Request Demo

Last update 29 Apr 2026

Cetuximab

Last update 29 Apr 2026

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Monoclonal antibody

Synonyms

Anti-EGFR monoclonal antibody 225, Cetuximab (Genetical Recombination), Cetuximab (genetical recombination) (JAN)

+ [16]

Target

EGFR

Action

antagonists

Mechanism

EGFR antagonists(Epidermal growth factor receptor erbB1 antagonists)

Therapeutic Areas

NeoplasmsDigestive System DisordersRespiratory Diseases+ [5]

Active Indication

BRAF V600E mutant Colorectal CancerRAS Wild Type Colorectal CancerHead and Neck Neoplasms+ [31]

Inactive Indication

Adenocarcinoma of EsophagusAdenocarcinoma of LungAdenocarcinoma of prostate+ [112]

Originator Organization

Merck Serono SA

Active Organization

Boehringer Ingelheim GmbH

Mirati Therapeutics, Inc.

Bristol Myers Squibb Co.

+ [18]

Inactive Organization

Hoffmann-La Roche, Inc.

Novartis Pharmaceuticals Corp.Wyeth AB

+ [13]

License Organization

Merck KGaA

Eli Lilly & Co.

Genfleet Therapeutics (Shanghai), Inc.

+ [10]

Drug Highest PhaseApproved

First Approval Date

Switzerland (01 Dec 2003),

Colorectal Cancer

RegulationAccelerated Approval (United States), Orphan Drug (United States), Priority Review (China)

Structure/Sequence

Sequence Code 43254L

Source: *****

Sequence Code 9505399H

Source: *****

1,236

Clinical Trials associated with Cetuximab

NCT07441681

/ Not yet recruitingPhase 3IIT

Radiotherapy With Concurrent Cetuximab vs. Carboplatin and Paclitaxel in Patients With Stage III-IVB Head and Neck Cancer With a Contraindication to Cisplatin: A Pragmatic Phase III Randomized Trial

This phase III trial compares cetuxumab to chemotherapy, carboplatin and paclitaxel, with intensity modulated radiation therapy for the treatment of patients with head and neck cancer who are unable to receive cisplatin. Cetuximab is in a class of medications called monoclonal antibodies. It binds to a protein called EGFR, which is found on some types of cancer cells. This may help keep cancer cells from growing. Carboplatin is in a class of medications known as platinum-containing compounds. It works in a way similar to the anticancer drug cisplatin, but may be better tolerated than cisplatin. Carboplatin works by killing, stopping or slowing the growth of cancer cells. Paclitaxel is in a class of medications called antimicrotubule agents. It stops cancer cells from growing and dividing and may kill them. Intensity modulated radiation therapy is a type of 3-dimensional radiation therapy that uses computer-generated images to show the size and shape of the tumor. Thin beams of radiation of different intensities are aimed at the tumor from many angles. This type of radiation therapy reduces the damage to healthy tissue near the tumor. It is not yet know if cetxiumab or chemotherapy, with intensity modulated radiation therapy works best for the treatment of patients with head and neck cancer who are unable to receive cisplatin.

Start Date06 Jan 2027

Sponsor / Collaborator

NRG Oncology

NCT06418724

/ Not yet recruitingPhase 2

Neoadjuvant PD-1 Inhibitor and EGFR Inhibitor in Locally Advanced Cutaneous Squamous Cell Carcinoma

The NEOPECS trial is a phase II prospective, single-arm, non-randomised interventional trial for patients with borderline resectable locally advanced cutaneous squamous cell carcinoma with a 6-participant safety lead in to ensure safety of the combination in the neoadjuvant setting across 3 sites in Australia.

Start Date30 Jul 2026

Sponsor / Collaborator

Melanoma & Skin Cancer Trials Ltd.

NCT07468071

/ Not yet recruitingPhase 1/2

KontRASt-R: An Open-label, Multi-center, Rollover Study for Participants Who Have Been Previously Enrolled Into a Novartis-sponsored Opnurasib (JDQ443) Study and Are Continuing to Benefit From Opnurasib as a Single Agent or in Combination With Other Study Treatments

The purpose of this study is to allow continued access to opnurasib (JDQ443) to participants who are benefitting from treatment with opnurasib as a single agent or in combination with other study treatments in pre-defined Novartis-sponsored opnurasib studies and to continue to assess safety in these participants.

Start Date15 Jun 2026

Sponsor / Collaborator

Novartis Pharmaceuticals Canada, Inc.

