug Database
BE

bevacizumab (BP 01 / Bevqolva / BP01)

✓ Approved

Aurobindo Pharma Limited · VEGFA · Monoclonal Antibodies

What is bevacizumab?

bevacizumab is a monoclonal antibodies developed by Aurobindo Pharma Limited. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesBP 01, Bevqolva, BP01
CompanyAurobindo Pharma Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetVEGFA
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

bevacizumab acts on 1 molecular target:

VEGFAvascular endothelial growth factor A (VPF, MVCD1)
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Therapeutic Indications

bevacizumab is developed for 9 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-small cell lung cancer stage IV✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-small cell lung cancer metastatic✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Ovarian cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Renal cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Colorectal cancer✓ Approved

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Soluble T-cell receptor (TCR)-based biologics (protein-based) are an emerging class of immunotherapeutic agents that recognize antigenic peptides presented by the human leukocyte antigen (HLA) on the surface of target cells. Furthermore, they simultaneously bind to cluster of differentiation 3 (CD3) subunits on T cells, recruit T cells to target cells, and promote T-cell activation and degranulation, ultimately eliminating tumor cells. Soluble TCR-based protein biologics target intracellular antigens that are inaccessible to conventional antibody-based drugs. Consequently, the development of soluble TCR-based protein biologics has generated significant interest. One soluble TCR-based protein biologic is already approved for marketing, and several other drugs are entering clinical stages. Soluble TCR-based protein biologics have substantial therapeutic benefits but may cause cytokine release syndrome (CRS), off-target toxicity, and drug resistance. This review outlines the structural characteristics and mechanisms of action of soluble TCR-based protein biologics, introduces nonclinical research concerning soluble TCR-based protein biologics, describes the clinical progress, discusses the quality control of TCR drugs, and explores the challenges and possible future improvements for soluble TCR-based protein biologics.

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WIN-MTB-2024002 - WIN International Molecular Tumor Board: A 52-year-old female with unmeasurable Stage IIIc colon cancer.

El-Deiry Wafik S WS, Hernando-Calvo Alberto A, Magidi Shai S, Bresson Catherine C et al.

Copyright: © 2026 El-Deiry et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Colorectal cancer (CRC) is a leading cause of cancer-related mortality, with a complex molecular profile that impacts tumor behavior and treatment response. This case report discusses a 52-year-old female diagnosed with Stage IIIc colon cancer, exhibiting KRAS, TP53, IDH1, and APC mutations, as well as a tumor microenvironment with high PD-L1 expression and elevated VEGFR1 and VEGFR3. Despite surgical resection and adjuvant treatment which included FOLFOX, FOLFIRI with bevacizumab and local radiation, the patient’s disease was difficult to track due to small, non-FDG-avid lymph nodes in the aortocaval region and persistent circulating tumor DNA (ctDNA). Following a review by an international Molecular Tumor Board (MTB), maintenance therapy options were discussed, including the personalized combinations of regorafenib, sulindac, and metformin, or fruquintinib, sulindac, and metformin, based on the patient’s molecular alterations. Alternatively, 5-FU with or without bevacizumab was suggested. In the event of relapse, the MTB recommended the combination of regorafenib, sulindac, and metformin, with the addition of trametinib and ivosidenib. The combination of regorafenib, ipilimumab, and nivolumab (RIN) was also considered due to the patient’s high PD-L1 expression. Further clinical trial options, such as pan-RAF inhibitors, NK cell agonists, and TAS-102 with bevacizumab, were also discussed. Additionally, the potential combination of PD-1 and TGFβ inhibitors was explored. This case underscores the critical role of molecular profiling in tailoring personalized treatment strategies for advanced CRC, providing novel avenues for managing recurrent disease, even in the absence of measurable disease.

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Advances in Treatment of Refractory Advanced and Recurrent Cervical Adenocarcinoma: Molecular Heterogeneity and Differences from Squamous Cell Carcinoma.

