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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

PubMedMolecules (Basel, Switzerland)2026-10-27

Advanced Paclitaxel Delivery Systems in Oncology and Cardiovascular Medicine: Current Formulations and Emerging Technologies.

Crețeanu Andreea A, Lungu Claudiu N CN, Gratiela Popa Eliza E, Tartau Liliana Mititelu LM et al.

Oncology and cardiology use paclitaxel, a powerful cell-division inhibitor. Paclitaxel-eluting coated metal stents in oncology prevent tumor growth by modulating proliferation, apoptosis, and angiogenesis. Paclitaxel-eluting stents reduce in-stent restenosis and maintain arterial patency in cardiology. Paclitaxel encapsulated in liposomes improves targeted administration, pharmacokinetics, and therapeutic efficacy. Liposome-loaded paclitaxel has a stronger anti-tumor effect than standard formulations. Paclitaxel plus sirolimus in a stent may synergistically prevent restenosis and inhibit tumors. Liposomal formulations with supplemental medications offer promising prospects for improving therapeutic accuracy and efficacy. Liposomal paclitaxel enhances targeted drug delivery, which may improve cancer treatment and cardiovascular treatments such as drug-eluting stents and drug-coated balloons in interventional radiology. Advanced delivery technologies have changed paclitaxel drug delivery methods for therapeutic use by overcoming its low solubility and systemic toxicity. Nanocrystals and liposomes enable high drug loading and precise targeted delivery, and, by eliminating toxic solvents such as Cremophor EL, they improve the safety and efficacy of cancer therapy.

PMID 42943723
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PubMedMedicine2026-10-27

Heterogeneity in nerve recovery patterns despite symptomatic improvement in paclitaxel-induced neuropathy: A longitudinal analysis.

Lim Ikhyun I, Moon Yong Wha YW, Suh MiRi M, Kim Seul-Gi SG

Chemotherapy-induced peripheral neuropathy (CIPN) is a common and potentially persistent toxicity of paclitaxel. This prospective study aimed to characterize longitudinal changes in paclitaxel-induced CIPN by integrating serial neurophysiological and clinical assessments. Twenty-six patients receiving paclitaxel-based chemotherapy for breast, ovarian, or endometrial cancer were prospectively enrolled. Assessments were scheduled at baseline (T0), completion of chemotherapy (T1), 3 months posttreatment (T2), and 1 year posttreatment (T3) and included nerve conduction studies (NCS), the self-reported Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS), and Common Terminology Criteria for Adverse Events (CTCAE) grading. Fourteen patients with available longitudinal outcome data were included in the analytic cohort. Longitudinal changes were analyzed using linear mixed-effects models, and associations between NCS parameters and clinical measures were explored using repeated-measures correlation. S-LANSS scores increased from 1.29 ± 4.81 at T0 to 14.29 ± 4.23 at T1 and subsequently decreased to 4.86 ± 5.88 at T3 (overall P < .001), although they remained higher than baseline (P = .008). NCS amplitudes showed heterogeneous recovery patterns. Sural SNAP amplitude markedly decreased at T1 but recovered thereafter and was not significantly different from baseline at T3. In contrast, ulnar SNAP amplitude remained significantly reduced at T3 (P < .001), whereas tibial compound motor action potential amplitude was no longer significantly different from baseline (P = .060). NCS amplitudes were inversely associated with clinical measures, with the strongest association observed between ulnar SNAP amplitude and CTCAE grade (r = -0.720, P < .001). Paclitaxel-induced peripheral neuropathy showed substantial symptomatic improvement after chemotherapy but heterogeneous electrophysiological recovery across peripheral nerves. Persistent abnormalities in selected nerves despite symptom improvement highlight the complementary roles of patient-reported outcomes and objective neurophysiological assessment in characterizing the longitudinal course of CIPN.

PMID 42937720
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PubMedPharmaceutics2026-10-27

Pirenzepine Reverses Chemotherapy-Induced Peripheral Neuropathy in Mice.

