Synopsis
0
API Suppliers
0
USDMF
0
CEP/COS
0
JDMF
0
EU WC
0
KDMF
0
NDC API
0
VMF
0
Listed Suppliers
0
EDQM
0
USP
0
JP
0
Others
0
FDF Dossiers
0
FDA Orange Book
0
Europe
0
Canada
0
Australia
0
South Africa
0
Listed Dossiers
DRUG PRODUCT COMPOSITIONS
0
US Patents
0
US Exclusivities
0
Health Canada Patents
US Medicaid
NA
Annual Reports
NA
Regulatory FDF Prices
NA
0
API
0
FDF
0
Data Compilation #PharmaFlow
0
Stock Recap #PipelineProspector
0
Weekly News Recap #Phispers
0
News #PharmaBuzz
1. Hydrogen-1
2. Protium
1. Molecular Hydrogen
2. Dihydrogen
3. 1333-74-0
4. Protium
5. Hydrogen-1
6. Dtxsid9029643
7. 7ynj3po35z
8. Chebi:18276
9. Hydrogen Atoms
10. Refchem:389053
11. Dtxcid00196437
12. 215-605-7
13. H
14. Atomic Hydrogen
15. Hydrogen Gas
16. H2
17. 1-butanol, Titanium(4+) Salt, Monohydrate, Homopolymer (9ci)
18. Hydrogen, Atomic
19. Hidrogeno
20. Hydrogene
21. Wasserstoff
22. Cellulose Powder
23. O-hydrogen
24. P-hydrogen
25. Hydrogen Molecule
26. Monoatomic Hydrogen
27. 3a Molecular Sieve
28. Hydrogen [hsdb]
29. Alpha-cellulose, 90mum
30. Hydrogen [mi]
31. T101 Monoclonal Antibody
32. Hydrogen [who-dd]
33. Coware 20ml With H-caps
34. Hydrogen, >=99.99%
35. Hydrogen, >=99.999%
36. Schembl29349524
37. Schembl29357126
38. Chebi:18140
39. Chebi:33251
40. Yzckveuigoorgs-uhfffaoysa-n
41. Bbl103822
42. Nsc356464
43. Stl557632
44. Alpha-cellulose, 25mum Particle Size
45. Alpha-cellulose, 65mum Particle Size
46. Akos016038407
47. Nsc-356464
48. Un 1049
49. Un 1966
50. E949
51. Hydrogen, Messer(r) Cangas, 99.999%
52. E 949
53. E-949
54. Ns00080750
55. C00282
56. Alpha-cellulose, Partical Size: D50,180-280mum
57. Alpha-cellulose, Partical Size: D50,90-150mum
58. Q3027893
59. 1-butanol,titanium(4+)salt,monohydrate,homopolymer(9ci)
60. 1h
61. H-h
| Molecular Weight | 2.016 g/mol |
|---|---|
| Molecular Formula | H2 |
| XLogP3 | 0 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 0 |
| Exact Mass | Da |
| Monoisotopic Mass | Da |
| Topological Polar Surface Area | 0 |
| Heavy Atom Count | 0 |
| Formal Charge | 0 |
| Complexity | 0 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/EXPL THER/ Hydrogen-rich saline (HRS) is a novel protection against various oxidative disorders and almost all types of inflammation. Moreover, its toxicity and side effects are rarely reported. We sought to clarify the protective effect of HRS against the oxygen-induced retinopathy (OIR) in C57BL/6 J model. The OIR in the HRS treated mice and the untreated controls were systematically compared. The retinas of both groups were analyzed using high-molecular-weight FITC-dextran staining of flat-mount preparations, hematoxylin and eosin (H&E) staining of cross-sections. The distribution and expression of the vascular endothelial growth factor (VEGF) were also evaluated by the immunohistochemical measurements between postnatal days 17 (P17) and P21. The leakage and non-perfusion areas of retinal blood vessels were not alleviated in the HRS treatment group. Moreover, the number of preretinal vascular endothelial cell in the HRS treatment group was similar to that in the untreated group after exposure to hyperoxia (P>0.05). The degree of OIR was positively correlated with the expression level of VEGF. Intriguingly, the preretinal vascular