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 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.
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 employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
P36888
UPID:
FLT3_HUMAN
Alternative names:
FL cytokine receptor; Fetal liver kinase-2; Fms-like tyrosine kinase 3; Stem cell tyrosine kinase 1
Alternative UPACC:
P36888; A0AVG9; B7ZLT7; B7ZLT8; F5H0A0; Q13414
Background:
Receptor-type tyrosine-protein kinase FLT3, also known as Fms-like tyrosine kinase 3, plays a pivotal role in the regulation of hematopoietic progenitor cells. This protein, acting as a cell-surface receptor for the cytokine FLT3LG, is crucial for the differentiation, proliferation, and survival of hematopoietic progenitor cells and dendritic cells. It promotes the phosphorylation of several key proteins, including SHC1, AKT1, and MTOR, facilitating the activation of vital signaling pathways.
Therapeutic significance:
The FLT3 protein is significantly implicated in acute myelogenous leukemia (AML), a malignant disease of bone marrow. Somatic mutations in FLT3, leading to its constitutive activation, are frequent in AML patients. These mutations disrupt normal kinase activity regulation, promoting cell proliferation and resistance to apoptosis. Understanding the role of FLT3 in AML pathogenesis opens doors to potential therapeutic strategies, focusing on targeting these mutations.