Studies have shown that the Bcl-2 oncogene may inhibit apoptosis in two ways; either by directly controlling the activation of caspases, or by disrupting the channels that allow proapoptotic factors from leaving the mitochondria.

Regarding the activation of caspases, there exists a gene called ced-9 in C. elegans that protects against cell death that is a part of the Bcl-2 family.

Cowpox is an orthopox virus that increases their chances of survival and infection by inhibition of specific caspases and preventing inflammatory responses and apoptosis.

Activity of XIAP is blocked by binding to DIABLO (Smac) and HTRA2 (Omi) proteins released from mitochondria after proapoptotic stimuli.

One recent example published in 2013 describes the synthesis and testing of peptidomimetics whose structure is based on the AVPI tetrapeptide IAP binding motif present in the N-terminus of mature Smac.

These peptidomimetic compounds were specifically noted for their exceptionally high level of binding to Livin, one of the important IAP family members yet to receive much attention from a drug discovery perspective.

A Phase I clinical trial determined that LCL161 is well tolerated in the treatment of patients with advanced solid tumors, though they experienced vomiting, nausea, fatigue, and loss of appetite.

[12] Xevinapant that targets the IAPs XIAP, c-IAP1, and c-IAP2 has entered phase III clinical trials for the treatment of squamous cell cancer.