BV02

BV02 is a 14-3-3 inhibitor and an antibacterial agent. BV02 enhances the cleavage of PARP and caspase-3. BV02 induces Apoptosis, Autophagy, and enhances Akt activation. BV02 has anti-B. melitensis infection and epilepsy-promoting effects. BV02 can also be used in colitis research. In Vitro:BV02 (5 μM; 24 h) induces apoptotic death and recruits cells into the sub-G₁ phase of the cell cycle in Bcr-Abl-expressing Ba/F3 cells, regardless of whether they express the wild-type Bcr-Abl or the T315I mutation^[1].
BV02 (5-50 μM; 24 h) significantly reduces the surface expression of wild-type K_2P5.1-GFP channels in HEK293T cells^[2].
BV02 (5 μM; 6 h) induces autophagy in C33A cells, with increasing the LC3-II level and decreasing the SQSTM1 level^[3].
BV02 (5 μM; 36 h) enhances Akt activation, as shown by increased phosphorylation of Akt at Thr308 and Ser473, and triggers apoptosis in SW480 cells^[4].
BV02 (20 μM; 24 h) decreases the invasion of Brucella into macrophages^[7].
In Vivo:BV02 (10 mg/kg; i.p.; once daily; 4 days during DSS-induced colitis) enhances Akt activation in the mucosa of colitic mice, increases apoptosis, and decreases cell proliferation, further shortening the colon length^[4].
BV02 (10 mg/kg; i.p.; 1 day prior to receiving PTZ) weakens the anti-epileptic effects of LV-14-3-3 and LV-HAP1 in Pentylenetetrazole (PTZ)-induced epileptic rats, increasing seizure severity, shortening latency and increasing generalized tonic clonic (GTC) values per rat^[5].
BV02 (3 mg/kg; i.p.; once daily; for 3 days starting 10 days post - infection) reduces the splenic load of B. melitensis in infected mice^[6].