K134 is an inhibitor of phosphodiesterase 3. The IC50s of K134 for PDE3A, PDE3B, PDE5, PDE2 and PDE4 are 0.1, 0.28, 12.1, >300 and >300 μM, respectively.

K134 (K-134) inhibits rat platelet aggregation caused by collagen and ADP in a dose-dependent manner in vitro. K134 also inhibits mouse platelet aggregation induced by collagen and ADP in a dose-dependent manner (IC50s: 5.5 μM and 6.7 μM, respectively), in vitro experiments. The half-maximal (50%) inhibitory concentration (IC50) values of K134 are 2.5 μM and 3.2 μM, respectively [1].

K134 obviously decreases the incidence of occlusive shunt thrombi at doses above 10 mg/kg (half-maximal effective dose: ED50=11 mg/kg). The effects of PDE3 inhibitors on thrombus formation are also investigated in an arteriovenous shunt model in rats. The plasma concentration of K134 is 0.43±0.08 μM (Cmax) at a dose of 10 mg/kg. K134 obviously prolongs middle cerebral artery (MCA) occlusion time at doses >10 mg/kg and decreases cerebral infarct size at 30 mg/kg in the stroke model (n?=?12, 87.5±5.6 vs. 126.8±7.5 mm3, P<0.01), indicating its potent antithrombotic effect. The overall bleeding risk of K134 is assessed in general in mice. K134 (30 mg/kg; Single oral administration) does not prolong bleeding time at a dose of compared to control (106±5 vs. 110±5 s, not significant). A sufficiently high enough plasma concentration of K134 (13.6±2.3 μM) is detected to inhibit platelet aggregation at 10 min after single administration in mice at a dose of 30 mg/kg, which is the same time point as the above test of bleeding time [1].

189362-06-9

C22H29N3O4

399.48

OPC33509;K134

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years