Drug Database
TR

trastuzumab (BP 02 / BP02)

✓ Approved

Aurobindo Pharma Limited · ERBB2 · Monoclonal Antibodies

What is trastuzumab?

trastuzumab 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 02, BP02
CompanyAurobindo Pharma Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetERBB2, LRP1
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

trastuzumab acts on 2 molecular targets:

ERBB2erb-b2 receptor tyrosine kinase 2 (NEU, CD340)
LRP1LDL receptor related protein 1 (LRP1A, A2MR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

trastuzumab is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Breast cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Gastric cancerBLA/NDA

Related Research Articles

PubMedBioelectrochemistry (Amsterdam, Netherlands)2026-08-30

Super-antifouling electrochemical biosensor based on a biomimetic gemini zwitterionic interface for sensitive detection of therapeutic antibodies.

Zhao Zheng Z, Yu Wanqing W, Li Haidong H, Hai MingFang M et al.

Biofouling, arising from the nonspecific adsorption of proteins, cells, and other biomolecules, remains a major challenge that compromises the stability and reliability of diagnostic and therapeutic platforms. To address this issue, a super-antifouling electrochemical aptasensor was developed by integrating a biomimetic "gemini" zwitterionic monomer (BSMMP) with polydopamine (PDA). The covalent assembly of BSMMP and PDA forms a multi-site anchoring layer that enables the stable functionalization of the affinity aptamer GC20. Owing to its dense hydration shell, the PDA-BSMMP hybrid interface acts as a physical barrier against nonspecific adsorption, maintaining electron-transfer stability in undiluted human serum. Differential pulse voltammetry confirmed that this interface markedly reduced biofouling-induced signal loss, limiting attenuation to less than 15%, nearly fourfold lower than that of the unmodified surface. The platform achieved a low limit of detection of 0.97 ng/mL, a broad linear range from 1 ng/mL to 100 μg/mL, and high selectivity for trastuzumab in a label-free format without secondary antibodies or additional signal amplification. Finally, this platform successfully quantified trastuzumab in serum from breast cancer patients, with results consistent with commercial ELISA kits. Overall, this super-antifouling aptasensor offers great potential for therapeutic drug monitoring, advancing zwitterionic interface-based biosensing strategies for point-of-care diagnostics.

PubMedJournal of translational autoimmunity2026-08-30

Immune dysregulation in osteoarthritis: Mechanisms, biomarkers, and therapeutic opportunities.

Enteshari-Moghaddam Afsaneh A, Khorramdelazad Hossein H, Abbasifard Mitra M

Osteoarthritis (OA) is increasingly recognized as a heterogeneous, immune-modulated joint disease in which chronic low-grade synovial inflammation contributes to structural degeneration and pain, challenging its historical classification as a purely mechanical disorder. Central to this paradigm shift is the recognition that synovial immune activation, particularly macrophage-driven inflammatory programs, is a key axis linking tissue damage to nociception and interacting with complementary inflammatory networks that collectively shape disease progression. However, translating these mechanistic insights into effective disease-modifying therapies has remained limited, with biologics targeting individual inflammatory mediators yielding inconsistent clinical benefit, thereby exposing a fundamental disconnect between molecular stratification and therapeutic response. This disconnect reflects the pronounced biological heterogeneity of OA, in which inflammatory activity is neither uniform nor temporally stable across disease stages. Emerging evidence supports the existence of distinct immunopathological endotypes, yet current therapeutic strategies remain largely unstratified and fail to account for this variability. Parallel advances in synovial biology and systems-level profiling have expanded the conceptual framework beyond single-cell pathways to encompass integrated immune-stromal interactions, but these insights have not yet translated into robust clinical decision-support tools. Therapeutically, multiple immune-modulatory approaches, including macrophage reprogramming, broader pathway modulation, and cellular or senescence-targeting strategies, have shown preclinical promise but remain constrained by limited clinical validation and inadequate patient selection frameworks. Across these approaches, a consistent barrier is the lack of reliable, reproducible biomarkers that link immunological heterogeneity to clinically actionable stratification. This review synthesizes current understanding of immune-driven mechanisms in OA, evaluates the translational performance of immunomodulatory interventions, and critically examines the limitations of existing biomarker strategies. It highlights the need for an integrated framework that links synovial immunobiology to endotype-specific patient classification, arguing that biomarker-guided stratification is a prerequisite for achieving precision immunomodulation and meaningful disease modification in OA.

PubMedFrontiers in pharmacology2026-08-29

Correction: Investigation of potential sex-based differences in trastuzumab-induced chronic cardiotoxicity in a rat model.

Losonczi Réka R, Galla Zsolt Z, Kis Merse M, Kupecz Klaudia K et al.

[This corrects the article DOI: 10.3389/fphar.2026.1809964.].

PubMedAdvanced materials (Deerfield Beach, Fla.)2026-08-29

Advanced Materials for Biologics Delivery to Brain Tumors.

Feng Yuran Y, Cao Yuxue Y, Kavallaris Maria M, Janjua Taskeen T et al.

