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 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q9NSV4
UPID:
DIAP3_HUMAN
Alternative names:
Diaphanous-related formin-3; MDia2
Alternative UPACC:
Q9NSV4; A2A3B8; A2A3B9; A2A3C0; Q18P99; Q18PA0; Q18PA1; Q2KPB6; Q3ZK23; Q5JTP8; Q5T2S7; Q5XKF6; Q6MZF0; Q6NUP0; Q86VS4; Q8NAV4
Background:
Protein diaphanous homolog 3, also known as Diaphanous-related formin-3 or MDia2, plays a pivotal role in actin nucleation and elongation. It is essential for the assembly of F-actin structures, such as actin cables and stress fibers, and is crucial for processes like cytokinesis and stress fiber formation. MDia2 functions by binding to the GTP-bound form of Rho and to profilin, facilitating actin polymerization in a Rho-dependent manner. Its activity is integral to the coupling of Rho and Src tyrosine kinase signaling and the regulation of actin dynamics, including in the nucleus to drive serum-dependent SRF-MRTFA activity.
Therapeutic significance:
MDia2's involvement in auditory neuropathy, autosomal dominant 1, highlights its potential as a target for therapeutic intervention. This condition, characterized by sensorineural hearing loss and abnormal auditory brainstem response, underscores the critical role of MDia2 in auditory pathways. Understanding the role of Protein diaphanous homolog 3 could open doors to potential therapeutic strategies.