100 Clinical Results associated with Cetuximab

100 Translational Medicine associated with Cetuximab

100 Patents (Medical) associated with Cetuximab

7,754

Literatures (Medical) associated with Cetuximab

01 Dec 2026·MOLECULAR BIOLOGY REPORTS

Non-Coding RNAs and cernas: emerging modulators of drug response in colorectal cancer

Review

Author: Abkenar, Elahe Daskar ; Sadeghi, Amir ; Mojarad, Ehsan Nazemalhosseini ; Nobili, Stefania ; Shams, Elahe ; Moghani, Mona Malekzadeh ; Sina, Negin ; Ebrahimi, Sara ; Fatemi, Nayeralsadat

Colorectal cancer (CRC) is still one of the most common cancers and a leading cause of cancer morbidity worldwide. A significant issue that should be paid much attention to is its resistance to anticancer agents. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been identified as important regulators of drug response and drug resistance in CRC. In this review, we provide a comprehensive assessment of the studies conducted in the field of investigating the role of ncRNAs in drug resistance to prominent anticancer agents used in CRC, including 5-fluorouracil (5-FU), oxaliplatin, cetuximab, bevacizumab, and regorafenib. We focussed specifically on the miRNAs, lncRNAs, and circRNAs associated with resistance to each drug individually, even within the context of combination therapies, such as FOLFOX. We also reviewed competing endogenous RNA (ceRNAs) networks and their relationship with drug sensitivity and resistance and new therapeutic strategies to manage drug resistance in CRC and also analyzed the role of ceRNA networks in modulating drug response and its implications for new approaches to overcome drug resistance in CRC. This article also discusses findings from human clinical trials, highlighting evidence from patient studies that validate the role of targeting ceRNA and ncRNA networks in improving drug sensitivity, overcoming resistance, and enhancing therapeutic outcomes in CRC. It supports the targeting of ncRNA and ceRNA networks as potential therapies to improve treatment outcomes and drug resistance in CRC.

01 Jun 2026·Biomaterials advances

Development of a HER1/CP2c dual-targeting biopharmaceutical for HER1-overexpressing head and neck cancer

Article

Author: Cheon, So Yeong ; Park, Dongsun ; Han, Sang-Woo ; Kim, Eun Byeol ; Lee, Inbeom ; Cho, Junmin ; Kim, Boram ; Byun, Kyu Tae ; Kim, Chan Gil ; Won, Hyung-Sik

With the development of pharmaceuticals, the death rate due to cancer continues to decrease. However, the incidence of major cancers remains high. Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent type of non-skin cancers and it predominantly expresses human epidermal growth factor receptor 1 (HER1). To selectively eliminate HNSCC, cetuximab was developed as a HER1 targeting monoclonal antibody (mAb) therapy. Despite approval from the US-FDA, Cetuximab- or other anticancer drugs-related complications, such as mucosal inflammation, rash, intracranial infections, and neurological deficits, have been reported. In order to address these limitations, we have developed an antibody-drug conjugates (ADCs)-like anticancer platform called dual-targeting anticancer therapeutics (DTAT), which consists of a positioning site for mAbs or single-chain fragment variable (scFv) targeting specific antigens and a cell-penetrant cytotoxic payload targeting an oncoprotein CP2c conjugated to a cleavable linker sequence (CLS), which is sensed and cleaved by matrix metalloproteinase-11 (MMP-11). Based on this DTAT platform, we generated DTAT-D351, which dual-targets HER1 and CP2c, as an anticancer biopharmaceutical for HNSCC. Our data showed that DTAT-D351 exhibited high productivity and a strong binding affinity for HER1. Moreover, DTAT-D351 showed high anticancer potency against HER1-overexpressing cancer cells and A431 epidermoid squamous carcinoma cells. Moreover, it showed no adverse reactions in immune cells and normal cells. In conclusion, DTAT-D351, herein called Cetuximab scFv-CPTin, is a promising and effective anticancer agent for the treatment of HER1-overexpressing cancer cells, including head and neck cancers.

01 May 2026·JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS

LC-MS peptide mapping of monoclonal antibodies using the mirror proteases trypsin and Tryp-N

Article

Author: Sargautis, Domantas ; Thiede, Bernd

Accurate characterization of the amino acid sequence and post translational modifications (PTMs) of monoclonal antibodies (mAbs) is essential for evaluating product quality. Peptide mapping through bottom-up LC/MS analysis is a key methodology for this purpose. While trypsin is commonly the first choice for mAb digestion, it typically yields high but incomplete sequence coverage. As a result, supplementary endoproteases such as Asp-N, chymotrypsin, Glu-C or Lys-C are often employed to enhance coverage. In this report, we evaluated another endoprotease, Tryp-N, which serves as an effective alternative to trypsin for mAb analysis. The sequence coverages achieved for bevacizumab, cetuximab, NISTmAb, and trastuzumab with Tryp-N were comparable to that of trypsin, and the combination of both enzymes slightly improved overall sequence coverage. Notably, both trypsin and Tryp-N generated identical peptides beside the N- and C-terminal ends. The presence of a basic amino acid at opposite ends of the peptide often resulted in complementary sequence coverage of the MS2 of the same peptide sequences. These complementary ion series can be leveraged for precise localization of PTMs, as demonstrated in detail for deamidation, and oxidation sites as well as single amino acid variants (SAVs).

