Administered via intraperitoneal injection at 5 mg/kg for 37 days, KIRA6 notably improves random glucose levels over time when compared to a vehicle, under a free-feeding regimen^[2].

Also, following 21 or 18 days post-injections, it elevates plasma insulin and C-peptide levels and sustains high levels of insulin-positive islet areas in the Akita Mouse, demonstrating its efficacy in glucose management and insulin secretion enhancement^[2].

It has an affinity for the cytoplasmic domain of KIT, with a Kd value of 10.8 μM, covering a concentration range from 1nM to 100μM^[1].

At concentrations of 10-1000 nM over a period of 72 hours, KIRA6 significantly diminishes the viability of the KIT-dependent HMC-1.1 cell line, an effect that is consistent with its ability to block KIT^[1].

Within just an hour of treatment at the same concentration range, KIRA6 lowers the signaling output of KIT, including the phosphorylation of KIT itself and its downstream effectors, PSTAT5, and phosphorylated ERK1/2^[1].

Furthermore, KIRA6 at 1 μM inhibits the decay of Ins1 mRNA resulting from IRE1α overactivation in a dose-responsive manner over 48 hours^[2].

Additionally, between 0.1 to 10μM for 72 hours, it systematically decreases the enhancement of Ins1 apoptosis triggered by 1NM-PP1 under ER stress conditions in a dose-dependent way^[2].