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cetuximab (Lupitux / Cetuxa / ENZ124)

✓ Approved

Lupin Limited · EGFR · Monoclonal Antibodies

What is cetuximab?

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

Drug Profile

Brand NamesLupitux, Cetuxa, ENZ124
CompanyLupin Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetEGFR
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Lupin Limited

Mechanism of Action

Molecular Targets

cetuximab acts on 1 molecular target:

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

cetuximab is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Head and neck cancer metastatic✓ Approved

Related Research Articles

PubMedESMO gastrointestinal oncology2026-08-28

Predictive biomarkers for cetuximab-based rechallenge therapy in metastatic colorectal cancer: a pooled analysis of the CAVE and CAVE-2 GOIM studies.

Ciardiello D D, Martini G G, Pietrantonio F F, Avallone A A et al.

Anti-epidermal growth factor receptor (EGFR) therapy is a therapeutic option in patients with molecularly selected metastatic colorectal cancer (mCRC). However, the identification of predictive factors represents an unmet need. We conducted a pooled analysis of individual patient data from the CAVE-GOIM (NCT04561336) and CAVE-2 GOIM (NCT05291156) studies to investigate the impact of several clinical variables on rechallenge with cetuximab with and without avelumab in circulating tumor DNA RAS/BRAF/EGFR-extracellular domain wild-type mCRC. Overall, 180 patients met the eligibility criteria: 136 received cetuximab-avelumab and 44 cetuximab. In patients receiving cetuximab monotherapy, median progression-free survival (mPFS) was 4.80 months [95% confidence interval (CI) 3.90-5.90] and median overall survival (mOS) 12.9 months (95% CI 11.1-not evaluable). Cetuximab activity was retained regardless of clinical factors. Patients treated with cetuximab-avelumab showed an mPFS of 5.00 months (95% CI 4.30-5.90) and mOS of 15.7 months (95% CI 13.0-19.9). In univariable analysis, a shorter progression-free survival was observed in patients with liver involvement [hazard ratio (HR) 2.19, 95% CI 1.51-3.20, P < 0.001] and anti-EGFR-free interval ≤16 months (HR 1.62, 95% CI 1.13-2.31, P < 0.008). Both variables retained statistical significance in multivariable analysis. In univariable analysis, lower overall survival was observed among patients treated with cetuximab-avelumab with >3 metastatic sites (HR 1.79, 95% CI 1.16-2.77, P < 0.009) and liver (HR 1.82, 95% CI 1.15-2.88, P < 0.011) and peritoneal metastases (HR 1.9, 95% CI 1.23-2.93, P < 0.004). In multivariable analysis, only liver and peritoneal metastases maintained statistical significance. Single-agent cetuximab activity is not influenced by clinical factors. In cetuximab-avelumab therapy, the absence of liver metastases and longer anti-EGFR-free interval might represent potential biomarkers.

PMID 42661856
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PubMedJournal of clinical oncology : official journal of the American Society of Clinical Oncology2026-08-27

Long-Term Survival Outcomes of Modified-FOLFOXIRI Plus Cetuximab Versus Bevacizumab in RAS/BRAF Wild-Type Metastatic Colorectal Cancer: Final Analysis of the DEEPER Trial.

Sunakawa Yu Y, Shiozawa Manabu M, Watanabe Takanori T, Ota Hirofumi H et al.

The randomized phase II DEEPER trial (jRCTs061180022) previously reported superior depth of response with modified 5-fluorouracil, leucovorin, oxaliplatin and irinotecan (m-FOLFOXIRI) plus cetuximab versus bevacizumab in patients with RAS wild-type metastatic colorectal cancer (mCRC). Here, we report updated final survival outcomes and exploratory subgroup analyses focusing on RAS/BRAF wild-type and left-sided tumors. Final overall survival (OS) and progression-free survival (PFS) were analyzed in the per-protocol set (PPS) with exploratory subgroup analyses according to the presence of liver-limited disease and sex, using extended follow-up data. There were no differences in PFS and OS in the PPS. In patients with RAS/BRAF wild-type and left-sided tumors, median PFS was longer with cetuximab than with bevacizumab (14.8 v 11.9 months; hazard ratio [HR], 0.71 [95% CI, 0.52 to 0.97]; P = .029). The median OS was 50.2 months for cetuximab and 40.2 months for bevacizumab (HR, 0.74 [95% CI, 0.53 to 1.05]). In the exploratory analyses, cetuximab-based therapy was associated with longer OS in male patients (HR, 0.59; P = .016) and in patients with extrahepatic disease (HR, 0.60; P = .014). In conclusion, the DEEPER trial suggests that m-FOLFOXIRI plus cetuximab achieves superior tumor shrinkage and may be associated with favorable outcomes in selected patients with RAS/BRAF wild-type and left-sided mCRC, with exploratory signals of benefit in male patients and those with extrahepatic disease.

