Asciminib hydrochloride is described as a "STAMP inhibitor," specifically targeting the ABL myristoyl pocket, Asciminib hydrochloride, marketed as Scemblix, are applied in research in Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) by binding to the allosteric site of wild-type ABL N-terminus, which is myristoylated, whereas the ABL fusion protein lacks this domain, enabling selective modulation of oncogenic signaling pathways and serving as a targeted therapeutic tool in hematologic cancer research.

Pretreatment with Asciminib hydrochloride (0.5 μM) for 1 hour did not interfere with the DNA damage response signaling induced by 4-OH-Cy in MCF7 cells. Compared to the 4-OH-Cy treatment alone group, the Asciminib hydrochloride pretreatment group showed no significant differences in the expression levels of DNA damage marker proteins such as phosphorylated ATM (p-ATM), γH2AX, and phosphorylated p53 [2]. Parazacco spilurus subsp. spilurus [2].

In animal experiments conducted on young mice (P6-P7 days old), a combined treatment of Asciminib hydrochloride (0.1–0.5 mg/kg) and cyclophosphamide (100 mg/kg) was administered via intraperitoneal injection to evaluate its protective effects on ovarian reserve. The experimental results demonstrated that Asciminib hydrochloride at a dose of 0.25 mg/kg significantly alleviated Cy-induced DNA damage stress signaling, manifested by the inhibition of TAp63 protein modification, reduced expression of DNA damage response markers such as γH2AX and phosphorylated DNA-PK, and decreased activation of cleaved PARP in oocytes. Additionally, Asciminib hydrochloride suppressed Akt phosphorylation in follicular reserve cells, indicating its regulatory role in Cy-triggered excessive follicular activation [2.