Kassahun Markos M, Tayarani Alireza A, Freedman Kyle K, Gastelum Sebastian S et al.

Background/Objectives: Mitochondrial dysfunction is a common feature of many peripheral neuropathies and agents that enhance mitochondrial function have potential as pan-neuropathy therapeutics. M1 receptor (M1R) antagonists enhance mitochondrial function and reverse multiple indices of neuropathy in rodents and humans with diabetic neuropathy. The present studies extend evaluation of the M1R-selective antagonist pirenzepine to mouse models of chemotherapy-induced peripheral neuropathy (CIPN), with a primary focus on pain relief. Results: Oxaliplatin-exposed mice developed allodynia to light touch that persisted for months before resolution. Systemic pirenzepine (1 mg/kg/day) starting prior to chemotherapy did not prevent allodynia but accelerated recovery. Topical delivery (4% pirenzepine in hydrogel) to the paw, beginning after onset of allodynia, also accelerated recovery, with efficacy persisting weeks after treatment cessation and accompanied by normalization of paw responses to heat. Allodynia in paclitaxel-exposed mice was also reversed, but not prevented, by systemic or topical pirenzepine, while heat hyperalgesia and nerve conduction slowing were dose-dependently normalized. Efficacy of pirenzepine was not associated with disruption of the cytotoxicity of chemotherapeutics, as pirenzepine did not alter the LD50 of paclitaxel when applied to breast or ovarian cancer tumor lines in vitro. Tumor suppression by a cisplatin/paclitaxel cocktail given to mice seeded with OVCAR-8 ovarian cancer cells was also not impacted by pirenzepine. In contrast, pirenzepine did not prevent or reverse allodynia caused by the proteasome inhibitor bortezomib. Conclusions: These studies position pirenzepine as a novel interventional treatment against established neuropathy caused by taxanes and platin-based agents and may guide design of therapeutic regimens for future clinical studies.

PMID 42942764
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PubMedChem & bio engineering2026-10-27

Ultrasound-Activated Paclitaxel Prodrug Potentiates Suppression of Tumor Growth and Metastasis.

Ren Xitong X, Jing Qitian Q, Sun Jiali J, Kong Chaoying C et al.

Paclitaxel (PTX) remains a first-line chemotherapeutic agent, yet its therapeutic index is limited by poor tumor selectivity, nonspecific biodistribution, and systemic toxicity. Here, we report an ultrasound (US)-activated PTX prodrug nanoplatform (PTX@TBR NPs) for tumor-selective and spatiotemporally controlled PTX activation. PTX was covalently masked with a US-responsive thioketal (TK) linker and conjugated to a polymer, while riboflavin tetrabutyrate (TBR), a vitamin B2-derived sonosensitizer, was coencapsulated to enable sonochemical activation. Upon US irradiation, TBR generated singlet oxygen (1O2), which oxidized the TK linker and triggered its cleavage, thereby enabling on-demand PTX release with an efficiency of up to 68.0%. In vivo, PTX@TBR NPs+US achieved potent tumor inhibition, with a tumor suppression rate of 80.1%. Unexpectedly, this treatment also markedly suppressed distant metastasis. Transcriptomic analysis revealed broad downregulation of genes associated with redox-related metabolism, extracellular matrix remodeling, and lipid metabolic pathways, suggesting that sonochemical activation and PTX release cooperatively disrupted redox homeostasis, cytoskeletal functions, and metabolic adaptation. This study establishes a sonochemically amplified prodrug activation strategy for selective PTX chemotherapy and the inhibition of tumor growth and metastasis.

PMID 42936443
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PubMedCancers2026-10-27

Early Local Tumour Control and Feasibility of Intratumoral P-32 Microparticle Implantation in Patients with Locally Advanced Pancreatic Cancer: A Prospective Single-Center Observational Cohort Study.

Kontos Athanasios A, Riris Ioannis I, Kypraios Dimitrios D, Alexakis Nikolaos N et al.

