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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q96S99
UPID:
PKHF1_HUMAN
Alternative names:
Lysosome-associated apoptosis-inducing protein containing PH and FYVE domains; PH and FYVE domain-containing protein 1; Phafin-1; Zinc finger FYVE domain-containing protein 15
Alternative UPACC:
Q96S99; Q96K11; Q9BUB9
Background:
Pleckstrin homology domain-containing family F member 1, also known as Phafin-1, plays a crucial role in apoptosis through the lysosomal-mitochondrial pathway. It facilitates the translocation to the lysosome, initiating lysosomal membrane permeabilization (LMP) and releasing CTSD and CTSL into the cytoplasm. This process triggers caspase-independent apoptosis by altering mitochondrial membrane permeabilization (MMP), leading to the release of PDCD8.
Therapeutic significance:
Understanding the role of Pleckstrin homology domain-containing family F member 1 could open doors to potential therapeutic strategies.