Monomethyl auristatin E and paclitaxel use different mechanisms to alter intracellular calcium signaling.

Antibody-drug conjugates (ADCs) are a promising class of targeted cancer therapies that deliver cytotoxic agents to cancer cells. Although designed to reduce side effects, ADCs utilizing a microtubule-targeting agent, exemplified by monomethyl auristatin E (MMAE), as the drug cargo, frequently induce chemotherapy-induced peripheral neuropathy (CIPN) at rates comparable to taxanes like paclitaxel (PTX). Despite their clinical success, ADC-associated neurotoxicity remains a significant challenge, necessitating a deeper mechanistic understanding and potential neuroprotective strategies.

Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury.

: Repeat low-level blast exposure has emerged as a significant concern for military populations exposed to explosive events. Blast-Related Traumatic Brain Injury (bTBI) is a unique form of brain trauma with poorly understood molecular mechanisms. Loss of calcium homeostasis has emerged as a mediator of early neuronal dysfunction after blast injury.