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

✓ Approved

Fresenius Kabi · TUBB · Small Molecule

What is paclitaxel?

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

Drug Profile

Brand NamesPNP, Dabur, DO/NDR/02, PNP, Dabur
CompanyFresenius Kabi
Drug ClassSmall Molecule
Molecular TargetTUBB
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Fresenius Kabi

Mechanism of Action

Molecular Targets

paclitaxel acts on 1 molecular target:

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 4 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)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

Related Research Articles

PubMedCell & bioscience2026-11-13

A synergistic strategy of subacute scar tissue resection and paclitaxel-loaded fibrin scaffold grafting for spinal cord injury repair.

Liu Baoguo B, Liu Sumei S, Bai Jun J, Li Kang K et al.

Scar tissue impede axonal regeneration and hinder functional recovery after spinal cord injury. Previous studies have demonstrated excision of scar tissue during the subacute phase (particularly on day 10) not only enhances neuronal regeneration but also identifies microtubule stabilization as a key contributor to axonal regeneration in this process. Here we grafted fibrin scaffolds loaded with paclitaxel (a microtubule-stabilizing agent) immediately after scar excision during subacute stage, with the aim of stabilizing axonal microtubules. Our results showed that paclitaxel promoted functional recovery of injured rats by enhancing neuronal regeneration and axonal elongation post resecting scars in subacute stage. In paclitaxel-fibrin-grafted group, the microenvironment post injury was significantly improved. The secretion of pro-regenerative factors (laminin, BDNF and NT-3) was upregulated and the deposition of CSPG, a key inhibitory component of the scar tissue, was reduced in injured spinal tissue under paclitaxel-fibrin. Moreover, BSCB (blood spinal cord barrier) was reconstructed that alleviated the continuous infiltration of immune cells into the lesion site. Collectively, these findings suggest that the administration of paclitaxel following scar resection during subacute stage may hold significant potential in the treatment of SCI.

PMID 43021407
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PubMedAnnals of surgical treatment and research2026-11-13

Patient-derived organoid model for predicting chemotherapy response in patients with ampulla of Vater cancer: a prospective observational study.

Lee Hye Ji HJ, Park Sung Hee SH, Seo Hyung Il HI, Kim Dong Uk DU et al.

Ampulla of Vater cancer (AoVca) is a rare periampullary malignancy with a high recurrence rate after surgical resection and no established standard adjuvant chemotherapy. This study aimed to predict chemotherapy responses using patient-derived tumor organoids (PDTOs) from surgically resected tissues to identify an appropriate adjuvant chemotherapy regimen for AoVca patients. PDTOs were cultured from surgically resected AoVca tissues of 14 patients. Morphological and phenotypic consistency between PDTOs and primary tumors was verified using H&E and immunohistochemical staining for cytokeratin 7 and caudal-type homeobox 2. Drug sensitivity for 5-fluorouracil (5-FU), cisplatin, oxaliplatin, irinotecan, gemcitabine, and paclitaxel was assessed by comparing the IC50 values. PDTOs were successfully cultured from 11 of the 14 patients, with a phenotypic concordance rate of 82% (9 of 11). Ten PDTOs were successfully expanded for drug screening. These PDTOs showed universal resistance to cisplatin (n = 10), followed by irinotecan (n = 9) and paclitaxel (n = 8). Conversely, gemcitabine demonstrated the highest sensitivity, with resistance observed in only 1 PDTO, followed by 5-FU, which showed resistance in 4 cases. Gemcitabine was identified as the most responsive chemotherapeutic agent for AoVca based on PDTO drug screening. For combination therapy, oxaliplatin may be more appropriate than cisplatin. However, further clinical studies are required to validate these findings.

PMID 43022863
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PubMedCatheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions2026-11-13

Low-Dose Versus High-Dose Drug-Coated Balloon After Jetstream Atherectomy for Severely Calcified Femoropopliteal Lesions: The JUPITER Multicenter Study.

Ogata Kenji K, Nishihira Kensaku K, Nakai Michikazu M, Tokuda Takahiro T et al.

