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IBMX is a broad-spectrum phosphodiesterase (PDE) inhibitor, with IC50s of 6.5, 26.3 and 31.7 μM for PDE3, PDE4 and PDE5, respectively.

At 100 μM, KMUP-1 (a xanthine derivative) and IBMX are the most effective at inducing tracheal relaxation; the magnitude of the relaxation responses induced by KMUP-1 and IBMX are not significantly different[1]. IBMX (100 μM) activates renal outer medullary K+ (ROMK) channels (n=6, P<0.05) and prevents further channel activation by ANG II (n=6, P=NS) or cGMP. Of note is that pretreatment of cortical collecting duct (CCDs) isolated from high-K+ (HK)-fed rats with IBMX (100 μM) for 20 min leads to a significant increase in tubular cAMP content to 1.43±0.35 pg/mm tubule length (n=14) compare with that measured in vehicle-treated controls (0.61±0.13 pg/mm tubule length, n=12, P<0.05)[2].

IBMX, a non-selective PDE inhibitor significantly decreases the liver glycogen storage (mg/g, IBMX 22±1.5 P<0.001). IBMX potentiates insulin release and in hepatocytes and adipocytes, they increase glycogenolysis and lipolysis. In comparison with the control group, IBMX and mc5 significantly increase plasma glucose (blood glucose, mg/dl, control=141±3, IBMX=210±17 P<0.001 and mc5=191±13 P<0.01) while other test compounds (mc1, mc6, MCPIP and milrinone) do not produce significant effect (control=141±3, mc1 160±7, mc6 175±9, MCPIP 179±8 and milrinone 116±2 P>0.05) also mc2 does not change plasma glucose (control=141±3 and mc2=145±5). IBMX has the highest efficacy on increasing plasma glucose[3]. Treatments with IBMX and Apocynin significantly decrease cold-induced elevation of right ventricular (RV) systolic pressure (23.5±1.8 and 24.2±0.6 mmHg, respectively) although they do not decrease RV pressure to the warm control levels. IBMX or Apocynin significantly reduces medial layer thickness (19.0±0.9, and 16.9±0.8 μm, respectively) and increases lumen diameter (62.7±4.2, and 59.5±4.3 μm, respectively) of small PAs in cold-exposed rats[4].

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