Commentary, J Pharm Sci Emerg Drugs Vol: 12 Issue: 2

A Therapeutic Approach of Vandetanib in Anaplastic Thyroid Cancer

Mabee Montamat^*

¹Department of Clinical Pharmacology, Toulouse University Hospital, Toulouse, France

*Corresponding Author: Mabee Montamat,
Department of Clinical Pharmacology, Toulouse University Hospital, Toulouse, France
E-mail: mmbee@univ.87.fr

Received date: 27 March, 2024 Manuscript No. JPSED-24-137474;

Editor assigned date: 29 March, 2024, PreQC No. JPSED-24-137474 (PQ);

Reviewed date: 12 April, 2024, QC No. JPSED-24-137474;

Revised date: 19 April, 2024, Manuscript No. JPSED-24-137474 (R);

Published date: 26 April, 2024, DOI: 10.4172/2380-9477.1000183.

Citation: Montamat M (2024) A Therapeutic Approach of Vandetanib in Anaplastic Thyroid Cancer. J Pharm Sci Emerg Drugs 12:2.

Description

Anaplastic Thyroid Cancer (ATC) is a rare and aggressive malignancy characterized by rapid tumor growth, early metastasis, and poor prognosis. Traditional treatment modalities, including surgery, radiation, and chemotherapy, have limited efficacy in advanced ATC cases. In recent years, targeted therapies have emerged as promising treatment options, aiming to exploit specific molecular alterations driving tumor growth and progression. Vandetanib, a multi-targeted tyrosine kinase inhibitor, has shown encouraging results in the management of ATC. Vandetanib is a small molecule inhibitor that targets multiple Receptor Tyrosine Kinases (RTKs), including Vascular Endothelial Growth Factor Receptor (VEGFR), Epidermal Growth Factor Receptor (EGFR), and rearranged during transfection (RET) proto-oncogene. By inhibiting these signaling pathways, vandetanib disrupts tumor angiogenesis, proliferation, and survival, thereby impeding cancer growth and metastasis. In ATC, dysregulation of RTK signaling pathways plays a pivotal role in tumor progression. Overexpression of VEGFR and EGFR promotes angiogenesis and tumor cell proliferation, while activating mutations in the RET gene drive oncogenic signaling cascades. Vandetanib exerts its antitumor effects by selectively inhibiting these aberrant signaling pathways, thereby suppressing tumor growth and metastasis.

Preclinical studies have demonstrated vandetanib's ability to inhibit tumor angiogenesis by blocking VEGFR-mediated signaling, leading to decreased microvascular density and tumor perfusion. Additionally, vandetanib inhibits EGFR signaling, which is implicated in tumor cell proliferation and survival. By targeting both angiogenesis and tumor cell proliferation, vandetanib exerts potent antitumor activity in ATC models. The clinical efficacy of vandetanib in ATC has been evaluated in several phase II clinical trials and retrospective studies. These studies have demonstrated vandetanib's ability to induce tumor regression, stabilize disease, and improve Progression-Free Survival (PFS) in patients with advanced ATC. In a phase II trial vandetanib treatment resulted in partial responses in 15% of patients and disease stabilization in an additional 39% of patients, with a median PFS of 11.1 weeks. Furthermore, vandetanib has shown synergistic effects when combined with other treatment modalities, such as radiation therapy and chemotherapy. In a study the combination of vandetanib and radiotherapy led to improved local control and prolonged survival in patients with unresectable ATC. These findings underscore the potential of vandetanib as a component of multimodal treatment regimens for ATC.

While vandetanib has demonstrated efficacy in ATC, its use is associated with a range of adverse effects, including gastrointestinal toxicity, dermatologic toxicity, cardiovascular events, and endocrine disturbances. The most common adverse reactions reported in clinical trials include diarrhea, rash, hypertension, and fatigue. Additionally, vandetanib has been associated with QT interval prolongation, potentially leading to life-threatening cardiac arrhythmias. Given the potential for serious adverse effects, careful monitoring of patients receiving vandetanib therapy is essential. Baseline cardiac assessments, including electrocardiograms and cardiac function tests, should be performed prior to initiating treatment. Regular monitoring of electrolytes, thyroid function, and blood pressure is recommended to detect and manage treatment-related toxicities promptly. Despite its promising efficacy, vandetanib monotherapy is often limited by the development of resistance and disease progression. Future study efforts should focus on elucidating mechanisms of resistance to vandetanib and identifying biomarkers predictive of treatment response. Additionally, combination therapies targeting complementary signaling pathways may overcome resistance and improve outcomes in patients with ATC. Furthermore, the identification of patient subgroups most likely to benefit from vandetanib therapy is important for optimizing treatment selection and improving patient outcomes. Molecular profiling of ATC tumors may help identify actionable mutations and guide personalized treatment strategies. Additionally, the integration of vandetanib into neoadjuvant and adjuvant treatment regimens may improve outcomes in patients with resectable ATC.

Conclusion

In conclusion, vandetanib represents a promising therapeutic approach for the management of ATC, offering significant antitumor activity and potential for improved clinical outcomes. However, its use is associated with notable adverse effects, necessitating careful patient selection and monitoring. Future study projects should focus on elucidating mechanisms of resistance, identifying predictive biomarkers, and exploring combination therapies to enhance the efficacy of vandetanib in ATC. With continued study and clinical innovation, vandetanib may emerge as a basis of treatment for this aggressive malignancy, offering hope to patients with limited therapeutic options.