Second-generation low-dose drug-coated balloons (LD-DCBs) have shown clinical efficacy comparable to high-dose DCBs (HD-DCBs) for femoropopliteal artery (FPA) lesions. Whether paclitaxel dose density remains clinically relevant after aggressive vessel preparation with atherectomy in severely calcified FPA lesions remains uncertain. This study aimed to compare 1-year clinical outcomes of second-generation LD-DCB and HD-DCB following Jetstream atherectomy in patients with severely calcified FPA lesions. This study aimed to compare 1-year clinical outcomes of second-generation LD-DCB and HD-DCB following Jetstream atherectomy in patients with severely calcified FPA lesions. This multicenter retrospective study included 262 patients with severely calcified FPA lesions who underwent endovascular therapy with Jetstream atherectomy followed by second-generation LD-DCB (n = 175) or HD-DCB (n = 87). Propensity-score matching yielded 79 well-balanced pairs. The primary outcome was 1-year primary patency; secondary outcomes included freedom from clinically driven target-lesion revascularization (TLR), limb salvage, and overall survival. In the overall cohort before matching, 1-year primary patency was similar between second-generation LD-DCB and HD-DCB (86.8% vs. 83.1%, log-rank p = 0.578), with comparable freedom from TLR, limb salvage, and overall survival. After propensity score matching, primary patency remained similar between groups (88.5% vs. 84.9%, log-rank p = 0.588), as did freedom from TLR, limb salvage, and overall survival. Findings were consistent across calcification-related subgroups. In an exploratory Cox analysis, second-generation LD-DCB was not associated with an increased risk of restenosis compared with HD-DCB. After Jetstream atherectomy for severely calcified FPA lesions, second-generation LD-DCB and HD-DCB were associated with comparable 1-year clinical outcomes, suggesting that either strategy may be a reasonable treatment option.

PMID 43021695
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PubMedMolecular cancer2026-11-13

IGF2BP3 promotes M2 macrophage polarization and ESCC progression by increasing USP36-mediated β-catenin stabilization.

Tian Zhongxian Z, Zhou Yongjia Y, Zhao Yunpeng Y, Li Peiwei P et al.

Esophageal squamous cell carcinoma is a highly aggressive malignancy with poor prognosis that is characterized by an immunosuppressive tumor microenvironment that critically contributes to tumor progression and therapeutic resistance. RNA-binding proteins are emerging regulators of cancer biology; however, their role in shaping the tumor immune microenvironment of esophageal squamous cell carcinoma remains largely unexplored. This study aimed to investigate the function and mechanism of the RNA-binding protein IGF2BP3 in esophageal squamous cell carcinoma progression and immune modulation. Single-cell RNA sequencing datasets including esophageal squamous cell carcinoma and adjacent normal tissues were integrated to identify dysregulated RNA-binding proteins. The functional role of IGF2BP3 was evaluated using in vitro assays, organoid models, and immunocompetent and immunodeficient mouse models. RNA immunoprecipitation, polysome profiling, ubiquitination assays, and luciferase reporter assays were employed to elucidate the underlying molecular mechanisms. Immune cell infiltration was analyzed by flow cytometry, immunohistochemistry, and multiplex immunofluorescence. Virtual screening, biolayer interferometry, and molecular docking were used to identify small-molecule inhibitors of IGF2BP3. Statistical analyses included Student's t tests, one-way analysis of variance, Kaplan‒Meier survival analysis, and correlation analyses. IGF2BP3 was specifically overexpressed in epithelial tumor cells, exhibited progressively increasing expression during esophageal squamous cell carcinoma progression, and correlated with poor clinical outcomes. IGF2BP3 promoted tumor growth by activating Wnt signaling through the stabilization of β-catenin. Mechanistically, IGF2BP3 increased the translation of the deubiquitinase USP36 without altering the stability of its messenger RNA, leading to the USP36-mediated deubiquitination and stabilization of β-catenin. Activation of β-catenin signaling increased the transcription and secretion of transforming growth factor beta, which promoted the polarization of macrophages toward the immunosuppressive M2 phenotype. Pharmacological inhibition of IGF2BP3 with digoxin disrupted the IGF2BP3-USP36-β-catenin axis, reduced transforming growth factor beta production, suppressed tumor growth, and increased the efficacy of paclitaxel and PD-1 blockade in preclinical models. This study identifies IGF2BP3 as a critical posttranscriptional regulator that links oncogenic signaling to immune suppression in esophageal squamous cell carcinoma. Targeting IGF2BP3 represents a promising therapeutic strategy to remodel the tumor microenvironment and improve responses to chemotherapy and immunotherapy.