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Treatment for locally advanced and recurrent cervical cancer has advanced substantially with immune checkpoint inhibitors, induction chemotherapy, bevacizumab, and antibody-drug conjugates. However, subgroup analyses of major phase III trials suggest that cervical adenocarcinoma (AC) may respond differently from squamous cell carcinoma (SCC). Therefore, novel treatment strategies based on the distinct biological characteristics of AC are needed. This review aimed to evaluate the efficacy of current treatments for AC by examining histology-specific subgroup analyses from major clinical trials and to identify potential therapeutic strategies for AC. We also reviewed ongoing AC-focused clinical trials of novel molecularly targeted agents and combination therapies for advanced or recurrent disease. A structured search of PubMed and ClinicalTrials.gov through 1 June 2026, identified studies of advanced or recurrent cervical adenocarcinoma. Randomized trials, prospective studies, and histology-specific subgroup analyses were included, while case reports, preclinical studies, and SCC-only studies were excluded. Survival and response outcomes were extracted, with histology-specific findings considered exploratory. AC exhibits distinct molecular and immunological features compared with SCC, including frequent alterations in ERBB2/3, KRAS, PIK3CA, PTEN, ARID1A, and STK11 and a relatively immune-cold tumor microenvironment. HPV-independent AC, particularly gastric-type adenocarcinoma, shows aggressive clinical behavior and resistance to conventional therapies. Although bevacizumab, immune checkpoint inhibitors, and tisotumab vedotin have improved outcomes in cervical cancer, evidence specific to AC remains limited because most pivotal trials predominantly enrolled SCC or reported combined AC/adenosquamous subgroups. Emerging strategies targeting HER2, CLDN18.2, TROP2, Nectin-4, FAK, PI3K/AKT/mTOR, and ROS1 may provide new therapeutic opportunities for AC. AC represents a biologically heterogeneous disease distinct from SCC, supporting treatment strategies based on histology and molecular characteristics. Future AC-specific clinical trials and molecular stratification according to HPV association, histological subtype, and actionable alterations are needed to establish biomarker-driven personalized therapy, particularly for treatment-resistant HPV-independent AC.

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Protein tyrosine phosphatase sigma (PTPσ) is a member of the leukocyte common antigen-related (LAR) family of receptor-type protein tyrosine phosphatases. Its architecture integrates an extracellular proteoglycan-sensing region, a single-pass transmembrane helix, and tandem intracellular phosphatase domains. In neural injury, inhibition of PTPσ signaling can relieve chondroitin sulfate proteoglycan (CSPG)-mediated restriction of axonal growth and plasticity. In rheumatoid arthritis (RA), by contrast, restoration of PTPσ activity in fibroblast-like synoviocytes can suppress pathogenic migration and invasion. Structural studies have established a proteoglycan-switch model in which glycosaminoglycan engagement of the N-terminal immunoglobulin-like domains and extracellular clustering regulate intracellular phosphatase activity. Recent work demonstrated that antibodies to the membrane-proximal fibronectin type III-like domain 9 (Fn9) can regulate PTPσ oligomerization and syndecan-4 association in rheumatoid arthritis. Structure-guided protein engineering has converted a poorly soluble PTPσ Ig1-Ig2 decoy into developable Fc-fusion variants with substantially improved solubility and expression yield while retaining glycosaminoglycan binding and cell-based activity. This review summarizes the structural basis of PTPσ regulation and evaluates therapeutic modalities and engineering strategies for advancing PTPσ-directed biologics toward clinical candidates.

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Achondroplasia (ACH) is the most common non-lethal skeletal dysplasia and is caused in the vast majority of cases by a heterozygous gain-of-function variant in fibroblast growth factor receptor 3 (FGFR3, p.Gly380Arg). Hyperactive FGFR3 signaling constrains endochondral bone growth by suppressing growth-plate chondrocyte proliferation and hypertrophic differentiation. In the past decade, management has expanded beyond supportive care, and several mechanism-based interventions have shown disease-modifying effects in clinical studies. These include the activation of the NPR2/CNP axis with vosoritide and navepegritide and the pharmacologic attenuation of FGFR signaling with infigratinib, while extracellular biologics designed to modulate ligand-receptor interactions remain investigational. In parallel, gene-based approaches are increasingly discussed as routes toward the etiology-directed control of the causal driver, ranging from the cartilage-biased tuning of FGFR3 expression to variant-level genome editing concepts. Here, we synthesize the current therapeutic landscape, explicitly distinguish pathway-targeted disease modification from etiology-directed genetic strategies, and highlight the key translational barriers for gene-based approaches, including target-tissue delivery to the growth-plate, dose control and durability across development, redosing and immunogenicity constraints, and long-term safety.

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