Brain cancer remains a major global health challenge due to its high morbidity and mortality. Current standard therapies are often limited by incomplete tumor resection, systemic toxicity, and the inability to effectively penetrate the blood-brain barrier (BBB), which restricts drug delivery to the tumor site. These challenges underscore the urgent need for innovative therapeutic strategies that can overcome these barriers and improve treatment outcomes. Biological materials encompass a diverse range of molecules, from small peptides to monoclonal antibodies, either derived from living organisms or synthetically synthesized. Unlike traditional therapies, biologics provide a more targeted approach, including specific tumor targeting, immune system modulation, and regenerating damaged cells. Although biologics offer significant promise for brain cancer treatment, major challenges associated with blood-brain and tumour barriers continue to limit their translation, and comprehensive reviews bridging therapeutic advances with delivery technologies remain scarce. While individual biologic classes have been extensively studied, a unified assessment of these modalities and their delivery optimization is still needed. This review addresses the current gap by critically examining recent advances in biologic therapies and evaluating emerging invasive and non-invasive delivery strategies to enhance their therapeutic efficacy in brain cancer.

PubMedAdvances in therapy2026-08-29

Effectiveness and Safety of Trastuzumab Deruxtecan in Chinese Patients with HER2-Mutant Metastatic Non-Small Cell Lung Cancer (RERUN): Study Protocol for a Real-World, Multicenter, Prospective, Observational Study.

Duan Jianchun J, Zhuo Minglei M, Su Chunxia C, Liu Yibing Y et al.

Trastuzumab deruxtecan (T-DXd) is a human epidermal growth factor receptor 2 (HER2)-targeting antibody-drug conjugate that has demonstrated encouraging efficacy and a manageable safety profile in the second-line or later setting for non-small cell lung cancer (NSCLC) harboring HER2 mutations. While T-DXd was approved for treating patients with locally advanced or metastatic HER2-mutant NSCLC in China, real-world data on its use in Chinese clinical practice are lacking. This study will collect real-world data on T-DXd to evaluate its effectiveness and safety in Chinese patients with HER2-mutant metastatic NSCLC, thereby providing additional evidence to the oncology community in China. RERUN is a prospective, multicenter, observational cohort study conducted at approximately 30 sites in China. Approximately 150 adult patients (≥ 18 years) with pathologically documented unresectable and/or metastatic non-squamous NSCLC harboring any known activating HER2 mutation are currently being enrolled. The follow-up period will last approximately 6 months after the last patient is enrolled, when sufficient progression-free survival (PFS) maturity (approximately 60% of patients with events) is expected to be reached. All data will be prospectively collected and analyzed descriptively. The primary outcome is real-world PFS assessed by investigators in patients receiving T-DXd as second-line or later therapy. Secondary outcomes include the time to treatment discontinuation or death, best overall response rate, overall survival, and safety and tolerability. This study will support treatment decision-making in routine oncology practice and improve outcomes for Chinese patients with HER2-mutant NSCLC across diverse healthcare settings. Study registration number NCT06809764.

PubMedClinical reviews in allergy & immunology2026-08-29

From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.

Luo Xin X, Li Yichuan Y, Feng Yinyi Y, Wang Ying Y et al.

Atopic dermatitis (AD) is a heterogeneous inflammatory skin disorder characterized by recurrent eczematous lesions and persistent pruritus. Its pathogenesis involves epidermal barrier dysfunction, immune dysregulation, microbial dysbiosis, and altered neuroimmune signaling. Genetic defects in structural proteins, particularly filaggrin, and altered epidermal lipids increase allergen and microbial penetration, perpetuating itch, scratching, tissue injury, and inflammation. Molecular evidence further reveals AD endotypes beyond conventional clinical phenotypes, with heterogeneity in immune polarization, barrier dysfunction, microbial colonization, and pruritic pathways. This heterogeneity may underlie differences in clinical presentation and treatment response. Conventional treatments, including skin hydration, antihistamines, and topical anti-inflammatory agents, often provide incomplete or transient control. Mechanism-based therapies targeting IL-4/IL-13, OX40/OX40L, JAK, and PDE4, together with AhR agonists, have broadened treatment options. However, efficacy must be balanced against treatment-specific risks. Biologics require monitoring for ocular and injection-site reactions, whereas systemic JAK inhibitors require monitoring for infections and laboratory abnormalities and carry regulatory class warnings regarding major adverse cardiovascular events, venous thromboembolism, and malignancy; however, these warnings are largely extrapolated from studies in older patients with rheumatoid arthritis, and the magnitude of these risks in patients with AD remains uncertain. Long-term safety and real-world evidence remain limited for several emerging therapies. This review synthesizes current knowledge of barrier dysfunction, immune heterogeneity, molecular endotypes, microbiome imbalance, neuroimmune signaling, and mechanism-based therapies. Integrating clinical phenotypes with molecular endotypes, predictive biomarkers, efficacy, and individualized safety assessment may enable more precise treatment selection and durable disease control.

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