PMID 43021338
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PubMedEpigenomics2026-11-12

METTL1-mediated tRNA m7G methylome remodeling drives macrophage M2 polarization and paclitaxel resistance in cervical cancer.

Yi Hanjie H, Han Yongqing Y, Wang Xia X, Li Qing Q et al.

Chemoresistance remains a major obstacle to effective treatment of cervical cancer. Emerging evidence suggests that RNA methylation plays a crucial role in shaping tumor-immune interactions. However, the role of METTL1-mediated tRNA m7G modification in macrophage polarization and drug resistance is largely unexplored. Functional effects of METTL1 were examined through gain- and loss-of-function experiments in vitro, and xenograft models. Trac-seq was performed to characterize tRNA m7G remodeling. METTL1 was significantly upregulated in cervical cancer tissues and was predominantly expressed in macrophages within paclitaxel-resistant tumor samples. METTL1 overexpression promoted M2-like macrophage polarization, whereas METTL1 knockdown produced the opposite effects. METTL1-overexpressing macrophages enhanced cervical cancer cell proliferation and attenuated paclitaxel-induced cytotoxicity in vitro and promoted tumor growth under paclitaxel treatment in vivo. Trac-seq revealed extensive remodeling of tRNA m7G methylome following METTL1 overexpression, with selective hypo- and hypermethylation across distinct tRNAs. Single-cell analysis identified reduced NLRP3 expression in METTL1-high macrophages, and METTL1 overexpression suppressed pyroptosis, whereas WDR4 depletion produced opposing effects and partially attenuated METTL1-mediated changes in macrophages. METTL1 promotes M2-like macrophage polarization and paclitaxel resistance in cervical cancer, accompanied by extensive remodeling of the tRNA m7G methylome, providing a potential epitranscriptomic link between macrophage reprogramming and chemoresistance.

PMID 43016285
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PubMedFrontiers in oncology2026-11-12

Case Report: Brain metastasis from cervical cancer treated with multimodal therapy.

Liu Juntong J, Wen Yunxin Y, Peng Yuyi Y, Zhang Huatang H et al.

Brain metastasis from cervical cancer is exceptionally rare, occurring in 0.4%-2.3% of cases and portending a dismal prognosis, with a median survival of approximately 6.2 months after the diagnosis of brain metastasis. Here we report a 51-year-old woman initially diagnosed with stage IVB papillary squamous cell carcinoma of the cervix. Initial therapy combining albumin-bound paclitaxel, cisplatin, and the anti-PD-1 antibody tislelizumab, followed by pelvic radiotherapy, achieved durable disease control. Nineteen months after diagnosis, she developed memory decline and headache; brain MRI disclosed large, radiologically presumed metastases in the right frontal-basal ganglia and left occipital lobe. As the patient declined surgery, she received bevacizumab, paclitaxel, and the bispecific PD-1/CTLA-4 antibody iparomlimab/tuvonralimab (Ipa-tuv), together with focal fractionated VMAT (3900 cGy in 13 fractions) to the brain lesions. The dominant lesion decreased from 66 × 54 × 58 mm to 45 × 54 × 49 mm, and neurological symptoms resolved. Because of financial constraints, Ipa-tuv was later discontinued and she was maintained on bevacizumab plus chemotherapy. At the last two imaging time points, an increase in perilesional edema was noted; no clear size-based progression was demonstrated, although progression, radiation-related change, and treatment-related necrosis could not be excluded. At the last radiological assessment (January 25, 2026), the overall survival was approximately 34 months from the initial diagnosis and approximately 15 months since the diagnosis of radiologically presumed brain metastases. This case describes the observed response to a multimodal treatment strategy, although the contribution of any single component cannot be determined, and further prospective trials are warranted.

PMID 43016508
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