Thiorphan is the first potent synthetic inhibitor of enkephalinase. Thiorphan displays antinociceptive activity after systemic administration. Thiorphan also inhibits to a lesser extent the widely distributed angiotensin-converting enzyme, a carboxydipeptidase implicated in blood pressure regulation. Thiorphan failed to potentiate allergen-induced airway responses in asthma. Thiorphan significantly reduced the castor oil-induced diarrhea in rats when administered intravenously but not when administered intracerebroventricularly. Racecadotril, via its active metabolite thiorphan, was consistently effective in animal models and patients with various forms of acute diarrhea by inhibiting pathologic (but not basal) secretion from the gut without changing gastro-intestinal transit time or motility.

Indolapril (CI-907) is a new orally active prodrug of nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor, developed by Warner-Lambert/Parke-Davis Pharmaceutical Research for treating hypertension. Indolapril is epimer of trandolapril, well-known ACE inhibitor currently in the market for hypertension treatment. Indolapril (Monoester form) and it’s active component (diacid form) produced concentration related ACE inhibition in guinea-pig serum (IC50 for monoester -- 0.1 mkM and for diacid -- 2.6 nM). In isolated rabbit aortic rings and in rat and dog autonomic studies, Indolapril is highly specific in suppressing the contractile or pressor responses to angiotensin I. In two-kidney, one-clip Goldblatt hypertensive rats, single daily doses (0.03-30 mg/kg p.o.) produced dose-dependent decreases in blood pressure; 3 mg/kg lowered blood pressure to normotensive levels. In the spontaneously hypertensive rat, subacute administration of Indolapril produced the same decrease in blood pressure as that obtained in the renal hypertensive rat. In diuretic-pretreated renal hypertensive dogs, 10 mg/kg normalized blood pressure. For equivalent drops in blood pressure, heart rate increases were less in Indolapril than in enalapril-treated renal hypertensive dogs. No side effects were observed with CI-907 in any of the conscious animals. The antihypertensive response to Indolapril (0.03-1.0 mg/kg p.o.) was found to correlate with inhibition of vascular tissue ACE, but not plasma or brain ACE in two-kidney, one-clip renal hypertensive rats.

Verticine is a steroidal alkaloid compound extracted from the Fritillaria species of medicinal plants. Verticine was not only able to block the Nav1.7 ion channel but also preferably inhibited the Kv1.3 ion channel. It inhibits the production of inflammatory cytokines induced by LPS through blocking MAPKs and NF-κB signaling pathways. Verticine inhibited the hERG peak tail currents in a concentration dependent manner. Verticine exhibits anti-inflammatory, antitussive, antihypertensive and pain suppression properties.

(±)-3A,7A-di-epi-Perindopril is a mixture of two isomers (S, RR, SS) and (R, SS, RR) each of which is an isomer of the antihypertensive drug perindopril. The first of which has the same activity as the compound while the second one is almost inactive.

(±)-2,3A-di-epi-Perindopril is a mixture of two isomers (S, SR, RR) and (R, RS, SS) which are both inactive epimers of the antihypertensive drug perindopril, although the (R, RS, SS) isomer possesses better activity.

(3AR)-3A-epi-Perindopril is an epimer (S, RS, SS) of the drug perindopril which is commonly used to treat high blood pressure, hypertension, heart failure, or stable coronary artery disease. This epimer possesses equal activity with the parent compound, perindopril.

(7AR)-7A-epi-Perindopril is an epimer (S, SR, SS) of the drug perindopril which is commonly used to treat high blood pressure, hypertension, heart failure, or stable coronary artery disease. This epimer possesses equal activity with the perindopril.

Spirapril (Renormax) is an ACE inhibitor antihypertensive drug used to treat hypertension. Spiraprilat, the active metabolite of spirapril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Spiraprilat may also act on kininase II, an enzyme identical to ACE that degrades the vasodilator bradykinin.