645

News (Medical) associated with Cetuximab

23 Apr 2026

·www.prnewswire.com

AACR 2026 | Abbisko Therapeutics Showcases Six Research Advances Highlighting pan-KRAS, 4th Generation EGFR, and Synthetic Lethality Approaches

SAN DIEGO, April 22, 2026 /PRNewswire/ -- Abbisko Therapeutics (HKEX: 02256) announced that the company presented six latest preclinical and translational research findings in poster sessions at the American Association for Cancer Research (AACR) Annual Meeting, held from April 17 to 22, 2026, in San Diego, USA. The presentations span multiple key innovation areas, including the pan-KRAS inhibitor ABSK211, the 4 th generation EGFR inhibitor ABK-EGFR-1, the CDK4 selective inhibitor ABK-CDK4, the MTA-cooperative PRMT5 inhibitor ABSK131, as well as a ctDNA-based study investigating resistance mechanisms to the FGFR2/3 inhibitor ABSK061. pan-KRAS Inhibitor ABSK211 ABSK211 is a potent, highly selective, and orally bioavailable small-molecule pan-KRAS inhibitor developed by Abbisko Therapeutics. It demonstrates broad inhibitory activity against multiple KRAS mutations, addressing significant unmet medical needs in KRAS-driven cancers. At AACR 2026, Abbisko presented preclinical data for both monotherapy and combination strategies of ABSK211. Monotherapy: Broad and Potent Inhibition Across KRAS Mutations KRAS mutations are highly prevalent across multiple cancers, including pancreatic (~90%), colorectal (~35%), and lung cancer (~25%). While several pan-KRAS inhibitors have entered clinical development, there remains a critical need for enhanced potency. In preclinical studies, ABSK211 demonstrated: Robust in vitro activity: ABSK211 significantly reduced cell viability across multiple KRAS alterations (including G12, G13, Q61, and WT amplification) at sub-nanomolar to nanomolar concentrations. Meanwhile ABSK211 displayed marginal inhibition in KRAS wild-type cell line with normal copy. Strong in vivo efficacy: Oral administration induced deep tumor regression in multiple KRAS G12V xenograft models, with robust target engagement. Broad mutation coverage: Consistent and significant antitumor activity was observed in models harboring KRAS G12D/C/S and G13D mutations. These findings support the clinical advancement of ABSK211, which is currently undergoing IND-enabling studies. Poster Information Title: Preclinical characterization of ABSK211: A highly potent, orally bioavailable and selective pan-KRAS inhibitor with broad and robust activity in KRAS-driven tumors Time: April 22, 2026, 9:00 AM – 12:00 PM (PT) Location: Poster Section 13, Board #10 Abstract #: 7090 Combination Therapy: Multi-Mechanistic Synergy Enhances Antitumor Activity Combination therapy is widely considered a key strategy to improve treatment outcomes in KRAS-mutant cancers. ABSK211 demonstrated synergistic antitumor activity with multiple therapeutic agents: In vitro synergy: Significant anti-proliferative synergy with PRMT5 inhibitors across KRAS mutations; strong synergy observed with EGFR monoclonal antibodies and chemotherapy in KRAS G12D/G12V models. Enhanced in vivo efficacy: Combination regimens with PRMT5 inhibitors, cetuximab, immunotherapies, and chemotherapy showed superior tumor growth inhibition and improved durability compared to monotherapy. These results demonstrate that ABSK211 can significantly enhance antitumor efficacy through multi-mechanistic synergy, supporting its further development in combination strategies. Poster Information Title: ABSK211, a highly potent and orally available pan-KRAS inhibitor, demonstrates robust antitumor efficacy in combination with multiple agents Time: April 22, 2026, 9:00 AM – 12:00 PM (PT) Location: Poster Section 13, Board #3 Abstract #: 7083 4 th Generation EGFR Inhibitor ABK-EGFR-1 ABK-EGFR-1 is a novel 4th generation EGFR inhibitor developed by Abbisko Therapeutics, specifically designed to target the EGFR C797S resistance mutation. It combines high selectivity with central nervous system (CNS) penetration to address key clinical challenges following resistance to 3rd generation EGFR TKIs. Targeting C797S-Mediated Resistance The EGFR C797S mutation is a clinically validated mechanism of resistance to third-generation EGFR TKIs, with an estimated 51,000–146,000 cases annually worldwide. Currently, no approved therapies specifically target this mutation, representing a significant unmet clinical need. Preclinical studies showed that ABK-EGFR-1: Exhibits high selectivity over wild-type EGFR and other kinases. Demonstrates significant in vivo antitumor activity in multiple EGFR C797S-driven xenograft models, effectively inhibiting tumor growth. Possesses excellent blood-brain barrier penetration and favorable drug-like properties. These findings support further development of ABK-EGFR-1 as a next-generation targeted therapy for EGFR-resistant cancers, particularly for patients with brain metastases. Poster Information Title: Discovery and characterization of ABK-EGFR-1, a 4th generation EGFR C797S Inhibitor with excellent selectivity and brain penetration Time: April 21, 2026, 2:00 PM – 5:00 PM (PT) Location: Poster Section 53, Board #7 Abstract #: LB350 CDK4 Selective Inhibitor ABK-CDK4 ABK-CDK4 