Bivalirudin TFA

Bivalirudin TFA is a hirudin analog and belongs to the class of specific, reversible direct thrombin inhibitors. Bivalirudin TFA exhibits high selectivity, with Ki values of 2.56 nM and 1.84 nM for α-thrombin and ζ-thrombin, respectively, and shows no significant activity against trypsin or γ-thrombin. Bivalirudin TFA also exhibits antiviral and anti-inflammatory activities. Bivalirudin TFA can be used in research on thrombotic diseases and other conditions.

Methods: HUVECs were incubated with 2 U/ml thrombin and 30 μg/ml Bivalirudin TFA for 10 minutes. Intracellular and extracellular S1P concentrations were measured by ELISA, and S1PR expression was assessed by Western blot.
Results: Thrombin significantly increased intracellular and extracellular S1P levels and S1PR2 expression; Bivalirudin TFA completely reversed the thrombin-induced increase in S1P and upregulation of S1PR2. [1]

Methods: 5- to 7-day-old C57BL/6 newborn mice were selected and anesthetized with ketamine / serazine (0.04 mL/0.02 kg), and a respiratory syncytial virus (RSV) infection model was established via intranasal instillation of 0.035 mL of a solution containing 5 × 10⁶ TCID₅₀ of RSV A2. Starting 1 day prior to viral infection, 2 mg/kg of Bivalirudin TFA was administered intravenously once every other day for 2 consecutive weeks.
Results: Following administration of Bivalirudin TFA, the inflammatory score in mouse lung tissue decreased by approximately 50%, and viral copy numbers decreased by approximately 60%. Concurrently, it corrected disorders in the coagulation-fibrinolysis system, downregulated pro-inflammatory factors and the TLR3/7 signaling pathways, and regulated the expression of inflammation-related microRNAs. No significant toxic reactions were observed in the mice during the treatment period. [2]
Methods: Wild-type (P2Y₁₂⁺/⁺) and heterozygous (P2Y₁₂⁺/⁻) mice were administered 0.2 mg/mL rhodamine 6G-labeled platelets via tail vein injection; Bivalirudin TFA (2 mg/kg) was administered intravenously 15 minutes prior to the procedure; injury was induced by treating the mesenteric artery with 12.5% FeCl₃-impregnated filter paper for 7 minutes, followed by continuous observation of thrombus formation and vascular occlusion time for 40 minutes.
Results: Bivalirudin TFA delayed vascular occlusion time in wild-type mice; in P2Y₁₂⁺/⁻ mice, Bivalirudin TFA completely blocked thrombus formation.[3]

DMSO: 80 mg/mL (34.87 mM), Sonication is recommended.

H2O: 40 mg/mL (17.43 mM), Sonication is recommended.