Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced activity, selectivity, and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We utilise our cutting-edge, exclusive workflow to develop focused 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 stands out due to several important features:
partner
Reaxense
upacc
P02538
UPID:
K2C6A_HUMAN
Alternative names:
Cytokeratin-6A; Cytokeratin-6D; Keratin-6A; Type-II keratin Kb6
Alternative UPACC:
P02538; A4QPC1; P48667; Q08AR4; Q6NT67; Q96CL4
Background:
Keratin, type II cytoskeletal 6A, known by alternative names such as Cytokeratin-6A, Cytokeratin-6D, Keratin-6A, and Type-II keratin Kb6, plays a pivotal role in epidermal integrity and repair. This protein is specifically involved in wound healing, activating follicular keratinocytes post-injury, and regulating epithelial migration by inhibiting SRC activity during wound repair.
Therapeutic significance:
Keratin, type II cytoskeletal 6A's mutation is linked to Pachyonychia congenita 3, a genodermatosis causing nail dystrophy, plantar keratoderma, oral leukokeratosis, and epidermal cysts. Understanding its role could lead to targeted therapies for this debilitating condition.