is a highly selective, brain-penetrant small-molecule CDK4 inhibitor developed by Abbisko Therapeutics. It is designed to selectively target CDK4, reduce CDK6-related toxicity, and expand treatment potential for patients with brain metastases. Differentiation Through Selectivity and CNS Penetration 1st generation CDK4/6 inhibitors (e.g., palbociclib, ribociclib, and abemaciclib) have demonstrated clinical benefit in breast cancer, but CDK6 inhibition is associated with dose-limiting hematologic toxicities. In addition, 20–40% of breast cancer patients develop brain metastases, while current therapies have limited CNS exposure. Preclinical studies showed that ABK-CDK4: High selectivity: Over 50-fold selectivity for CDK4 versus CDK6, potentially reducing CDK6-related toxicity. CNS penetration: Favorable CNS exposure (Kpuu > 0.5) and drug-like properties. Antitumor activity: Effective inhibition of Rb phosphorylation and tumor growth in HR+/HER2− breast cancer models These results suggest that ABK-CDK4 may overcome key limitations of current CDK4/6 inhibitors and provide a differentiated therapeutic option. Poster Information Title: Discovery of ABK-CDK4, a selective and brain-penetrant CDK4 inhibitor Time: April 20, 2026, 9:00 AM - 12:00 PM (PT) Location: Poster Section 20, Board #13 Abstract #: 1905 MTA-cooperative PRMT5 inhibitor ABSK131 ABSK131 is a potent and selective small-molecule MTA-cooperative PRMT5 inhibitor developed by Abbisko Therapeutics, targeting MTAP-deleted tumors, and is currently in clinical development. Broad Synergy Across Multiple Therapeutic Modalities MTAP homozygous deletion occurs in approximately 10–15% of solid tumors and frequently co-exists with oncogenic drivers such as KRAS and EGFR. In addition, MTAP abnormities are associated with poor prognosis following standard-of-care therapies across multiple cancer types. Therefore, there remains a significant unmet need for novel and effective combination therapies centered on MTA-cooperative PRMT5 inhibitor for MTAP-deleted tumors, with the potential to enable precision patient stratification and deliver synergistic therapeutic benefits. Preclinical studies demonstrated that ABSK131 exhibits strong synergistic activity with multiple therapies: KRAS inhibitors: Enhanced tumor growth inhibition in KRAS-mutant, MTAP-deleted models when combined with AMG 510 or ABSK141. EGFR inhibitors: Improved anti-proliferative and in vivo antitumor activity in EGFR-mutant, MTAP-deleted NSCLC models when combined with osimertinib. MAT2A inhibitors: Consistent synergistic effects across multiple tumor models when combined with IDE397. Chemotherapy: Synergistic activity observed both in vitro and in vivo when combined with carboplatin in NSCLC models. These findings support ABSK131 as a potential backbone therapy for combination strategies in MTAP-deleted tumors. Poster Information Title: Synergistic antitumor activity of the MTA-cooperative PRMT5 inhibitor ABSK131 in combination with multiple therapeutic agents in diverse cancer models Time: April 21, 2026, 9:00 AM - 12:00 PM (PT) Location: Poster Section 14, Board #23 Abstract #: 4504 FGFR2/3 Inhibitor ABSK061 ABSK061 is a highly potent and selective small-molecule FGFR2/3 inhibitor developed by Abbisko Therapeutics. It has demonstrated encouraging efficacy and safety in Phase I studies and is currently being evaluated in a Phase II trial for gastric cancer. ctDNA Analysis Reveals Resistance Mechanisms Acquired resistance remains a major challenge limiting the long-term benefit of targeted therapies. Using ctDNA-based next-generation sequencing (NGS), Abbisko conducted longitudinal genomic analyses comparing baseline and progression samples to elucidate resistance mechanisms to ABSK061: On-target resistance: Polyclonal acquired FGFR2 mutations in the FGFR2 kinase domain were commonly observed in gastric cancer and cholangiocarcinoma. Off-target resistance: FGFR2-Atered NSCLC was prone to develop acquired alterations in genes involved in RTK/RAS pathways. These findings provide important molecular insights into resistance mechanisms and inform the design of future combination and sequential treatment strategies. Poster Information Title: Circulating tumor DNA (ctDNA)-based profiling of acquired resistance to the fibroblast growth factor receptor (FGFR)2/3 inhibitor lavengratinib(ABSK061) in patient(pt)s with advanced solid tumors Time: April 21, 2026, 9:00 AM - 12:00 PM (PT) Location: Poster Section 45, Board #14 Abstract #: 5319 At AACR 2026, Abbisko Therapeutics showcased the latest preclinical and translational research advances across multiple pipeline programs, demonstrating its strong capabilities in drug discovery and development. As these programs continue to advance into clinical stages, the company is further strengthening its globally competitive R&D platform. Looking ahead, Abbisko Therapeutics will continue to focus on addressing unmet medical needs and accelerating the translation of innovative discoveries into clinical applications, with the goal of delivering more first-in-class and best-in-class therapies to patients worldwide. SOURCE Abbisko Therapeutics 21% more press release views with Request a Demo

