Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q16611
UPID:
BAK_HUMAN
Alternative names:
Apoptosis regulator BAK; Bcl-2-like protein 7
Alternative UPACC:
Q16611; C0H5Y7; Q6I9T6; Q92533
Background:
The Bcl-2 homologous antagonist/killer, also known as Apoptosis regulator BAK or Bcl-2-like protein 7, plays a pivotal role in the mitochondrial apoptotic process. It promotes mitochondrial outer membrane permeabilization by forming pores, releasing apoptogenic factors like cytochrome c into the cytosol. This activation of caspase 9 leads to the activation of effector caspases, crucial for cell death.
Therapeutic significance:
Understanding the role of Bcl-2 homologous antagonist/killer could open doors to potential therapeutic strategies.