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 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.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted 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.
Our library distinguishes itself through several key aspects:
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.