AACRPhase 1Phase 2Clinical Result

23 Apr 2026

·www.biospace.com

BBOT Presents Preclinical Data Demonstrating pan-KRAS Inhibitor BBO-11818 Has Robust Anti-Tumor Activity in KRAS-Mutant Preclinical Models at the AACR Annual Meeting 2026

BBO-11818 targets KRAS in both its ON (active GTP-bound) and OFF (inactive GDP-bound) states, potently suppressing MAPK signaling and inhibiting cell proliferation in KRAS-mutant cell lines BBO-11818 demonstrates robust anti-tumor activity as monotherapy and in combination across KRAS-mutant tumor models Updated Phase 1 clinical data are expected in the second half of 2026 SOUTH SAN FRANCISCO, Calif., April 22, 2026 (GLOBE NEWSWIRE) -- BridgeBio Oncology Therapeutics, Inc. (“BBOT”) (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, today presented new preclinical data for BBO-11818, a selective, orally bioavailable non-covalent inhibitor that targets mutant KRAS in both the ON (active GTP-bound) and OFF (inactive GDP-bound) states with robust anti-tumor activity in KRAS-mutant preclinical models. The data underscore BBO-11818’s differentiated activity across multiple KRAS-mutant cancer types. The data were presented at the American Association for Cancer Research (AACR) Annual Meeting 2026. "BBO-11818 addresses a significant unmet need by targeting multiple KRAS variants for which no approved therapies exist, including KRAS G12D and KRAS G12V ,” said Pedro J. Beltran, PhD, Chief Scientific Officer of BBOT. “Its ability to inhibit KRAS in both its inactive and active states drives potent tumor regressions in pancreatic, lung, and colorectal cancer models — and its efficacy is meaningfully amplified in combination with BBO-10203, cetuximab, and anti-PD-1, underscoring its potential as a combination backbone in KRAS-mutant cancers." Highlights from the poster include: BBO-11818 potently inhibits ERK phosphorylation and proliferation in KRAS-dependent cell lines in vitro . BBO-11818 demonstrates robust efficacy in KRAS G12D and KRAS G12V CDX models. BBO-11818 exhibits in vivo combination effect with BBO-10203, a RAS:PI3K⍺ breaker, and cetuximab in KRAS-mutant CDX and PDX models. BBO-11818 also shows combination benefit with anti-PD-1 treatment, resulting in complete tumor regressions and the induction of an adaptive immune response in the CT26 syngeneic model. The presentation is titled “ BBO-11818: an orally bioavailable, highly potent and selective non-covalent pan-KRAS (ON) and (OFF) inhibitor with robust anti-tumor activity in KRAS-mutant preclinical models .” A copy of the poster will be available on the “ Publications ” page of the BBOT website following the conference. About BBO-11818 BBO-11818 is a selective, orally bioavailable non-covalent inhibitor that targets KRAS in both the ON and OFF states, has high selectivity over HRAS and NRAS, and displays strong activity in KRAS-mutant preclinical models, including KRAS G12D and KRAS G12V . In addition, it potently suppresses MAPK signaling and inhibits cell proliferation in KRAS-mutant cell lines. BBO-11818 is currently being evaluated in the Phase 1 KONQUER-101 trial in subjects with locally advanced unresectable or metastatic KRAS-mutant solid tumors. About BBOT BBOT is a clinical-stage biopharmaceutical company advancing a next-generation pipeline of novel small molecule therapeutics targeting RAS and PI3Kα malignancies. BBOT has the goal of improving outcomes for patients with cancers driven by the two most prevalent oncogenes in human tumors. For more information, please visit and follow us on LinkedIn . Forward-Looking Statements This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995, as amended, and other federal securities laws. Any statements in this press release that are not historical facts may be deemed forward-looking statements, which generally are accompanied by words such as “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” “should,” “would,” “plan,” “predict,” “potential,” “seem,” “seek,” “future,” “outlook” and similar expressions that predict or indicate future events or trends. These statements are based on various assumptions, whether or not identified in this press release, and are the current expectations of BBOT’s management and are not predictions of actual performance. Many actual events and circumstances are beyond the control of BBOT. These forward-looking statements are subject to a number of risks and uncertainties, including changes in domestic and foreign business, market, financial, political, and legal conditions; risks related to the timing of expected regulatory and business milestones, including the progress of enrollment in clinical trials and availability of data from ongoing and planned clinical trials; and those factors discussed in documents BBOT has filed or will the U.S. Securities and Exchange Commission. In addition, forward-looking statements reflect BBOT’s expectations, plans, or forecasts of future events and views as of the date of this press release and are qualified in their entirety by reference to the cautionary statements herein. BBOT anticipates that subsequent events and developments will cause BBOT’s assessments to change. These forward-looking statements should not be relied upon as any guarantee, assurance, prediction or definitive statement of fact or probability or as representing BBOT’s assessments as of any date subsequent to the date of this press release. Neither BBOT, nor any of its affiliates undertake any obligation to update these forward-looking statements, except as required by law. BBOT Contacts: Investor Contact: Heather Armstrong, Head of Investor Relations BBOT Investors@BBOTx.com Media Contact: Jake Robison Inizio Evoke Comms Jake.robison@inizioevoke.com

