GYY4137 is a Slow Releasing H2S Donor with Vasodilator and Antihypertensive Activity

Hydrogen sulfide (H2S), a recognized environmental pollutant, comes from a wide range of sources. For example, H2S will be produced in the process of plant protein corruption, the decomposition of domestic sewage and garbage, food processing (wine brewing), etc. and once the concentration is too high, it will cause significant damage of environment and human body. Besides, H2S is a ubiquitous small gaseous signaling molecule. H2S join nitric oxide and carbon monoxide in the group of signaling agents termed gasotransmitters. H2S plays an improtant role in oxidative stress processes, cell protection, signal transduction and related diseases. In the last decade, H2S shows anti-inflammatory, anti-oxidant, mitochondrial protection, anti-apoptosis, and angiogenesis effects. H2S plays a key role in the homeostasis of the cardiovascular system.

Endogenous concentrations of H2S are generally low, making it difficult to discern precise biological functions. As such, probing the physiological roles of H2S is aided by exogenous delivery of the gas in cell and animal studies. This need for an exogenous source of H2S provides a unique challenge for chemists to develop chemical tools that facilitate the study of H2S under biological conditions.

GYY4137 is a slow releasing H2S donor.

Compounds that degrade in response to a specific trigger to release H2S, termed H2S donors. GYY4137 is a slow-releasing H2S donor. Therefore, GYY4137 exhibits vasodilator and antihypertensive activity. Meanwhile, it does not influence vascular smooth muscle cell viability in culture. When given intravenously, it is effective in rats, in either the acut or chronic hypertension models. What’s more, GYY4137 also exhibits anti-inflammatory and anticancer activities.

All in all, GYY4137 is a slow releasing H2S donor with vasodilator and antihypertensive activity. In addition, it shows anti-inflammatory and anticancer effects.

Powell CR, et, al. Biochem Pharmacol. 2018 Mar;149:110-123.