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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

PubMedGynecologic oncology reports2026-09-20

Temozolomide and olaparib for the treatment of an ARID1A-mutated uterine carcinosarcoma: A case report.

Liu Chrissy C, Abozenah Yasmin Y, Rutherford Thomas J TJ, Andikyan Vaagn V et al.

Pathogenic ARID1A mutations are common in uterine carcinosarcoma (UCS) and may confer vulnerability to the combination of temozolomide (TMZ) and a poly (ADP-ribose) polymerase inhibitor (PARPi) through synthetic lethality. Clinical experience with this regimen in gynecologic cancers is limited and has not been reported in UCS. A 54-year-old woman with stage IIIB UCS harboring a pathogenic ARID1A mutation developed isolated cavitating pulmonary metastases shortly after completing chemoradiation, surgery, and adjuvant carboplatin/paclitaxel with dostarlimab. She received off-label temozolomide and olaparib on a 21-day cycle. After four cycles, she achieved a complete radiographic response and has remained in clinical remission with normal CA-125 and negative circulating tumor DNA. Treatment was complicated by reversible grade 3-4 thrombocytopenia. This case suggests that TMZ/PARPi may produce durable responses in biomarker-selected UCS and supports prospective evaluation of this regimen in genomically characterized, ARID1A-defined gynecologic cancers.

PMID 42763538
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PubMedClinical colorectal cancer2026-09-19

A Phase I Study of Nab-Paclitaxel, Gemcitabine and AZD1775 for Treatment of Metastatic Adenocarcinoma of the Pancreas: ECOG-ACRIN EA2131.

Eads Jennifer R JR, Lee Ju-Whei JW, Chee Cheng E CE, Meropol Neal J NJ et al.

Pancreatic adenocarcinoma is a devastating disease for which there are limited treatment options. Identification of novel agents to enhance the activity of existing regimens is much needed. We hypothesized that the disruption of the DNA damage response by AZD1775, an oral Wee1 inhibitor, added to the nab-paclitaxel and gemcitabine chemotherapy backbone would be safe and effective. A phase I trial to evaluate the dose-limiting toxicities and maximum tolerated dose of AZD1775 in combination with nab-paclitaxel and gemcitabine was conducted in patients with metastatic or locally advanced, unresectable pancreatic adenocarcinoma (NCT02194829). A total of 7 patients received nab-paclitaxel and gemcitabine intravenously on days 1, 8, and 15 of a 28-day treatment cycle, along with AZD1775 by mouth on days 1, 2, 8, 9, 15, and 16. Toxicities were assessed using CTCAE version 4 criteria. Two patients were treated at the initial dose level of nab-paclitaxel, gemcitabine, and AZD1775, and both experienced dose-limiting toxicities (dehydration, elevated bilirubin, oral mucositis, increased AST, and Candida intertrigo). Under a revised study design, 5 patients were treated, and 2 of them also developed dose-limiting toxicities (anemia, thrombocytopenia, neutropenia, hyponatremia, and febrile neutropenia). Progression-free survival (PFS) and overall survival (OS) among these 7 patients were 5.26 months (95% confidence interval [CI] [2.73, 12.16]) and 5.29 months (95% CI [2.73, 20.17]), respectively. The combination of nab-paclitaxel, gemcitabine, and AZD1775 was determined to be too toxic when administered in patients with metastatic or locally advanced, unresectable pancreatic adenocarcinoma.

PMID 42763280
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PubMedBrain, behavior, & immunity - health2026-09-19

T cell-dependent modulation of pain behaviors in a rat model of recurring paclitaxel-induced peripheral neuropathy.

Bakare Ahmed Olalekan AO, Austin Paul J PJ, Curatolo Michele M, Stephens Kimberly E KE et al.

Advances in preventing or treating chemotherapy-induced peripheral neuropathy (CIPN) have been limited because most preclinical models do not capture the repeated cycles of chemotherapy exposure common in clinical practice. Consequently, the mechanisms driving CIPN across successive chemotherapy cycles remain incompletely understood. Here, we investigated the contribution of T cells to recurrent paclitaxel (PTX)-induced peripheral neuropathy (PIPN) using homozygous RNU rats (T cell-deficient) and heterozygous littermates (T cell-competent). PTX (8 mg/kg total) was administered intraperitoneally over two treatment cycles to model repeated chemotherapy exposure and its effects on neuropathic pain. Pain sensitivity testing with von Frey filaments, dry-ice, and acetone assays revealed distinct pain phenotypes across cycles. Mechanical allodynia was transient, resolving between cycles, with a smaller reduction in mechanical withdrawal threshold during the observed period following the second cycle, independent of T cell status. In contrast, cold hyperalgesia persisted in T cell-competent rats but did not reach significance in T cell-deficient rats, whereas cold allodynia was transient, resolving between cycles, and developed exclusively in T cell-competent rats. T cell frequencies in peripheral neural tissues were higher after the second PTX cycle than after the first, while natural killer cell populations showed T cell- and tissue-specific differences across cycles. CD163+ M2-like macrophage abundance remained relatively stable across cycles in peripheral neural tissues, whereas CD206+ M2-like and CD86+ M1 macrophage populations showed tissue-specific changes. Repeated exposure also reduced satellite glial cell gliosis and was associated with gene-specific transcriptional changes, including T cell-dependent effects linked to immune-glial signaling in the sciatic nerve. Together, these findings indicate that repeated paclitaxel exposure produces distinct transient and persistent pain phenotypes and engages tissue-specific neuroimmune mechanisms, with T cells selectively shaping sensory outcomes in PIPN.

