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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8NFM7
UPID:
I17RD_HUMAN
Alternative names:
IL17Rhom; Interleukin-17 receptor-like protein; Sef homolog
Alternative UPACC:
Q8NFM7; Q2NKP7; Q58EZ7; Q6RVF4; Q6UWI5; Q8N113; Q8NFS0; Q9UFA0
Background:
Interleukin-17 receptor D (IL17RD), also known as Sef homolog and IL17Rhom, plays a critical role in regulating several signaling pathways. It acts as a feedback inhibitor of fibroblast growth factor (FGF) mediated Ras-MAPK signaling and ERK activation. IL17RD regulates nuclear ERK signaling by preventing the nuclear translocation of activated ERK. Additionally, it may mediate JNK activation and influence apoptosis, inhibit FGF-induced FGFR1 tyrosine phosphorylation, and play a role in the specification of GnRH-secreting neurons.
Therapeutic significance:
IL17RD's involvement in Hypogonadotropic hypogonadism 18 with or without anosmia highlights its potential as a therapeutic target. Understanding the role of IL17RD could open doors to potential therapeutic strategies for treating this disorder, which is characterized by low levels of circulating gonadotropins and testosterone, and in some cases, anosmia, cleft palate, and sensorineural hearing loss.