endothelial cell count in the retinas of pups reared in room air with HRS treatment was 15.21+/-2.98. The preretinal vascular endothelial cell count of the HRS treated mice was significantly higher than that of the untreated group reared in room air. In summary, HRS therapy (at the dose of 10mL/day, applied between P12 and P17) did not inhibit retinal neovascularization in OIR; On the contrary, it would induce the retinal neovascularization during the development of normal retinas. /Hydrogen-rich saline/
PMID:27091652 Zhang Q et al; Life Sci 153: 17-22 (2016)
/EXPL THER/ Acute pancreatitis (AP) is an inflammatory disease mediated by damage to acinar cells and pancreatic inflammation. In patients with AP, subsequent systemic inflammatory responses and multiple organs dysfunction commonly occur. Interactions between cytokines and oxidative stress greatly contribute to the amplification of uncontrolled inflammatory responses. Molecular hydrogen (H2) is a potent free radical scavenger that not only ameliorates oxidative stress but also lowers cytokine levels. The aim of the present study was to investigate the protective effects of H2 gas on AP both in vitro and in vivo. For the in vitro assessment, AR42J cells were treated with cerulein and then incubated in H2-rich or normal medium for 24 hr, and for the in vivo experiment, AP was induced through a retrograde infusion of 5% sodium taurocholate into the pancreatobiliary duct (0.1 mL/100 g body weight). Wistar rats were treated with inhaled air or 2% H2 gas and sacrificed 12 hr following the induction of pancreatitis. Specimens were collected and processed to measure the amylase and lipase activity levels; the myeloperoxidase activity and production levels; the cytokine mRNA expression levels; the 8-hydroxydeoxyguanosine, malondialdehyde, and glutathione levels; and the cell survival rate. Histological examinations and immunohistochemical analyses were then conducted. The results revealed significant reductions in inflammation and oxidative stress both in vitro and in vivo. Furthermore, the beneficial effects of H2 gas were associated with reductions in AR42J cell and pancreatic tissue damage. In conclusion, our results suggest that H2 gas is capable of ameliorating damage to the pancreas and AR42J cells and that H2 exerts protective effects both in vitro and in vivo on subjects with AP. Thus, the results obtained indicate that this gas may represent a novel therapy agent in the management of AP.
PMID:27115738 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4845997 Zhou HX et al; PLoS One 11 (4): e0154483 (2016)
/EXPL THER/ Hydrogen gas inhalation (HI) ameliorates cerebral and cardiac dysfunction in animal models of post-cardiac arrest syndrome (PCAS). HI for human patients with PCAS has never been studied. Between January 2014 and January 2015, 21 of 107 patients with out-of-hospital cardiac arrest achieved spontaneous return of circulation. After excluding 16 patients with specific criteria, 5 patients underwent HI together with target temperature management (TTM). No undesirable effects attributable to HI were observed and 4 patients survived 90 days with a favorable neurological outcome. HI in combination with TTM is a feasible therapy for patients with PCAS.
