Administered in doses of 25, 50, and 100 mg/kg, LFM-A13 displays no noticeable toxicity in rats. When given at a dose of 50 mg/kg, three times a week intraperitoneally (i.p.), it mitigates mammary tumorigenesis in mice. LFM-A13, either alone or combined with paclitaxel, significantly affects breast tumor incidence, mean tumor numbers, average tumor weight, and size in BALB/c mice. Moreover, at 50 mg/kg (i.p., three times a week), it significantly lowers the expression of PLK1, cyclin D1, CDK-4, P53, and Bcl-2, while increasing the levels of p21, IκB, Bax, and caspase 3 expression in mice^[4].

At 200 mg/kg, LFM-A13 is not associated with hematologic toxicity in rats. Doses of 10 or 50 mg/kg, administered intraperitoneally, demonstrate dose-dependent anti-tumor effects in the MMTV/Neu transgenic mouse model of breast cancer^[4].

LFM-A13 significantly reduces BTK activity, with an IC50 value of 17.2 ± 0.8 μM (equivalent to 6.2 ± 0.3 μg/mL). The inhibitory constants (Ki) of LFM-A13 against various kinases, including BTK, JAK1, JAK3, IRK, EGFR, and HCK, have been found to be 1.4 μM, 110 μM, 148 μM, 31.6 μM, 166 μM, and 214 μM, respectively. At a concentration of 200 μM, LFM-A13 notably enhances the susceptibility of ALL-1 cells to apoptosis induced by ceramide^[1].

At 100 μM, LFM-A13 impedes Epo-induced phosphorylation of various proteins including EpoR, Jak2, Btk, Stat5, and Erk1/2 in R10 cells. Additionally, at the same concentration, it hinders the auto-phosphorylation of Jak2, Tec, and Btk, but not of Lyn kinase, in COS cells^[2].

LFM-A13 exhibits potent inhibition of Plx1 with an IC50 value of 10 μM and demonstrates inhibitory activity against BRK, BMX, and FYN, with IC50 values of 267 μM, 281 μM, 240 μM, and 215 μM, respectively^[3].