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paclitaxel

✓ Approved

Shanghai Yizhong Pharmaceutical · EGFR · 小分子

什么是 paclitaxel?

paclitaxel 是一种小分子,由Shanghai Yizhong Pharmaceutical研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Intravenous (IV)。

药物档案

公司Shanghai Yizhong Pharmaceutical
药物类别小分子, 单克隆抗体, 抗体
分子靶点EGFR, ERBB2, TUBB
给药途径Injectable (Others), Intravenous (IV)
状态Approved

作用机制

分子靶点

paclitaxel 作用于 3 个分子靶点:

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
ERBB2erb-b2 receptor tyrosine kinase 2 (HER-2, c-ERB-2)
TUBBtubulin beta class I (TUBB1, CSCSC1)
需要更深入的分析?Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

paclitaxel 针对 5 个适应症,涉及 1 个治疗领域。

治疗领域疾病/病症分期
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

相关研究文献

PubMedCurrent oncology (Toronto, Ont.)2026-10-26

A New Era of Treatment Sequencing in Platinum-Resistant Ovarian Cancer: Integrating Immunotherapy, Antibody-Drug Conjugates, and Targeted Therapies.

Mabuchi Seiji S, Kusakabe Ai A, Takimoto Yumi Y

Platinum-resistant ovarian cancer (PROC) has historically been treated with sequential non-platinum chemotherapy, with bevacizumab added when appropriate. The therapeutic landscape has expanded with positive randomized phase III data for pembrolizumab plus weekly paclitaxel with or without bevacizumab (KEYNOTE-B96), mirvetuximab soravtansine (MIRV) in FRα-high disease (MIRASOL), and relacorilant plus nab-paclitaxel (ROSELLA). Trastuzumab deruxtecan (T-DXd) has also shown substantial activity in previously treated HER2-expressing ovarian cancer, although its ovarian cohort was small, nonrandomized, and not restricted to PROC. These trials enrolled different populations and do not establish a cross-trial efficacy hierarchy. We therefore review the development of immunotherapy leading to KEYNOTE-B96, compare newer strategies with established PROC treatments, distinguish phase III evidence from regulatory approval and routine availability, and propose an evidence-informed framework for treatment selection and sequencing. The framework prioritizes current treatment opportunity while accounting for biomarker eligibility, prior treatment, residual toxicity, treatment and financial burden, patient priorities, and the feasibility of later-line therapy.

PMID 42930189
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PubMedCureus2026-10-26

Locally Advanced Primary Cervical Endometrial Stromal Sarcoma: A Case Report.

Bali Asmae A, Khater Kaouthar K, Jebrouni Fadoua F, Chibani Hind H et al.

Primary cervical endometrial stromal sarcoma (ESS) is a challenging mesenchymal neoplasm that may present with non-specific clinical manifestations and advanced local disease at diagnosis. We report the case of a 50-year-old diabetic woman presenting with metrorrhagia and pelvic pain. Clinical examination revealed a large ulcerative cervical mass infiltrating the vaginal walls. Histopathology with immunohistochemistry supported the diagnosis of ESS. Imaging demonstrated extensive loco-regional invasion of the bladder, lower vagina, and rectal wall, consistent with FIGO stage IVA disease. The patient was treated with systemic chemotherapy (carboplatin-paclitaxel). This case highlights the diagnostic challenges of cervical ESS, the importance of histopathological and immunohistochemical evaluation, and the therapeutic considerations in locally advanced disease.

PMID 42928860
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PubMedRheumatology and immunology research2026-10-25

Paclitaxel-induced scleroderma: A scoping review of reported cases with an illustrative case from our center.

Bogojevic Milan M, Medjedovic Rifat R, Janjic Nevenka Lukovac NL, Vukovic Ivana I et al.

