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Related Experiment Video

Updated: Jul 14, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Arterial thrombosis and thalidomide.

Mustafa Goz¹, M Nesimi Eren, Omer Cakir

¹Department of Cardiovascular Surgery, Dicle University School of Medicine, Diyarbakir, Turkey. mustafagoz@dicle.edu.tr

Journal of Thrombosis and Thrombolysis

|May 22, 2007

Summary

Thalidomide, an antiangiogenic cancer drug, can increase arterial thrombosis risk. Physicians should consider this serious vascular complication when diagnosing arterial thromboembolism in patients undergoing thalidomide treatment.

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Last Updated: Jul 14, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

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Published on: September 5, 2011

Area of Science:

Oncology
Hematology
Vascular Medicine

Background:

Thalidomide is an antiangiogenic agent utilized in cancer treatment, particularly for multiple myeloma.
Arterial emboli are frequently indicative of underlying cardiac conditions.
An increased incidence of venous thrombosis has been observed during thalidomide therapy.

Observation:

This report details two cases of arterial thrombosis in patients with multiple myeloma receiving thalidomide treatment.
These patients underwent standard emergency interventions for their condition.

Findings:

The study identified arterial thrombosis as a potential adverse effect of thalidomide in multiple myeloma patients.
Postoperative management included enoxaparin, warfarin, and aspirin (ASA).

Implications:

The findings highlight the necessity of considering thalidomide-induced arterial thrombosis in differential diagnoses.
Given the life-threatening nature of this vascular complication, discontinuing thalidomide treatment is suggested.