PMID:27334126 Tamura T et al; Circ J. 80 (8): 1870-3 (2016)
/EXPL THER/ Premature ovarian failure (POF) is a disease that affects female fertility but has few effective treatments. Ovarian reserve function plays an important role in female fertility. Recent studies have reported that hydrogen can protect male fertility. Therefore, we explored the potential protective effect of hydrogen-rich water on ovarian reserve function through a mouse immune POF model. To set up immune POF model, fifty female BALB/c mice were randomly divided into four groups: Control (mice consumed normal water, n = 10), hydrogen (mice consumed hydrogen-rich water, n = 10), model (mice were immunized with zona pellucida glycoprotein 3 [ZP3] and consumed normal water, n = 15), and model-hydrogen (mice were immunized with ZP3 and consumed hydrogen-rich water, n = 15) groups. After 5 weeks, mice were sacrificed. Serum anti-Mullerian hormone (AMH) levels, granulosa cell (GC) apoptotic index (AI), B-cell leukemia/lymphoma 2 (Bcl-2), and BCL2-associated X protein (Bax) expression were examined. Analyses were performed using SPSS 17.0 (SPSS Inc., Chicago, IL, USA) software. Immune POF model, model group exhibited markedly reduced serum AMH levels compared with those of the control group (5.41 +/- 0.91 ng/ml vs. 16.23 +/- 1.97 ng/mL, P = 0.033) and the hydrogen group (19.65 +/- 7.82 ng/mL, P = 0.006). The model-hydrogen group displayed significantly higher AMH concentrations compared with that of the model group (15.03 +/- 2.75 ng/mL vs. 5.41 +/- 0.91 ng/mL, P = 0.021). The GC AI was significantly higher in the model group (21.30 +/- 1.74%) than those in the control (7.06 +/- 0.27%), hydrogen (5.17 +/- 0.41%), and model-hydrogen groups (11.24 +/- 0.58%) (all P < 0.001). The GC AI was significantly higher in the model-hydrogen group compared with that of the hydrogen group (11.24 +/- 0.58% vs. 5.17 +/- 0.41%, P = 0.021). Compared with those of the model group, ovarian tissue Bcl-2 levels increased (2.18 +/- 0.30 vs. 3.01 +/- 0.33, P = 0.045) and the Bax/Bcl-2 ratio decreased in the model-hydrogen group. Hydrogen-rich water may improve serum AMH levels and reduce ovarian GC apoptosis in a mouse immune POF model induced by ZP3. /Hydrogen-rich water/
PMID:27647193 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040020 He X et al; Chin Med J (Engl) 129 (19): 2331-7 (2016)
For more Therapeutic Uses (Complete) data for Hydrogen (24 total), please visit the HSDB record page.
Molecular hydrogen (H2) is an agent with potential applications in oxidative stress-related and/or inflammatory disorders. H2 is usually administered by inhaling H2-containing air (HCA) or by oral intake of H2-rich water (HRW). Despite mounting evidence, the molecular mechanism underlying the therapeutic effects and the optimal method of H2 administration remain unclear. Here, we investigated whether H2 affects signaling pathways and gene expression in a dosage- or dose regimen-dependent manner. We first examined the H2 concentrations in blood and organs after its administration and found that oral intake of HRW rapidly but transiently increased H2 concentrations in the liver and atrial blood, while H2 concentrations in arterial blood and the kidney were one-tenth of those in the liver and atrial blood. In contrast, inhalation of HCA increased H2 equally in both atrial and arterial blood ...
PMID:25707580 Sobue S et al; Mol Cell Biochem 403 (1-2): 231-41 (2015)
Hydrogen exerts beneficial effects in disease animal models of ischemia-reperfusion injury as well as inflammatory and neurological disease. Additionally, molecular hydrogen is useful for various novel medical and therapeutic applications in the clinical setting. In the present study, the hydrogen concentration in rat blood and tissue was estimated. Wistar rats were orally administered hydrogen super-rich water (HSRW), intraperitoneal and intravenous administration of hydrogen super-rich saline (HSRS), and inhalation of hydrogen gas. A new method for determining the hydrogen concentration was then applied using ... sensor gas chromatography, after which the specimen was prepared via tissue homogenization in airtight tubes. This method allowed for the sensitive and stable determination of the hydrogen concentration. The hydrogen concentration reached a peak at 5 minutes after oral and intraperitoneal administration, compared to 1 minute after intravenous administration. Following inhalation of hydrogen gas, the hydrogen concentration was found to be significantly increased at 30 minutes and maintained the same level thereafter. These results demonstrate that accurately determining the hydrogen concentration in rat blood and organ tissue is very useful and important for the application of various novel medical and therapeutic therapies using molecular hydrogen. /Hydrogen super-rich water or saline/
PMID:24975958 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074787 Liu C et al; Sci Rep 4: 5485 (2014)
The ability of mammalian tissues to oxidize hydrogen under conditions similar to those encountered by deep divers breathing mixtures containing hydrogen was investigated. The kidneys, livers, spleen, heart, lungs, and quadriceps muscle were removed from guinea-pigs and rats. After mincing or homogenization, the tissues, along with myocytes prepared from rat hearts and porcine cerebral cortex capillary endothelial cells were placed in petri dishes and exposed to tritium tagged hydrogen at a pressure of 1 or 5 megapascals (MPa) for 1 hour in a specially designed exposure system. Helium at a pressure of 1 MPa was used as a carrier. Petri dishes filled with distilled water or saline served as negative controls. After decompression, the extent of hydrogen oxidized by the mammalian tissues and cells was determined by measuring the amounts of incorporated tritium by liquid scintillation counting. The tissues and cells incorporated tritium only at the rate of 10 to 50 nanomoles per gram per minute (nmol/g/min), rates that were similar to those of the negative controls. The authors conclude that mammalian tissues do not oxidize hydrogen under hyperbaric conditions. The small amounts of tritium label incorporation observed in the tissues is probably due to radioisotope phenomena, which sets the detection limit for determining hydrogen oxidation at 100 nmol/g/min.
