h2s

H2S Donor 5a is a H2S donor that could mimic the slow and continuous H(2)S generation process.

H2S scavenger 1 triflate (Compound 7b) serves as a selective H2S depleting agent, particularly against glutathione. This compound impedes the formation of bacterial biofilms and enhances the sensitivity of Staphylococcus aureus to gentamicin or photosensitizers by depleting H2S.

Difluorinated H2S probe 1 is a fluorescent probe for hydrogen sulfide (H2S).1It selectively fluoresces in the presence of H2S over Zn2+, Fe3+, S2O32-, ClO-, SO32-, H2O2, NO2-, cysteine (Cys), homocysteine (Hcy), and glutathione (GSH) when used at a concentration of 1 μM. Difluorinated H2S probe 1 displays excitation/emission maxima of 365/450 nm, respectively. 1.Zhang, J., Gao, Y., Kang, X., et al.o,o-Difluorination of aromatic azide yields a fast-response fluorescent probe for H2S detection and for improved bioorthogonal reactionsOrg. Biomol. Chem.15(19)4212-4217(2017)

H2S probe 1 (compound 1NND), a derivative of nitrobenzofurazan (NBD), exhibits antitumor activity. It demonstrates cytotoxicity towards human pancreatic cancer cells, MIA PaCa-2, with an IC50 value of 77.9 nM, and shows high affinity for the human telomeric G-quadruplex with a Kd of 1.72 μM. H2S probe 1 is utilized for cancer research.

GYY4137 (GYY 4137 morpholine salt) is a novel water-soluble and slow releasing H2S donor with vasodilator and antihypertensive activity. GYY4137 also exhibits anti-inflammatory and anticancer activity.

L-Cysteine hydrochloride (L-Cysteine HCl) is a conditionally essential amino acid,L-Cysteine hydrochloride suppresses ghrelin and reduces appetite in rodents and humans

L-Cysteine hydrochloride hydrate (L-Cysteine hydrochloride monohydrate) is a conditionally essential amino acid, which acts as a precursor for biologically active molecules such as hydrogen sulphide (H2S), taurine and glutathione. L-Cysteine hydrochloride hydrate suppresses ghrelin and reduces appetite in rodents and humans.

Anethole trithione (Anetholtrithion) is a bile secretion-stimulating drug that restores salivation and relieves the discomfort of dry mouth in chemotherapy-induced xerostomia.

Sodium Hydrogen Sulfide (hydrate) is, like nitric oxide, an important gaseous mediator that has significant effects on the immunological, neurological, cardiovascular and pulmonary systems of mammals. Sodium Hydrogen Sulfide (hydrate) is an H2S donor commonly used in cellular and whole animal experimental systems. For example, it has been used to suggest that H2S promotes neutrophil migration, reduces airway inflammation, and protects neurites, heart, and intestine from chemical or ischemic-reperfusion damage.

D-Cysteine, the D-isomer of cysteine, is a powerful inhibitor of E. coli growth and is mediated by D-amino acid oxidase to produce H2S, serving as a neuroprotective agent against cerebellar ataxia. Additionally, D-cysteine can inhibit the growth and cariogenicity of a two-species biofilm formed by Streptococcus mutans and Streptococcus hemoglobin.

MitoA is a ratiometric mass spectrometry probe that can be used for assessing changes in H2S within mitochondria in vivo. MitoA contains a triphenylphosphonium cation component that drives its accumulation in mitochondria where its aryl azide moiety selectively reacts with H2S to produce an amine product, MitoN. Quantifying the MitoN/MitoA ratio by LC-MS/MS reflects the mitochondrial matrix H2S concentration. In a mouse model of acute myocardial infarction with MitoA administered prior to ischemia, the MitoN/MitoA ratio is increased only in the region of ischemia.

Desmethylanethol trithione (ADT-OH) is a derivative of anethole dithiolethione (ADT) and synthetic hydrogen sulfide (H2S) donor. In the in vitro glucose-oxygen deprivation (OGD) model, Desmethylanethol trithione markedly attenuated tPA-enhanced Akt activation and VEGF expression in brain microvascular endothelial cells. Finally, Desmethylanethol trithione improved functional outcomes in mice subjected to MCAO and tPA infusion. H2S donors reduced tPA-induced cerebral hemorrhage by possibly inhibiting the Akt-VEGF-MMP9 cascade. Administration of H2S donors has potential as a novel modality to improve the safety of tPA following the stroke.

