cbfβ-runx1

Ro5-3335 (CBFβ-Runx1 inhibitor II) is core binding factor (CBF) inhibitor; preferentially kills human leukemia cell lines with CBF fusion proteins (IC50 = 1.1 μM). Ro5-3335 represses RUNX1/CBFβ-dependent transactivation in reporter assays and inhibits transcriptional regulation by RUNX1 and CBFβ. Ro5-3335 also reduces the leukemia burden in a mouse model. Attenuates RUNX1-dependent hematopoiesis in zebrafish embryos. It also is a Tat antagonist and inhibits HIV-1 replication in vitro.

Kartogenin (KGN) is an activator of the smad4/smad5 pathway, and promotes the selective differentiation of multipotent mesenchymal stem cells into chondrocytes.

CBFβ Inhibitor (5-Ethyl-4-(4-methoxy-phenyl)-thiazol-2-ylamine) is a cell-permeable CBFβ inhibitor and inhibits its association with Runx1.

NSC-140873 is the RUNX1-CBFβ interaction inhibitor.

AI-10-49 is a selective inhibitor of the binding of CBFβ-SMMHC to RUNX1 with IC50 of 260 nM.

WUN40378 is compound first reported in PCT Int. Appl. (2019), WO 201909959, in which it was described as CBFβ-RUNX1 inhibitor. WUN40378 is very similar to Ro 5-3335 but with an F instead of Cl. WUN40378 is also analog of Ro 24-7429. This product has no formal name at the moment. For the convenience of communication, a temporary code name was therefore proposed according to MedKoo Chemical Nomenclature (see web page: https://www.medkoo.com/page/naming).

Kartogenin (KGN) sodium acts as an inducer of chondrogenic tissue formation (EC 50: 100 nM). It promotes chondrogenesis by binding to fibrin A, disrupting its interaction with the transcription factor core binding factor beta subunit (CBFβ), and modulating the CBFβ-RUNX1 transcriptional program. Additionally, Kartogenin sodium aids tendon-bone junction (TBJ) wound healing by stimulating collagen synthesis. It is extensively utilized in cell-free therapies for cartilage regeneration and protection, tendon-bone healing, wound healing, and limb development. The compound is also vital for cartilage repair, coordinating limb development, and osteoarthritis (OA) research [1] [2] [3] [4].