PMID 42659588
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PubMedSheng wu gong cheng xue bao = Chinese journal of biotechnology2026-08-25

[Experimental and computational analyses of altered cetuximab binding induced by EGFR mutations].

Li Yifan Y, Yang Haotong H, Zhu Jianwei J, Wu Mingyuan M

Acquired mutations in the extracellular domain of epidermal growth factor receptor (EGFR) are major causes of cetuximab resistance. However, the structural mechanisms by which different mutations impair antibody binding remain to be clarified. In this study, four clinically reported EGFR mutations, S492R, G465R, S464L, and I491M, were selected for investigation. Corresponding mutant EGFR fusion proteins were constructed, expressed, and purified. Enzyme-linked immunosorbent assay was performed to evaluate their binding ability to cetuximab. In parallel, SAAMBE-3D, FoldX, and Rosetta were employed to analyze mutation-induced changes in binding free energy, interfacial geometric complementarity, and local interaction patterns. The results showed that the half-maximal effective concentration (EC50) of cetuximab binding to wild-type EGFR was 0.05 nmol/L. S492R, G465R, and S464L completely abolished cetuximab binding, whereas I491M only increased the EC50 to 0.23 nmol/L, showing a weaker effect on antibody binding. Binding free energy analysis showed that all the four mutations reduced the stability of the EGFR-cetuximab complex, with I491M exerting a comparatively mild effect. Further analyses of interfacial geometric complementarity and structural features revealed that S492R and G465R mainly impaired interfacial matching by introducing marked steric hindrance and unfavorable repulsive effects, and S464L weakened antigen-antibody interactions by disrupting a critical hydrogen-bond network. I491M caused only mild perturbations in local hydrophobic interactions and conformational stability. In summary, by integrating in vitro binding assays with multiple structure-based computational methods, this study demonstrates that extracellular domain mutations of EGFR can attenuate cetuximab binding through enhanced steric hindrance, reduced interfacial complementarity, and disruption of key interaction networks. These findings provide experimental and theoretical evidence for understanding the structural basis of acquired cetuximab resistance and offer a reference for the rational design of antibodies targeting mutant EGFR.

PMID 42638061
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PubMedFrontiers in pharmacology2026-08-25

Cost-effectiveness analysis of triplet therapy of encorafenib, binimetinib, and cetuximab for treatment of metastatic BRAF V600E-mutated colorectal cancer in China.

Liu Mengmeng M, Liu Tong T

This study evaluates the cost-effectiveness of triplet therapy of encorafenib, binimetinib, and cetuximab in contrast to doublet therapy of encorafenib and cetuximab or a control group of cetuximab plus FOLFIRI as second-line or subsequent treatment for advanced or metastatic colorectal cancer (mCRC) patients with BRAF V600 E mutation-positive status in China. An economic evaluation using a 3-state partitioned survival model assessed the cost-effectiveness of triplet therapy versus doublet therapy, triplet therapy versus the control group, or doublet therapy versus the control group. The anticipated costs for triplet therapy, doublet therapy and control therapy were 58,614.81 USD, 46,521.37 USD and 15,710.17 USD, respectively. The estimated utilities of triplet therapy, doublet therapy and control therapy were 0.84 QALYs, 0.76 QALYs and 0.53 QALYs. The ICER of triplet-therapy vs. doublet-therapy or triplet-therapy vs. control therapy or doublet-therapy vs. control therapy was 154,675.20 USD/QALY, 140,355.45 USD/QALY, or 135,434.11 USD/QALY. Our results suggested that triplet therapy was not cost-effective compared to doublet therapy and control therapy as second-line or subsequent treatment for advanced or mCRC patients with BRAF V600 E mutation at a WTP threshold of 40,000 USD/QALY.