Background: Evidence regarding EUS-guided intratumoral phosphorus-32 (P-32) microparticle implantation for locally advanced pancreatic cancer (LAPC) remains limited. This prospective pilot study evaluated its technical feasibility, preliminary safety, and early disease-control outcomes when administered in combination with gemcitabine plus nab-paclitaxel. Methods: Seventeen patients with unresectable LAPC underwent EUS-guided intratumoral P-32 microparticle implantation through a 22-gauge fine-needle aspiration needle during the fourth week of systemic chemotherapy. Intratumoral distribution was assessed using Bremsstrahlung SPECT/CT. Tumour response was evaluated according to RECIST version 1.1, and treatment-emergent adverse events were graded according to CTCAE version 4.0. The main secondary endpoint was local disease control rate at approximately 16 weeks (LDCR16w). All analyses were descriptive. Results: Implantation was technically successful in all 17 patients (100.0%; exact 95% CI, 80.5-100.0%), and SPECT/CT confirmed intratumoral distribution in every case. No implantation-related procedural complications were recorded (0/17; exact 95% CI, 0.0-19.5%). At approximately 16 weeks, CT assessment was available for 16 patients: seven had a partial response and nine had stable disease. The LDCR16w was 16/16 among evaluable patients (100.0%; exact 95% CI, 79.4-100.0%) and 16/17 in the all-treated analysis (94.1%; exact 95% CI, 71.3-99.9%). A reduction in CA19-9 of at least 50% was observed in 13/16 evaluable patients. Four patients underwent subsequent R0 resection (4/17, 23.5%; exact 95% CI, 6.8-49.9%). Adverse events were predominantly grade 1-2; one grade 3 abdominal pain event and no grade 4-5 events were recorded. Only three deaths occurred during a median OS follow-up of 15.6 months, making survival estimates exploratory and statistically immature. Conclusions: In this small, single-center pilot cohort of highly selected patients, EUS-guided intratumoral P-32 microparticle implantation combined with gemcitabine plus nab-paclitaxel was technically feasible and provided preliminary safety information. Because of the absence of a chemotherapy-only comparator, the small sample size, and the limited follow-up, the radiographic, biomarker, resection, and survival outcomes cannot be attributed specifically to P-32 implantation and should be considered descriptive and hypothesis-generating. Larger controlled studies with longer follow-up are required to determine clinical efficacy.

PMID 42938864
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PubMedBiology2026-10-27

FXR and Nrf2 Mediate the Effect of Carbon Ion Irradiation on Drug Transporter OATP1A2 in Cancer Cells.

Li Zichong Z, Zhang Ziqi Z, Li Zhixing Z, Yuan Jiajian J et al.

Organic anion transporting polypeptides (OATPs, gene symbol SLCO) are recognized as key factors in the absorption, distribution, and excretion of a wide range of endogenous and xenobiotic compounds, including many anti-neoplastic drugs. Several OATPs, such as OATP1A2, OATP1B1, and OATP1B3, have been found to be expressed in tumor cells and/or tissues, making them potential therapeutic targets for chemotherapy. Previous studies in our laboratory demonstrated that both X-ray and carbon ion irradiation induced the expression of OATP1A2 in the breast cancer cell line MCF7, resulting in enhanced killing effects of methotrexate, 5-fluorouracil, and paclitaxel following irradiation. In the present study, we evaluated the effect of carbon ions on the expression of OATP1A2, OATP1B1, and OATP1B3 in different cell lines (HCT116, HepG2, A549, and MCF7). It was found that only HepG2 and MCF7 cells exhibited an upregulation of OATP1A2 after irradiation. Mechanistically, carbon ions induced the expression of FXR and Nrf2, both of which specifically bind to the upstream regulatory sequence of SLCO1A2, the encoding gene for OATP1A2. Modulators of these transcription factors altered the induction of OATP1A2 following irradiation. Additionally, combined treatment of these modulators, methotrexate, and carbon ion irradiation resulted in a more significant killing effect on these cancer cells.

PMID 42939487
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