23 Apr 2026

·www.biospace.com

Fulgent Selected to Present Rapid Oral Abstract Within the Head and Neck Cancer Track Session at the 2026 ASCO Annual Meeting

EL MONTE, Calif.--(BUSINESS WIRE)--Fulgent Genetics, Inc. (NASDAQ: FLGT) (“Fulgent” or the “Company”), a technology-based company with a well-established laboratory services business and a therapeutic development business, today announced that its abstract was selected to be presented within the Head and Neck Cancer Track of the American Society of Clinical Oncology (ASCO) rapid oral abstract session on June 1, 2026, from 4:30pm to 6:00pm (CDT) in hall D1 of McCormick Place, Chicago. The abstract is entitled “ FID-007 in combination with cetuximab in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC) ”, clinical trial identifier, NCT06332092. This is a Phase 2 study designed to evaluate the efficacy of different dosing regimens as well as to characterize the pharmacokinetics (PK) and safety and tolerability of FID-007 in combination with cetuximab in patients with disease progression after treatment with PD-L1-based immune checkpoint inhibitor. Ming Hsieh, Chairman of the Board of Directors and Chief Executive Officer, said, “We are honored to be selected by ASCO to present our findings on the interim data of our Phase 2 results for FID-007. We are encouraged by the clinical progress achieved so far and believe in the potential of FID-007 for the treatment of (R/M) HNSCC patients, currently having very few effective treatment options.” Details of the presentation are as follows: Abstract Title: FID-007 in combination with cetuximab in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC) . Session: Head and Neck Cancer Track Rapid Oral Abstract Session from 4:30pm to 6pm (CDT) within hall D1 of McCormick Place, Chicago. Presenter: Guilherme Rabinowits, MD, senior member of the Head and Neck-Endocrine Oncology Department at Moffitt Cancer Center. Authors: Guilherme Rabinowits, Christine H. Chung, Aditya Shreenivas, Eric S. Nadler, Donald A. Richards, Nabil F. Saba, Ray Yin, Jorge J. Nieva, Jacob S. Thomas. Presentation Date and Time: Monday, June 1, 2026, from 4:30pm to 6:00pm. Presentation Type: Rapid Oral Abstract Session within the Head and Neck Cancer Track Session. Abstract #6020. The abstract will be available on the ASCO® website on May 21, 2026, at 5:00pm EST. The full presentation will be available on Fulgent’s investor relations website at the start of the session. About Fulgent Fulgent is a technology-based company with a well-established laboratory services business and a therapeutic development business. Fulgent’s laboratory services business includes technical laboratory and testing services and professional interpretation of laboratory results by licensed physicians. Fulgent’s therapeutic development business is focused on developing drug candidates for treating a broad range of cancers using a novel nanoencapsulation and targeted therapy platform designed to improve the therapeutic window and pharmacokinetic pro new and existing cancer drugs. The Company aims to transform from a diagnostic business into a fully integrated precision medicine company. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Examples of forward-looking statements in this press release include statements about, among other things: future performance; Fulgent’s research and development efforts, including any implications that the results of earlier clinical trials will be representative or consistent with later clinical trials, the expected timing of enrollment and regulatory filings for these trials and the availability of data or results of these trials, including any implication that interim or preliminary data will be representative of final results. Forward-looking statements are statements other than historical facts and relate to future events or circumstances or Fulgent’s future performance, and they are based on management’s current assumptions, expectations, and beliefs concerning future developments and their potential effect on Fulgent’s business. These forward-looking statements are subject to a number of risks and uncertainties, which may cause the forward-looking events and circumstances described in this press release to not occur, and actual results to differ materially and adversely from those described in or implied by the forward-looking statements. These risks and uncertainties include, among others: the success of Fulgent’s development efforts, including its ability to progress its candidates through clinical trials on the timelines expected; its compliance with the various evolving and complex laws and regulations applicable to its business and its industry; and its ability to protect its proprietary technology and intellectual property. As a result of these risks and uncertainties, forward-looking statements should not be relied on or viewed as predictions of future events. The forward-looking statements made in this press release speak only as of the date of this press release, and Fulgent assumes no obligation to update publicly any such forward-looking statements to reflect actual results or to changes in expectations, except as otherwise required by law. Fulgent files reports filed with the U.S. Securities and Exchange Commission, or the SEC, including its annual report on Form 10-K for the fiscal year ended December 31, 2025, filed with the SEC on February 27, 2026, and the other reports it files from time to time, including subsequently filed annual, quarterly and current reports, are made available on Fulgent’s website upon their filing with the SEC. These reports contain more information about Fulgent, its business and the risks affecting their business.en@blueshirtgroup.com Contacts Investor Relations Contact: The Blueshirt Group Lauren Sloane, Lauren@blueshirtgroup.com

