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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q96MF2
UPID:
STAC3_HUMAN
Alternative names:
-
Alternative UPACC:
Q96MF2; B4DUK9; Q96HU5
Background:
SH3 and cysteine-rich domain-containing protein 3 plays a pivotal role in skeletal muscle function. It is essential for normal muscle contraction, responding to membrane depolarization by facilitating Ca(2+) release from the sarcoplasmic reticulum. This protein enhances CACNA1S channel activity and expression, crucial for muscle excitation-contraction coupling, and also modulates the calcium channel CACNA1C, slowing its inactivation rate.
Therapeutic significance:
Linked to Congenital myopathy 13, a disease characterized by muscle weakness, skeletal abnormalities, and susceptibility to malignant hyperthermia, understanding the role of SH3 and cysteine-rich domain-containing protein 3 could open doors to potential therapeutic strategies.