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paclitaxel (PNP, Dabur / DO/NDR/02 / PNP, Dabur)

✓ Approved

Fresenius Kabi · TUBB · 小分子

什么是 paclitaxel？

paclitaxel 是一种小分子，由Fresenius Kabi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

商品名PNP, Dabur, DO/NDR/02, PNP, Dabur
公司Fresenius Kabi
药物类别小分子
分子靶点TUBB
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Fresenius Kabi

作用机制

分子靶点

paclitaxel 作用于 1 个分子靶点：

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 4 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)Breast cancer✓ Approved
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)Ovarian cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-small cell lung cancer metastatic✓ Approved

相关研究文献

PubMedACS applied materials & interfaces2026-09-10

Functionalized Red Blood Cell Membrane Nanoplatform for Paclitaxel and Artesunate Induces Ferroptosis and Immunogenic Cell Death against Triple-Negative Breast Cancer.

Li Kaiming K, Zhu Xiaole X, Wu Haisi H, Li Jiang J et al.

Triple-negative breast cancer (TNBC) tends to exhibit extremely large rates of tumor recurrence and mortality owing to the absence on effective therapeutic targets. Paclitaxel is the chemotherapeutic drug of choice, but the clinical efficacy in TNBC is limited. In the present study, we developed a folic acid (FA)-modified red blood cell membrane biomimetic drug delivery system encapsulating both paclitaxel and artesunate (PA@LRM-FA) against TNBC, aimed at enhancing ferroptosis and promoting immunogenic cell death to improve paclitaxel efficacy. The morphology, particle size, zeta potential, particle stability, paclitaxel and artesunate loading capacity, and paclitaxel and artesunate encapsulation efficiency of the formulations were studied. Through a cellular assay, we discovered that PA@LRM-FA inhibited the 4T1 cell proliferation, induced ROS accumulation, and promoted ferroptosis and immunogenic cell death. In tumor-bearing mice, PA@LRM-FA effectively targeted tumor tissues for the delivery of paclitaxel and artesunate and significantly induced ferroptosis, promoting immunogenic cell death and active immune cells in 4T1 tumors, resulting in a marked inhibition of tumor growth. Taken together, this work demonstrated a feasible therapeutic approach to inhibit TNBC by enhancing tumor ferroptosis and immunogenic cell death through PA@LRM-FA delivery of paclitaxel and artesunate.

PMID 42717767
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PubMedMolecular oncology2026-09-10

Paclitaxel induces NM2-dependent cellular contraction through GEF-H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells.

Asensio-Juárez Gloria G, Pérez-Díaz Rafael R, Ramos-Solano Hugo H, Garrido-Casado Marina M et al.

In this study, we have investigated the crosstalk between microtubule dynamics and actomyosin contractility in cancer cells treated with taxanes, which are chemotherapeutic agents used to treat solid tumors. We found that paclitaxel (PTXL) induced cell contraction through a mechanism that involved the rapid dissociation of GEF-H1 from microtubules, and the phosphorylation and acute activation of NM2 in a RhoA-dependent manner. Mutation of a major α-tubulin regulatory site (K40R) markedly slowed and reduced the efficiency of PTXL-induced GEF-H1 dissociation, indicating that this site is required for the full, rapid release of GEF-H1 from the microtubule lattice. Inhibitors of tubulin deacetylase HDAC6 promoted a slow release of GEF-H1 from microtubules and a lagged accumulation of phosphorylated NM2. Unexpectedly, depletion of tubulin acetyltransferase αTAT1 also induced NM2 phosphorylation, indicating that microtubule acetylation is involved in the maintenance of contractile homeostasis. Together, these results indicate that PTXL induces rapid cellular contraction dependent on the GEF-H1-RhoA-ROCK axis, in which K40 of α-tubulin gates the efficiency of GEF-H1 dissociation from microtubules, whereas homeostatic, αTAT1-dependent microtubule acetylation maintains appropriate levels of cellular contractility through long-term control of NM2 phosphorylation and actomyosin organization.

PMID 42719948
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PubMedJournal of ginseng research2026-09-10

Context-dependent modulation of the TAK1-MAPK axis by ginsenoside-based formulations along the NAFLD-HCC continuum.

Lim Hyun Kyung HK, Oh Jae-Yong JY, Chung Kyu Nung KN, Yoo Byong Chul BC et al.

