The simultaneous inhibition of other PDE subtypes, such as PDE7A, PDE3A, or PDE1B may possibly augment the therapeutic effect in LPS-induced endotoxemia, as GRMS-55, which demonstrates strong PDE1B and PDE7A and moderate PDE3A inhibitory properties, was ~5.5 more potent than (±)-LSF in inhibiting TNF-α release, while it is only ~2 times more potent as a PDE4B inhibitor. The gene discussed is PDE3A; the disease is serum lipopolysaccharide activity.