CI-930 

CI-930 is a selective, orally active phosphodiesterase 3 (PDE3) inhibitor. CI-930 exerts positive inotropic and vasodilatory effects by inhibiting cAMP hydrolysis. CI-930 also regulates hemodynamics, inhibits the proliferation of coronary artery smooth muscle cells, and suppresses the proliferation of mouse splenocytes. CI-930 can be used in research related to heart failure, atherosclerosis, and asthma^{[1][2][3][4][5]}.

CI-930 (0.10-100.00 μM; 10 min) significantly inhibits soluble PDE activity in human coronary artery smooth muscle cells (HCASMCs) derived from a 32-year-old male donor, reaching a maximum inhibition rate of approximately 43% at concentrations of 10-100 μM^[3].
PDE3, the PDE isoform inhibited by CI-930 (10 μM), is expressed in both soluble and particulate fractions of quiescent HCASMC derived from 48-year-old and 58-year-old male donors, accounting for 42%-44% of total PDE activity^[3].
CI-930 (10 μM) inhibits PDE3, a PDE that is expressed in both the soluble and particulate fractions of proliferative HCASMC derived from 32-year-old and 58-year-old male donors, accounting for 44%-45% of total PDE activity^[3].
CI-930 (10-20 μM; 24-30 h) inhibits the proliferation of human coronary artery smooth muscle cells (HCASMCs) derived from specific donors: at a concentration of 10 μM, the proportion of S-phase cells from a 61-year-old female donor decreases significantly by 33%; at a concentration of 20 μM, the proportion of S-phase cells from a 58-year-old male donor also decreases significantly^[3].
CI-930 (20 μM; 15-25 h) alone does not induce a statistically significant increase in cAMP levels in HCASMC derived from male donors aged 32, 48, or 58 years^[3].
CI-930 (10 μM; 6 h) does not affect the steady-state level of IL-2 mRNA in human Jurkat leukemia T cells activated by PHA/PMA^[4].
CI-930 (1 nM-10 μM; 72 h) inhibits Concanavalin A (Con A, HY-P2149, 2.5 μg/mL)-induced proliferation of mouse splenocytes with an IC₅₀ of 4.4 μM, and results from MTT-based cell viability assays demonstrate that the inhibitory effect on cells is not caused by cell death^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

CI-930 (1-3 mg; oral administration; single dose) reaches peak plasma concentration at 0.5-3.0 h in patients with congestive heart failure, with favorable oral bioavailability^[2].
CI-930 (0.3-10 mg/kg; p.o.; twice daily) completely inhibits antigen-induced pulmonary eosinophilia and neutrophilia in Brown Norway rats, with ED₅₀ values of 0.4 mg/kg and 0.5 mg/kg for twice-daily administration, respectively, showing comparable potency^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

254.29

C₁₄H₁₄N₄O

86798-59-6

O=C1NN=C(C(C1)C)C2=CC=C(N3C=NC=C3)C=C2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Murali S, et al. Acute Hemodynamic and Hormonal Effects of CI-930, a New Phosphodiesterase Inhibitor, in Severe Congestive Heart Failure. The American Journal of Cardiology. 1987;59(15):1356-1360.

  [2]. Jafri SM, et al. Hemodynamic, Pharmacokinetic and Clinical Response to CI-930 in Congestive Heart Failure Due to Ischemic or Dilated Cardiomyopathy. The American Journal of Cardiology. 1987;59(11):1126-1130.

  [3]. Johnson-Mills K, et al. Effect of CI-930 [3-(2H)-pyridazinone-4,5-dihydro-6-[4-(1H-imidazolyl) phenyl]-5-methyl-monohydrochloride] and rolipram on human coronary artery smooth muscle cell proliferation. Biochemical pharmacology. 1998 Oct 15;56(8):1065-73.

  [4]. Lewis GM, et al. Effects of rolipram and CI-930 on IL-2 mRNA transcription in human Jurkat cells. Agents and actions. 1993;39 Spec No:C89-92.

  [5]. Howell RE, et al. Inhibition of antigen-induced pulmonary eosinophilia and neutrophilia by selective inhibitors of phosphodiesterase types 3 or 4 in Brown Norway rats. Pulmonary pharmacology. 1995;8(2-3):83-9.