Broad spectrum caspase inhibitor. Causes concentration-dependent inhibition of only TNFα-stimulated apoptosis (IC50 value 39 μM). Boc-D-FMK could significantly promote the survival of spinal motoneurons after root avulsion in neonates, but not in adult rats. Boc-D-FMK treatment reduces acute cell death after traumatic brain injury (TBI) by inhibiting mitochondrial release of cytochrome c, possibly via a mechanism involving initiator caspases-2, and -3-like, but not -8).

KEYWORS: Boc-D-FMK | supplier | Caspase inhibitor | apoptosis | TNF | boc-Aspartyl(OMe)-fluoromethylketone | BAF | traumatic | Brain injury | TBI | survival | motoneurons