PMID 42638785
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PubMedValue in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research2026-08-25

How Long Should We Wait? The Impact of Immature Data on Colorectal Cancer Decision Modeling.

Sim Jaemin J, Shin Gyeongseon G, Lee Donghwan D, Choi Gyeyoung G et al.

To identify a practical data maturity threshold at which model-based long-term survival projections become sufficiently reliable to inform health technology assessment (HTA). This retrospective modeling study used real-world, patient-level data from the Korea Clinical Data Utilization Network for Research Excellence registry. Patients with KRAS wild-type advanced colorectal cancer receiving first-line cetuximab- or bevacizumab-based chemotherapy between 2013 and 2021 (N = 1,208) were included. Hypothetical immature datasets were created by right-censoring at 30%, 50%, and 70% maturity (30%, 50%, and 70% of deaths observed). Partitioned survival analysis (PartSA) and state-transition model (STM) were developed for each maturity level and validated against observed 6-year overall survival and life expectancy using absolute prediction error and coverage within observed 95% confidence intervals. With highly immature data at 30% maturity, 6-year survival prediction errors ranged from 2.4%-11.1% (PartSA) and 4.5%-16.3% (STM). Prediction stability improved substantially at 50% maturity (PartSA 0.4%-5.8%, STM 0.04%-7.7%), with only modest gains at 70% maturity (0.2%-3.9% and 0.3%-6.1%). Life-expectancy deviations showed a similar pattern, narrowing from up to 0.4 years (PartSA) and 0.8 years (STM) at 30% maturity to within ±0.3 years at 50% and ±0.2 years at 70% maturity, regardless of modeling framework. In this first-line advanced colorectal cancer case study, prediction stability improved substantially once 50% maturity was reached. This threshold may provide a practical benchmark for planning reassessment or evidence-updating strategies in HTA; however, its applicability to other cancers, treatment settings, and data structures requires further evaluation.

PMID 42641950
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PubMedThe Journal of international medical research2026-08-24

Ras homolog family member A expression is associated with reduced cetuximab sensitivity in head and neck squamous cell carcinoma.

Bian ChaoRong C, Zhao Xiaotong X, Shen Ping P, Wang Runbang R et al.

ObjectivesGiven that intrinsic and acquired resistance to cetuximab substantially limits its therapeutic efficacy in head and neck squamous cell carcinoma, we sought to elucidate the role of Ras homolog family member A in mediating cetuximab resistance and delineate the mechanisms in both in vitro and in vivo models.MethodsOver 8 months, cetuximab-sensitive parental head and neck squamous cell carcinoma cells were exposed to progressively higher concentrations of cetuximab to develop a cetuximab-resistant head and neck squamous cell carcinoma cell line (HN31-R). Ribonucleic acid sequencing revealed significant upregulation of Ras homolog family member A and Rho-associated protein kinase in resistant cells compared with that in parental cells. The correlation between Ras homolog family member A overexpression and resistance to cetuximab was evaluated using Western blot analysis, immunofluorescence staining, and Cell Counting Kit-8 assays. Epigallocatechin-3-gallate was administered to Ras homolog family member A-overexpressing cells, and its effects on cetuximab sensitivity and tumor growth were evaluated in vitro and in a xenograft mouse model.ResultsElevated Ras homolog family member A expression is significantly associated with resistance to cetuximab. Ras homolog family member A knockdown restored cetuximab sensitivity and significantly reduced tumor growth in nude mice. Epigallocatechin-3-gallate treatment was associated with decreased Ras homolog family member A and Rho-associated protein kinase 2 expression and enhanced cetuximab sensitivity in both in vitro and xenograft models.ConclusionsRas homolog family member A may contribute to the development of cetuximab resistance and could be a candidate therapeutic target for future investigation aimed at improving treatment response in head and neck squamous cell carcinoma. The current findings suggest that modulation of the Ras homolog family member A-Rho-associated protein kinase axis is associated with cetuximab sensitivity in head and neck squamous cell carcinoma.

PMID 42635798
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