HTS07545 is a potent sulfide:quinone oxidoreductase inhibitor (IC50: 30 nM) that reduces the rate of hydrogen sulfide (H2S) decomposition and has been used in heart failure studies.

FW1256 is a phenyl analog. It also a slow-releasing hydrogen sulfide (H2S) donor. FW1256 inhibits NF-κB activity and causes cell apoptosis. FW1256 shows potent anti-inflammatory effects. It also has the potential for cancer and cardiovascular disease trea

Anti-inflammatory agent 89 (5c) exhibits significant effects in alleviating pulmonary inflammation and restoring lung structure through its corticosteroid and H2S releasing components, making it a promising candidate for asthma research. It inhibits all characteristics of asthma.

AP39 Prodrug 1 (Compound M1) is a mitochondria-targeted H2S prodrug. In hepatocytes, it induces ROS-dependent mild mitochondrial uncoupling, activates mitochondria-associated AMPK, and inhibits Palmitic acid (PA)-induced lipid accumulation.

SPRC is a novel synthetic molecule exerting antioxidant effects via elevating the generation of endogenous H2S. SPRC activates Gp130-mediated STAT3 and prevents doxorubicin-induced cardiotoxicity.

JK-2 is a hydrogen sulfide (H2S) donor. At acidic pH, it shows a greatly accelerated H2S release upon protonation-induced intramolecular cyclization.

CAY10732 is a fluorophore for the detection of hydrogen sulfide for H2S imaging in living cells.

ZYZ-803 is a slow H2S-NO-releasing hybrid, attenuating cardiac dysfunction after heart failure.

Zofenoprilat, an angiotensin-converting enzyme (ACE; IC50 = 8 nM for rabbit lung enzyme) inhibitor and the active metabolite of the prodrug zofenopril, effectively counters angiotensin I- or bradykinin-induced contractions in isolated guinea pig ileum (EC50s = 3 and 1 nM, respectively). At a concentration of 10 nM, Zofenoprilat not only diminishes basal endothelin-1 secretion and nitric oxide (NO) production but also safeguards against TNF-α-stimulated increases in reactive oxygen species (ROS) and reductions in glutathione (GSH) levels within human umbilical vein endothelial cells (HUVECs). Furthermore, at 10 µM, it delivers protection to primary human cardiac microvascular endothelial cells from doxorubicin-induced toxicity and enhances hydrogen sulfide (H2S) production, along with the adhesion, migration, and proliferation of HUVECs. Additionally, Zofenoprilat (400 µM) mitigates end diastolic pressure and lactate dehydrogenase (LDH) release, demonstrating therapeutic potential in a Langendorff isolated perfused rat heart model of ischemia-reperfusion injury.

NA-Ir is a ferroptosis (Ferroptosis) inducer that targets mitochondrial DNA (mtDNA) and activates the cGAS-STING pathway to stimulate ferritin autophagy (). It also induces the production of reactive oxygen species (ROS) through photodynamic therapy (PDT), depletes glutathione (GSH), and downregulates glutathione peroxidase 4 (GPX4), thereby triggering lipid peroxidation and ferroptosis. NA-Ir exhibits enhanced anticancer activity under light exposure and selectively inhibits cancer cells with high H2S content.

AP39 is a compound used to increase hydrogen sulfide (H2S) levels within mitochondria; it consists of a mitochondria-targeting motif (triphenylphosphonium) coupled to an H2S-donating moiety (dithiolethione) by an aliphatic linker. AP219, as a control compound for AP39, contains the triphenylphosphonium scaffold but lacks the H2S-releasing portion.

S-Diclofenac is a novel NSAID formed by linking diclofenac to an H2S-releasing moiety. S-Diclofenac spares the gastric mucosa of injury despite markedly suppressing prostaglandin synthesis [1].