Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
Q9Y283
UPID:
INVS_HUMAN
Alternative names:
Inversion of embryo turning homolog; Nephrocystin-2
Alternative UPACC:
Q9Y283; A2A2Y2; Q2NKL0; Q5W0T6; Q8IVX8; Q9BRB9; Q9Y488; Q9Y498
Background:
Inversin, also known as Nephrocystin-2, plays a pivotal role in renal development and the establishment of the body's left-right axis. It functions as a molecular switch in Wnt signaling pathways, inhibiting the canonical Wnt pathway by targeting DVL1 for degradation, thus opposing the repression of tubular epithelial cell differentiation. Additionally, Inversin collaborates with NPHP1, NPHP4, and RPGRIP1L/NPHP8 in organizing apical junctions in kidney cells, although it is not strictly necessary for ciliogenesis.
Therapeutic significance:
Inversin's mutation leads to Nephronophthisis 2, an autosomal recessive disorder causing end-stage renal disease characterized by early onset, rapid progression, and symptoms like enlarged kidneys and metabolic acidosis. Understanding the role of Inversin could open doors to potential therapeutic strategies for this debilitating condition.