PMID 42761819
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PubMedJournal of chromatography. B, Analytical technologies in the biomedical and life sciences2026-09-19

Unveiling the in vivo fate of albumin-bound paclitaxel nanoparticles by UPLC-MS/MS based on free, protein bound, and total drug.

Miao Yu Y, Zhang Ning N, Zhang Guolei G, Ye Runyi R et al.

Paclitaxel (PTX) has poor water solubility. Traditional formulations requiring solubilizers can induce allergic reactions and disrupt pharmacokinetics. Albumin-bound PTX nanoparticles (PTX-Nab) provide a solvent-free nanodelivery system that enhances solubility and may enable receptor-mediated tumor targeting. Comprehensive studies comparing its systemic pharmacokinetics, particularly the dynamics of free versus total drug concentrations and excretion routes, are still lacking. This study established a sensitive ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method coupled with ultrafiltration to simultaneously quantify free, protein-bound, and total PTX in rats following intravenous administration of PTX-Nab and conventional PTX-injection. PTX-Nab profoundly altered the pharmacokinetic profile. Despite a double dose (10 mg/kg), it exhibited significantly lower dose-normalized initial concentration (C0/Dose) and systemic exposure (AUC/Dose) along with a longer elimination half-life (t1/2) than the injection group (5 mg/kg), indicating sustained drug release and prolonged circulation. Tissue distribution showed preferential accumulation of PTX-Nab in lung and spleen.  Excretion studies showed a change in the primary excretion route. Unlike the renal-excreted conventional injection, PTX-Nab enhanced fecal excretion (56.14% versus 16.50%). These findings elucidate how the albumin carrier reshapes the in vivo fate of PTX through sustained release, tissue targeting, and clearance redirection, providing crucial pharmacokinetic evidence for its clinical application and future nanocarrier development.

PMID 42762797
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PubMedFrontiers in oncology2026-09-19

Case Report: Neuroendocrine-low POU2F3-positive small cell lung cancer presenting as a diagnostically unstable thoracic malignancy.

Ma Ying Y, Chen Wenlong W, Guo Fangfei F, Han Songchen S

POU2F3-positive small cell lung cancer (SCLC) is a tuft-cell-like, neuroendocrine-low subtype that may be difficult to classify in small specimens. We report a 61-year-old man with a left-upper-lobe high-grade thoracic malignancy radiographically staged as cT2aN2bM0. The cN2b component was imaging-based, and inflammatory nodal uptake could not be fully excluded because of previous pulmonary tuberculosis. Bronchoscopic biopsy from the opening of the left-upper-lobe lingular bronchus and CT-guided core biopsy of the primary mass sampled anatomically distinct sites within the same tumor process. Both samples showed morphology favoring small cell carcinoma, but conventional neuroendocrine markers were absent, focal, or weak and the immunophenotype varied by specimen and review. Morphology and specimen-specific immunophenotyping, integrated with specialist consultation, supported small cell carcinoma; POU2F3 nuclear positivity supported subtype assignment and explained the neuroendocrine-low phenotype rather than establishing the diagnosis alone. Nab-paclitaxel, cisplatin, and pembrolizumab were used as an empiric bridge strategy while histologic classification remained unresolved. After four induction cycles and marked radiographic response, a highly selected multidisciplinary decision led to surgery for pathologic assessment. Resection showed pCR/ypT0N0M0, followed by four postoperative cycles of TP plus pembrolizumab. On May 26, 2026, surveillance imaging showed no recurrence or metastasis; no ctDNA was detected on subsequent plasma testing, which was interpreted as MRD-negative. This single case is illustrative and does not define a treatment standard, a POU2F3-specific response phenotype, or evidence of cure.

PMID 42760987
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PubMedInternational journal of clinical oncology2026-09-19

Association between ABCB1 genetic polymorphisms with treatment outcomes in patients with metastatic pancreatic cancer.

Hatori Masahiro M, Arafune Rei R, Suzuki Kenichi K, Yokokawa Takashi T et al.

Gemcitabine plus nanoparticle albumin-bound-paclitaxel (GnP) therapy cause sometimes severe neutropenia in all the treatment period, which was reported to association with overall survival (OS). However, the relationship between pharmacokinetics-related genetic polymorphisms and both OS and early severe neutropenia in patients with metastatic pancreatic cancer receiving GnP therapy has not been adequately examined. We aimed to examine the associations between pharmacokinetic genetic polymorphisms involved in GnP, early severe neutropenia, and OS in Japanese patients with metastatic pancreatic cancer treated with GnP as first-line chemotherapy. This multicenter prospective observational study enrolled 122 patients with metastatic pancreatic cancer who received GnP therapy. Twenty-two genetic polymorphisms related pharmacokinetics of GnP including ABCB1 were analyzed. Multivariable logistic regression and time-dependent Cox proportional hazards models were used to evaluate associations between these genotypes and early severe neutropenia up to day 14 and OS after applied inverse probability of treatment weighting. The significance level was set at 5%. Patients who developed early severe neutropenia had significantly longer median OS (523 vs. 249 days; adjusted hazard ratio [HR], 0.47; 95% confidence interval, 0.26-0.85; p = 0.012). The combination of ABCB1 rs2032582 non-GG and rs1045642 non-CC were significantly associated with severe neutropenia (adjusted odds ratio, 2.75; p = 0.020) and OS (adjusted HR, 0.56; p = 0.017). Early-onset severe neutropenia could be associated with prolonged OS in patients with metastatic pancreatic cancer treated with GnP. The combination of ABCB1 rs2032582 non-GG and rs1045642 non-CC may help predict the risk of severe neutropenia and OS. UMIN 000012720.

PMID 42762424
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