Paclitaxel-induced scleroderma is a rare but increasingly recognized adverse effect of taxane chemotherapy. Most cases present with distal edema and cutaneous sclerosis, usually without disease-specific autoantibodies or visceral involvement. This study aimed to map all published cases of paclitaxel-induced scleroderma and present a unique case characterized by dual anticentromere (ACA) and anti-cyclic citrullinated peptide (ACPA) antibody positivity. A scoping review of English-language literature was performed in PubMed and Scopus up to May 2025 using the terms "paclitaxel" OR "taxane" AND "scleroderma" OR "systemic sclerosis. " Only human case reports or case series describing paclitaxel- or nab-paclitaxel-induced scleroderma were included. Data were extracted on demographics, cancer type, clinical features, serology, and outcomes, and summarized descriptively. Nineteen publications describing 21 patients were analyzed. Most patients were female (85.7%), with a mean age of 58.1 years. Cutaneous involvement was predominant, affecting both upper and lower extremities in 85.7% of cases. Raynaud's phenomenon occurred in 28.6%, and visceral involvement was uncommon (9.5% interstitial lung fibrosis; 9.5% scleroderma renal crisis). Autoantibody profiles were largely negative; antinuclear antibodies (ANA) positivity was seen in 33.3% and ACA in only one case. Nearly all patients improved after paclitaxel withdrawal, with corticosteroids and/or methotrexate used in refractory disease. The presented patient developed scleroderma-like changes with ACA and ACPA positivity-an unprecedented serologic finding-together with transient synovitis and Raynaud's phenomenon, confirming an immune-mediated overlap phenotype. Paclitaxel-induced scleroderma typically manifests as a reversible cutaneous fibrosing reaction distinct from idiopathic systemic sclerosis. However, rare cases with autoimmune serology suggest underlying immune activation in genetically predisposed individuals. The coexistence of ACA and ACPA positivity in the current case broadens the immunologic spectrum of taxane-induced scleroderma and highlights the need for further mechanistic and immunogenetic studies.

PMID 42924234
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PubMedAsiaIntervention2026-10-25

Reply: Paclitaxel- versus limus-coated balloons in the treatment of ISR.

Sagris Marios M

PMID 42923723
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PubMedAsiaIntervention2026-10-25

Letter: Paclitaxel- versus limus-coated balloons in the treatment of ISR.

Jonsson Anders A, Oldroyd Keith G KG, Chen Xiang X

PMID 42924213
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PubMedMolecular carcinogenesis2026-10-25

PPP1R14B Promotes Lung Adenocarcinoma Tumorigenesis and Paclitaxel Resistance by Increasing ARPC1A Expression.

Yang Yanna Y, You Wenjie W, Wang Xin X, Shang Bin B et al.

To investigate the biological functions of PPP1R14B in lung adenocarcinoma and further elucidate its underlying regulatory mechanisms. The Cancer Genome Atlas clinical cohorts, single-cell sequencing, Kaplan-Meier survival analysis, immunohistochemistry, qRT-PCR, and Western blot were performed to assess the expression and prognostic value of PPP1R14B in lung adenocarcinoma. Then, PPP1R14B-silenced A549 cells and PPP1R14B-overexpressing H1650 cells were constructed. Colony formation, CCK-8, EdU assay, flow cytometry, scratch, and Transwell chamber assays were utilized to evaluate cell proliferation, apoptosis, migration, invasion, and paclitaxel (PTX) resistance. To elucidate the molecular mechanism of PPP1R14B, transcriptome sequencing (RNA-seq) and co-immunoprecipitation assays were conducted. Additionally, a xenograft tumor mouse model was established to explore the in vivo role of PPP1R14B. PPP1R14B exhibited high expression in lung adenocarcinoma and correlated with an unfavorable prognosis. Silencing of PPP1R14B markedly suppressed the proliferation, migration, and invasion of A549 cells, while concurrently promoting apoptosis and sensitizing cells to PTX. Nevertheless, overexpression of PPP1R14B in H1650 cells displayed an opposite trend. PPP1R14B directly interacted with ARPC1A and promoted its expression. Overexpression of ARPC1A reversed the inhibitory effects of PPP1R14B silencing on the malignant biological behaviors of A549 cells. In vivo, silencing of PPP1R14B repressed tumor growth, as evidenced by smaller tumor volume, lower tumor weight, fewer Ki67-positive cells, and more TUNEL-positive cells. PPP1R14B directly binds ARPC1A and increases its expression to facilitate lung adenocarcinoma tumorigenesis and PTX resistance.

PMID 42927607
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