Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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 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 employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9BQL6
UPID:
FERM1_HUMAN
Alternative names:
Kindlerin; Kindlin syndrome protein; Kindlin-1; Unc-112-related protein 1
Alternative UPACC:
Q9BQL6; D3DW10; Q8IX34; Q8IYH2; Q9NWM2; Q9NXQ3
Background:
Fermitin family homolog 1, known by alternative names such as Kindlerin, Kindlin syndrome protein, and Kindlin-1, plays a crucial role in cell adhesion and integrin activation. It is essential for keratinocyte proliferation, polarization, and migration, facilitating normal wound healing processes. This protein's interaction with talin enhances ITGA2B activation, contributing to cell shape and adhesion to extracellular matrices like fibronectin and laminin.
Therapeutic significance:
Kindler syndrome, a skin disorder characterized by blistering, photosensitivity, and increased cancer risk, is linked to mutations in the FERMT1 gene encoding Fermitin family homolog 1. Understanding the role of Fermitin family homolog 1 could open doors to potential therapeutic strategies, offering hope for targeted treatments for Kindler syndrome and related conditions.