Role of Paclitaxel in Endometriosis: An Insight into its Safety Profile andBiomolecular Approaches

Dinesh Kumar Yadav, Mansi Aggarwal, Sapna Salar, Santosh Kumar, Mohit Singh, Vijay Kumar
In: Current Cancer Therapy Reviews · 2026 · vol. 22 · doi:10.2174/0115733947401692251204075304 · W7153443610
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Paclitaxel shows potential as an anti-endometriotic treatment by stabilizing microtubules, inhibiting angiogenesis, modulating immune responses, and impacting key signaling pathways involved in the disease.

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This review analyzes the pharmacological and biomolecular mechanisms by which paclitaxel functions as an anti-endometriotic agent. The authors describe how the drug stabilizes microtubules to inhibit cell division, suppresses angiogenesis by targeting VEGF, and modulates immune responses through pathways involving TGF-β and NF-κB. While highlighting its potential to reduce lesion vascularization and inflammation, the paper notes that further research is required to establish optimal dosing schedules and combination therapies for clinical application. This paper is centrally about endometriosis — specifically exploring paclitaxel as a therapeutic intervention for the condition.

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Abstract

Abstract: The chemotherapeutic agent paclitaxel is being presented as a promising antiendometriotic treatment. Endometriosis is a common gynecological disorder that leads to chronic peritoneal pain and infertility. It is characterized by the presence of endometrial tissue outside the uterus. In this review, the anti-endometriotic features of paclitaxel are analyzed and discussed from both pharmacological and biomolecular perspectives. Paclitaxel acts pharmacologically as a microtubule- stabilizing agent, interfering with the cell cycle and preventing the formation of new cells. It also exhibits anti-angiogenic activity, inhibiting the growth of new blood vessels and thereby reducing the vascularization of endometriotic lesions. Moreover, paclitaxel modulates immune responses, inducing an anti-inflammatory environment during endometriosis. At the biomolecular level, paclitaxel affects important signaling pathways involved in endometriotic pathogenesis. It acts on molecules such as transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-κB), and matrix metalloproteinases (MMPs), which play roles in inflammation, neovascularization, and tissue remodeling associated with endometriosis. This review provides detailed insights into the research conducted on paclitaxel, including its safety and efficacy as a treatment for endometriosis. It also examines different methods of administration, dosage schedules, and combination strategies aimed at enhancing its therapeutic effects. In conclusion, paclitaxel represents a potential therapeutic strategy for endometriosis by acting not only through its pharmacological properties but also through its biomolecular effects on the disease. Additional investigations are needed to elucidate its mechanisms of action, determine optimal treatment schedules, and explore new combination therapies to improve outcomes in patients with endometriosis.
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Abstract

The chemotherapeutic agent paclitaxel is being presented as a promising antiendometriotic treatment. Endometriosis is a common gynecological disorder that leads to chronic peritoneal pain and infertility. It is characterized by the presence of endometrial tissue outside the uterus. In this review, the anti-endometriotic features of paclitaxel are analyzed and discussed from both pharmacological and biomolecular perspectives. Paclitaxel acts pharmacologically as a microtubule- stabilizing agent, interfering with the cell cycle and preventing the formation of new cells. It also exhibits anti-angiogenic activity, inhibiting the growth of new blood vessels and thereby reducing the vascularization of endometriotic lesions. Moreover, paclitaxel modulates immune responses, inducing an anti-inflammatory environment during endometriosis. At the biomolecular level, paclitaxel affects important signaling pathways involved in endometriotic pathogenesis. It acts on molecules such as transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-κB), and matrix metalloproteinases (MMPs), which play roles in inflammation, neovascularization, and tissue remodeling associated with endometriosis. This review provides detailed insights into the research conducted on paclitaxel, including its safety and efficacy as a treatment for endometriosis. It also examines different methods of administration, dosage schedules, and combination strategies aimed at enhancing its therapeutic effects. In conclusion, paclitaxel represents a potential therapeutic strategy for endometriosis by acting not only through its pharmacological properties but also through its biomolecular effects on the disease. Additional investigations are needed to elucidate its mechanisms of action, determine optimal treatment schedules, and explore new combination therapies to improve outcomes in patients with endometriosis.

Keywords

Paclitaxel, gynecological disorders, endometriosis, apoptosis induction, angiogenesis, biomolecular. 1

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endometriosisinfertility

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