Phase 2ASCOImmunotherapy

100 Deals associated with Cetuximab

External Link

KEGG	Wiki	ATC	Drug Bank
D03455	Cetuximab	L01XC06	DB00002

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
BRAF V600E mutant Colorectal Cancer	China	Merck Europe BV	30 Sep 2025
RAS Wild Type Colorectal Cancer	Australia	Merck Healthcare Pty Ltd.	25 Sep 2007
Head and Neck Neoplasms	United States	Eli Lilly & Co.	01 Mar 2006
Metastatic Colorectal Carcinoma	European Union	Merck Europe BV	29 Jun 2004
Metastatic Colorectal Carcinoma	Iceland	Merck Europe BV	29 Jun 2004
Metastatic Colorectal Carcinoma	Liechtenstein	Merck Europe BV	29 Jun 2004
Metastatic Colorectal Carcinoma	Norway	Merck Europe BV	29 Jun 2004
Squamous Cell Carcinoma of Head and Neck	European Union	Merck Europe BV	29 Jun 2004
Squamous Cell Carcinoma of Head and Neck	Iceland	Merck Europe BV	29 Jun 2004
Squamous Cell Carcinoma of Head and Neck	Liechtenstein	Merck Europe BV	29 Jun 2004
Squamous Cell Carcinoma of Head and Neck	Norway	Merck Europe BV	29 Jun 2004
Colorectal Cancer	Switzerland	Merck & Co., Inc.	01 Dec 2003

