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paclitaxel

✓ Approved

Shanghai Yizhong Pharmaceutical · EGFR · Small Molecule

What is paclitaxel?

paclitaxel is a small molecule developed by Shanghai Yizhong Pharmaceutical. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyShanghai Yizhong Pharmaceutical
Drug ClassSmall Molecule, Monoclonal Antibodies, Antibody
Molecular TargetEGFR, ERBB2, TUBB
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Shanghai Yizhong Pharmaceutical

Mechanism of Action

Molecular Targets

paclitaxel acts on 3 molecular targets:

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
ERBB2erb-b2 receptor tyrosine kinase 2 (HER-2, c-ERB-2)
TUBBtubulin beta class I (TUBB1, CSCSC1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

paclitaxel is developed for 5 unique indications across 1 therapeutic area.

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)Breast cancerPhase III
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Rectosigmoid cancerPhase I
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Pancreatic carcinomaPreclinical

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Unrecognized Charcot-Marie-Tooth Disease Unmasked by Chemotherapy-Induced Neurotoxicity.

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Chemotherapy-induced peripheral neuropathy (CIPN) is among the most prevalent and clinically significant toxicities from systemic cancer treatments, with taxanes being a leading cause. It is characterised by a length-dependent, predominantly sensory axonal neuropathy that can stabilise or improve after treatment discontinuation. However, the clinical course can be profoundly altered by underlying peripheral nerve pathology. We report the case of a 68-year-old woman with luminal B, HER2-negative breast cancer who developed severe peripheral neuropathy during adjuvant chemotherapy with doxorubicin/cyclophosphamide followed by weekly paclitaxel. Treatment was discontinued after 9 of 12 planned paclitaxel cycles due to grade 3 peripheral neuropathy ( Common Terminology Criteria for Adverse Events (CTCAE) v5.0). Despite cessation of the offending agent and initiation of duloxetine, symptoms continued to worsen, with progressive motor impairment and significant gait instability. Nerve conduction studies revealed a severe sensorimotor demyelinating polyneuropathy, atypical for the predominantly axonal pattern of taxane-induced CIPN. Inflammatory, infectious, paraneoplastic, and metabolic causes were excluded, and empirical corticosteroids and intravenous immunoglobulin proved ineffective. Genetic testing identified a peripheral myelin protein 22 (PMP22) duplication (17p11.2), confirming Charcot-Marie-Tooth disease type 1A (CMT1A), a hereditary demyelinating neuropathy previously subclinical. This case report underscores the value of serial clinical and electrophysiological assessment when neuropathy is atypical, disproportionately severe, or refractory to standard treatment.

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Breast cancer is the most frequently reported cancer in women, with high mortality and morbidity globally. Paclitaxel, doxorubicin, tamoxifen, cisplatin, and 5-fluorouracil are cornerstones of standard-of-care treatment for primary and advanced breast cancers, targeting distinct molecular mechanisms. However, the evolution of acquired resistance primarily leads to treatment failure and progression to metastasis, ultimately to patient mortality. Furthermore, their effectiveness is limited by potential toxicities in various organs. These limitations present an extreme challenge for the management of breast cancer at the advanced stage. This review uncovers recent updates on acquired resistance mechanisms toward standard-of-care treatments driven by deeply rooted heterogeneity and aggressive nature through direct counteracting of its core action, hyperactivation of survival pathways, silencing of core cell death pathways, derepressing the expression of multidrug resistance proteins, metabolic reprogramming, epigenetic modifications, and exosome-mediated horizontal transfer of resistance phenotype. In addition, we discuss recent updates on potential strategies to overcome resistance and toxicities induced by standard-of-care treatments. Ultimately, this review helps to identify novel strategies targeting pathways to reverse resistance and reduce toxicity in breast cancer patients.

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Epstein-Barr virus-associated gastric cancer (EBVaGC) is a distinct molecular subtype of gastric cancer, but reliable biomarkers linking EBV-related biology, prognosis, and microenvironmental remodeling remain limited. Differentially expressed genes associated with EBVaGC were identified from TCGA and GEO datasets. Weighted gene co-expression network analysis and machine learning were used to screen core genes. Functional enrichment, diagnostic and prognostic modeling, immune infiltration analysis, single-cell transcriptomic analysis of a public scRNA-seq dataset, cell-cell communication analysis, drug sensitivity prediction, external cohort validation, and RT-qPCR validation in gastric cancer cell lines were subsequently performed. Five core genes (ASPA, CHODL, GNG7, P2RY14, and PI16) were identified. The combined classifier showed high apparent diagnostic performance in the discovery datasets (AUC = 1.000 in the EBV cohort and 0.981 in TCGA-STAD) and retained value in GSE27342 (AUC = 0.771). RT-qPCR confirmed differential expression of these genes between a gastric epithelial cell line and a gastric cancer cell line, providing general tumor-versus-normal experimental support rather than EBV-specific validation. A five-gene risk signature stratified overall survival, with 1-, 2-, and 3-year AUCs of 0.634, 0.645, and 0.622, which improved to 0.716, 0.768, and 0.693 after integration with age and stage. Single-cell analysis localized the strongest signature signal to fibroblasts and B cells and revealed enhanced MIF-, PTN-, and TNFSF13B-related communication in tumors. High-risk tumors showed higher predicted IC50 values for paclitaxel and 5-fluorouracil. We identified a five-gene signature with strong diagnostic value and biologically meaningful prognostic relevance in EBVaGC, highlighting fibroblast- and B-cell-associated microenvironmental programs in aggressive disease.

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