Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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 high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
O15105
UPID:
SMAD7_HUMAN
Alternative names:
Mothers against decapentaplegic homolog 8; SMAD family member 7
Alternative UPACC:
O15105; B7Z773; K7EQ10; O14740; Q6DK23
Background:
Mothers against decapentaplegic homolog 7 (SMAD7), also known as SMAD family member 7, plays a pivotal role in cellular processes by acting as an antagonist of TGF-beta signaling. It inhibits TGF-beta and activin signaling pathways by associating with their receptors, thus blocking SMAD2 access. SMAD7 also recruits SMURF2 to the TGF-beta receptor complex and the PPP1R15A-PP1 complex to TGFBR1, enhancing dephosphorylation and positively regulating PDPK1 kinase activity.
Therapeutic significance:
Given its crucial role in modulating TGF-beta signaling, SMAD7 is directly linked to the pathogenesis of Colorectal cancer 3. Its involvement suggests that targeting SMAD7 could offer a novel therapeutic approach for managing colorectal cancer, particularly in cases where genetic susceptibility is influenced by variants affecting this gene.