Non-alcoholic fatty liver disease (NAFLD) is a dynamic metabolic liver disorder that can progress to hepatocellular carcinoma (HCC). Stress-responsive signaling pathways, particularly the transforming growth factor-β-activated kinase 1 (TAK1)-mitogen-activated protein kinase (MAPK) axis, play context-dependent roles in hepatocyte survival, disease adaptation, and tumorigenesis. Two ginseng-derived formulations with distinct biological properties were investigated: a non-cytotoxic Rg5/Rk1-triterpene complex and a cytotoxic Rg3/paclitaxel liposomal formulation. Cytotoxicity and signaling responses were evaluated in HepG2 hepatocellular carcinoma cells, MKN1 gastric cancer cells, and HEK293T cells. Cell viability was assessed using MTT assays. TAK1-MAPK signaling was analyzed by Western blotting and overexpression experiments, and cellular thermal shift assays were performed to examine target engagement. Rg5/Rk1-triterpene enhanced TAK1 autophosphorylation and activated downstream MAPK signaling without inducing cytotoxicity, consistent with an adaptive stress-response profile. This modulation was accompanied by selective upregulation of the RNA editing enzyme ADAR2, while global translational regulators such as eIF6 remained unchanged. In contrast, Rg3/paclitaxel liposomes induced cytotoxic stress and suppressed MEK-ERK signaling in hepatic and gastric cancer cells, supporting a pro-apoptotic mechanism. These opposing effects demonstrate formulation-dependent regulation of the TAK1-MAPK signaling axis. These findings suggest that ginseng-derived formulations differentially modulate the TAK1-MAPK pathway and may represent a context-dependent signaling framework relevant to different stages of liver disease progression.

PMID 42718885
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PubMedFrontiers in oncology2026-09-10

Distal cholangiocarcinoma mimicking pancreatic ductal adenocarcinoma successfully converted to resection following PD-1/CTLA-4 bispecific immunotherapy (cadonilimab) combined with nab-paclitaxel-based chemotherapy: a case report providing preliminary real-world insight.

Li Yongzhao Y, Sheng Xiyang X, Mi Chen C, Du Yongyue Y et al.

Distal cholangiocarcinoma (dCCA) and pancreatic ductal adenocarcinoma (PDAC) share highly overlapping clinical presentations and radiological features, often leading to preoperative misdiagnosis. Therapeutic strategies for these malignancies differ substantially. While PDAC is commonly treated with gemcitabine plus nab-paclitaxel (AG regimen) or FOLFIRINOX as neoadjuvant or conversion therapy, first-line treatment for cholangiocarcinoma (CCA) typically consists of gemcitabine plus cisplatin (GC regimen), with or without immunotherapy. In recent years, increasing attention has been paid to immunotherapy-based combination strategies in biliary tract cancers, although their role in conversion therapy remains to be fully elucidated. A 70-year-old male presented with upper abdominal discomfort. Imaging findings and endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) suggested moderately differentiated ductal adenocarcinoma. Based on the tumor location in the pancreatic uncinate process and associated vascular involvement, the lesion was initially considered borderline resectable PDAC. The patient received neoadjuvant therapy consisting of a programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) bispecific antibody (cadonilimab) combined with the AG regimen for seven cycles. Post-treatment imaging demonstrated marked tumor regression and reduced vascular involvement. The patient subsequently underwent pancreaticoduodenectomy, with partial resection and reconstruction of the superior mesenteric vein (SMV), as well as arterial divestment of the superior mesenteric artery (SMA), achieving R0 resection. However, postoperative pathological evaluation revealed that the tumor originated from the distal bile duct, confirming a final diagnosis of dCCA. This case highlights the limitations of EUS-FNA in accurately determining the primary tumor origin in periampullary and pancreatobiliary junction malignancies, while immunohistochemistry lacks sufficient specificity in this setting. Importantly, it demonstrates that the AG regimen combined with PD-1/CTLA-4 bispecific immunotherapy, commonly used in PDAC, may exert significant antitumor activity in dCCA, providing a novel perspective for conversion therapy in biliary tract cancers. This report offers a preliminary real-world therapeutic insight from a single case, suggesting that dual immune checkpoint blockade combined with chemotherapy may enable conversion surgery in selected patients with CCA. Further studies are warranted to elucidate the underlying immunological mechanisms.

PMID 42719709
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PubMedClinical cancer research : an official journal of the American Association for Cancer Research2026-09-10

Response-Adapted Surgery after Neoadjuvant Immunochemotherapy in Locally Advanced Head and Neck Squamous Cell Carcinoma (REMATCH): A Single-Arm Phase II Trial.

Zhang Xiaomeng X, Zhou Yan Y, Huang Jing J, Peng Gang G et al.

We assessed the feasibility and efficacy of a response-adapted surgical strategy in patients with locally advanced head and neck squamous cell carcinoma (LA-HNSCC) achieving major tumor regression after neoadjuvant immunochemotherapy (NAICT). This phase II, single-arm, prospective trial enrolled patients with resectable, human papillomavirus-negative stage III to IVA LA-HNSCC. All received three cycles of NAICT (penpulimab, nab-paclitaxel, and cisplatin). Pre-cycle 3 imaging and laryngoscopy guided surgery: Patients with ≥50% primary tumor regression underwent reduced-volume surgery (RVS); those with <50% regression received standard-volume surgery (SVS). All received risk-adapted adjuvant radiotherapy. The primary endpoint was 2-year disease-free survival (DFS). Fifty patients completed NAICT, with an objective response rate of 94% [95% confidence interval (CI), 84%-99%]. At a median follow-up of 34.0 months (IQR, 30.1-39.5), the 2-year DFS for the per-protocol cohort was 83% (95% CI, 69%-91%). The RVS group (n = 42) achieved a 2-year DFS of 90% (95% CI, 77%-96%) with 100% laryngeal preservation in laryngeal/hypopharyngeal cancers, whereas the SVS group (n = 5) had a 2-year DFS of 20% (95% CI, 0.8%-58%). Grade 3 adverse events (AE) occurred in 16% of patients related to NAICT and in 15% related to surgery; there were no grade 4 or 5 AEs. At 9 months after radiotherapy, most quality-of-life scores improved or stabilized compared with baseline. The REMATCH trial provides the first prospective evidence that a response-adapted surgical strategy after NAICT is feasible. Patients achieving ≥50% primary tumor regression derived promising survival and universal laryngeal preservation. These findings support the initiation of phase III randomized trials to validate this de-escalation strategy.

PMID 42717678
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PubMedFrontiers in oncology2026-09-10

Immune checkpoint inhibitor-based combination therapy for platinum-resistant or platinum-refractory recurrent ovarian cancer: a systematic review and meta-analysis of prospective trials.

Xu Jing J, Zhang Lin L, Yang Wen-Ying WY, Cai Xiao-Jing XJ et al.

The clinical value of immune checkpoint inhibitor (ICI)-based combinations in platinum-resistant or platinum-refractory recurrent ovarian cancer remains regimen-dependent and uncertain. We updated the evidence base and separated nonrandomized response evidence from randomized comparative evidence. PubMed/MEDLINE, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched from inception to 23 July 2026, supplemented by reference and citation searching. Eligible reports were peer-reviewed prospective phase II or III trials of an ICI-containing combination in adults with platinum-resistant or platinum-refractory recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer. Front-line, maintenance-only, ICI-monotherapy, retrospective, phase I-only, protocol-only, and mixed platinum-status cohorts without extractable resistant/refractory data were excluded. Objective response rate (ORR) and disease control rate (DCR) from compatible nonrandomized cohorts were synthesized as proportions using a logit random-effects model with Paule-Mandel variance estimation and Hartung-Knapp confidence intervals. Randomized hazard ratios were synthesized descriptively and were not pooled. Twenty-one eligible prospective reports were included, comprising 14 nonrandomized reports and 7 randomized trials. Of the 14 nonrandomized reports, 13 provided compatible confirmed response data for the pooled ORR analysis, yielding 112 objective responses among 490 participants and a pooled ORR of 21.9% (95% CI, 13.1%-34.3%; I² = 70.7%). The remaining nonrandomized report was retained for narrative synthesis only because it reported an unconfirmed response. Ten nonrandomized reports contributed 211 disease-control events among 354 participants, yielding a pooled DCR of 59.9% (95% CI, 46.4%-72.1%; I² = 71.7%). The seven randomized trials were summarized separately and were not pooled with the nonrandomized reports. KEYNOTE-B96 demonstrated improved progression-free survival (HR, 0.70; 95% CI, 0.58-0.84) and overall survival (HR, 0.82; 95% CI, 0.69-0.97), whereas JAVELIN Ovarian 200, EORTC 1508, NRG-GY023, and AGO-OVAR 2.29 did not meet their primary efficacy objectives. ICI-based combinations show measurable but highly heterogeneous activity in platinum-resistant/refractory ovarian cancer. The evidence does not support a uniform class effect: a survival benefit is established for pembrolizumab plus weekly paclitaxel in KEYNOTE-B96, whereas several other randomized strategies were negative. Future trials should prioritize regimen-specific validation, biomarker enrichment, and harmonized toxicity reporting.

PMID 42718730
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