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Adenocarcinoma	Phase 3	United States	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	China	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Japan	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Argentina	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Australia	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Brazil	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Canada	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Chile	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Colombia	Merck Sharp & Dohme LLC	16 Jul 2025
Adenocarcinoma	Phase 3	Finland	Merck Sharp & Dohme LLC	16 Jul 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NRG-HN004 (AACR2026)	Not Applicable	Squamous Cell Carcinoma of Head and Neck	6,299	Radiation with chemotherapy (RT-C)	smkprcorhe(haclsykukc) = daoseirbem hgbnzaxlqu (cuuyiuthvn, 63.8 - 66.3) View more	Negative	22 Apr 2026
NRG-HN004 (AACR2026)	Not Applicable	Squamous Cell Carcinoma of Head and Neck	6,299	Radiation with immunotherapy (RT-I)	smkprcorhe(haclsykukc) = hqqqxnsgih hgbnzaxlqu (cuuyiuthvn, 49.2 - 57.0) View more	Negative	22 Apr 2026
AACR2026	Not Applicable	BRAF V600E mutant Colorectal Cancer Second line BRAF-V600E mutation \| WEE1 expression	15	Encorafenib plus cetuximab with or without binimetinib (high-WEE1)	fyfpzwwgrd(nrmwnxxrle) = pgzvrideok ayutugxfat (lnkxnathvj )	Positive	22 Apr 2026
AACR2026	Not Applicable		15	Encorafenib plus cetuximab with or without binimetinib (low-WEE1)	fyfpzwwgrd(nrmwnxxrle) = skzrwjbsys ayutugxfat (lnkxnathvj )	Positive	22 Apr 2026
SWOG S0819 (AACR2026)	Phase 3	Non-Small Cell Lung Cancer Serial CTRS	1,275	Cetuximab + carboplatin/paclitaxel	vtrxeaxiwp(pbqtvvbwjf) = BOR achieved 35% (33–37%) power hvnpkdhweo (qtlwuhfhvv ) View more	Positive	20 Apr 2026
SWOG S0819 (AACR2026)	Phase 3	Non-Small Cell Lung Cancer Serial CTRS	1,275	Bevacizumab + cetuximab + carboplatin/paclitaxel		Positive	20 Apr 2026
NCT05756153 (KROCUS, Pubmed \| Lancet Oncol)	Phase 1/2	KRAS mutant Non-small Cell Lung Cancer First line KRAS G12C	47	Fulzerasib 600 mgCetuximab 500 mg/m² + Fulzerasib 600 mgCetuximab 500 mg/m² (KRAS G12C-mutated NSCLC)	syzmcsjkid(coeghuzjzj) = xaishbzemw gxeudzygtt (imtyxshpwk, 56 - 80) View more	Positive	01 Apr 2026
NCT03693807 (CTgov)	Phase 2	Colorectal Liver Metastases \| Colorectal Cancer \| Bile Duct Neoplasms	35	Cetuximab+Gemcitabine+Floxuridine (FUDR)+Oxaliplatin+Irinotecan (CPT-11)+Panitumumab+Fluorouracil (Group 1: Unresectable Liver Metastases From Colorectal Cancer)	gmpvpcmbnx(yeyxqfvjij) = joisxuenvr kfkuqfdzsi (twyduefwkl, ougtssnygb - xtbiwumdfx) View more	-	06 Feb 2026
NCT03693807 (CTgov)	Phase 2		35	Cetuximab+Gemcitabine+Floxuridine (FUDR)+Oxaliplatin+Irinotecan (CPT-11)+Panitumumab+Fluorouracil (Group 2: Resectable Liver Metastases From Colorectal Cancer)	gmpvpcmbnx(yeyxqfvjij) = ztnxiocaom kfkuqfdzsi (twyduefwkl, xfzrrbwdcn - dnmkcdjcxt) View more	-	06 Feb 2026
NCT02979977 (Phase 2 trial of dual EGFR inhibition with cetuximab and afatinib, CTgov)	Phase 2	Advanced Head and Neck Squamous Cell Carcinoma	50	Afatinib+cetuximab	holvdxdkqg(tzeujrjkem) = mvluxjmbba irxiuvuari (mhnjqxykzh, angwrgzmcq - wektfydagi) View more	-	04 Feb 2026
NCT04587128 (ASCO_GI2026)	Phase 2	Metastatic Colorectal Carcinoma First line RAS/RAF wildtype	21	Panitumumab or Cetuximab	bytvmfflzu(rgaruzmxcm) = xhnzalcphi wecetfzrro (uuwuekoyez ) View more	Positive	08 Jan 2026
NCT06358430 (ASCO_GI2026)	Phase 1	Colorectal Cancer	14	TROP2 CAR-engineered IL-15-transduced cord blood-derived NK cells+cetuximab	hufrzymbac(jhndzbnisa) = updtlsaoyi bckxmgxpyj (iocexzqmcn ) View more	Positive	08 Jan 2026
NCT06978400 (ASCO_GI2026)	Phase 2	BRAF V600E mutant Colorectal Cancer First line BRAF V600E mutation \| MSS	64	FOLFOX with dabrafenib and cetuximab/panitumumab (MSS and BRAF V600E mutation + metastatic colorectal cancer)	lmwapgnkay(lumsktpils) = xxnbgtvktf bkvtydnkzh (cdvrgylxvx )	Positive	08 Jan 2026
NCT06321081 (ASCO_GI2026)	Phase 2	RAS/BRAF wild-type \| MSS	20	Irinotecan + Cetuximab + Envafolimab	ssinbifhtt(vxawpqdqsn) = lmsdaskxlq qzhpsgkylw (cyqjdkrqyh ) View more	Positive	08 Jan 2026

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Biosimilar

Competitive landscape of biosimilars in different countries/locations. Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis