Tirofiban（MK383） hydrochloride monohydrate is a non-peptide glycoprotein IIb/IIIa antagonist.

ADP:70 ng/ml, Collagen:200 ng/ml, Thrombin:5,000 ng/ml

METHODS: HUVEC cells were cultured in 24-well plates. The effect of 0.12, 0.25, 1, and 3 μg/ml Tirofiban（MK383） hydrochloride monohydrate on cell growth was determined using cell counting method. Cells were harvested after 72 h and counted using trypan blue.
RESULTS At a concentration of 0.25 μg/ml, the number of cells in the Tirofiban group increased compared with the group without Tirofiban. Tirofiban can induce the growth of HUVEC cells. [1]
METHODS:HUVEC cells were treated with Tirofiban (1mg/mL) at different time points (0, 1, 2, 3, 4 and 5 hours).
RESULTS After Tirofiban treatment, the amount of VEGF produced by HUVECs gradually increased and reached a peak at 2 hours. [2]

METHODS: Rats were intravenously injected with Tirofiban（MK383） hydrochloride monohydrate (200 μg/kg). Fifteen minutes later, the left renal pedicle was occluded with a small microvascular forceps, and renal ischemia was induced for 45 minutes. Blood was collected 24 hours after reperfusion, and the left kidney was taken for analysis.
RESULTS Tirofiban can reduce SCR and BUN levels in I/R-injured kidneys, improve renal tissue pathological changes, and reduce ROS generation, cell apoptosis, and leukocyte infiltration. [3]
METHODS: 60 μg/kg Tirofiban was administered as an intravenous bolus injection through the tail vein of rats 30 minutes before reperfusion, and the cardiac function of the rats was observed.
RESULTS Tirofiban improved cardiac function, with lower left ventricular end-systolic blood pressure levels, left ventricular pressure maximum change rates of increase and decrease, heart rate, and left ventricular end-diastolic pressure levels. [4]