Kayar SR et al; Undersea and Hyperbaric Medicine 21 (3): 265-275 (1994)
Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/
PMID:27477846 Hara F et al; Circ J 80 (9): 2037-46 (2016)
Amyloid beta (Abeta) peptides are identified /as a/ cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Abeta-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Abeta-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Abeta-induced cytotoxicity /in SK-N-MC cells/. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Abeta-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Abeta-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Abeta-induced neurotoxicity. /Hydrogen-rich water/
PMID:26271894 Lin CL et al; Chem Biol Interact 240: 12-21 (2015)
The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1beta, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubiquitination, a non-transcriptional priming signal of NLRP3 in response to the stimulation of LPS. Additionally, the removal of mtROS by H2 reduced the generation of oxidized mitochondrial DNA and consequently decreased its binding to NLRP3, thereby inhibiting the NLRP3 inflammasome activation. Our findings have, for the first time, revealed the novel mechanism underlying the inhibitory effect of molecular hydrogen on LPS-caused NLRP3 inflammasome activation, highlighting the promising application of this new antioxidant in the treatment of LPS-associated inflammatory pathological damage.
PMID:26488087 Ren JD et al; Biochim Biophys Acta 1863 (1): 50-5 (2016)
... H2 decreased the tyrosine nitration level and suppressed oxidative stress damage in retinal cells. S-nitroso-N-acetylpenicillamine treatment decreased the cell numbers in the ganglion cell layer and inner nuclear layer, but the presence of H2 inhibited this reduction. These findings suggest that H2 has a neuroprotective effect against retinal cell oxidative damage, presumably by scavenging peroxynitrite. H2 reduces cellular peroxynitrite, a highly toxic reactive nitrogen species. Thus, H2 may be an effective and novel clinical tool for treating glaucoma and other oxidative stress-related diseases.
PMID:25801048 Yokota T et al; Clin Exp Ophthalmol 43 (6): 568-77 (2015)
Endothelial injury is a primary cause of sepsis and sepsis-induced organ damage. Heme oxygenase-1 (HO-1) plays an essential role in endothelial cellular defenses against inflammation by activating nuclear factor E2-related factor-2 (Nrf2). We found that molecular hydrogen (H2) exerts an anti-inflammatory effect. Here, we hypothesized that H2 attenuates endothelial injury and inflammation via an Nrf2-mediated HO-1 pathway during sepsis. First, we detected the effects of H2 on cell viability and cell apoptosis in human umbilical vein endothelial cells (HUVECs) stimulated by LPS. Then, we measured cell adhesion molecules and inflammatory factors in HUVECs stimulated by LPS and in a cecal ligation and puncture (CLP)-induced sepsis mouse model. Next, the role of Nrf2/HO-1 was investigated in activated HUVECs, as well as in wild-type and Nrf(-/-) mice with sepsis. We found that both 0.3 mmol/L and 0.6 mmol/L (i.e., saturated) H2-rich media improved cell viability and cell apoptosis in LPS-activated HUVECs and that 0.6 mmol/L (i.e., saturated) H2-rich medium exerted an optimal effect. H2 could suppress the release of cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1), and pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-a, interleukin (IL)-1beta and high-mobility group box 1 protein (HMGB1). Furthermore, H2 could elevate anti-inflammatory cytokine IL-10 levels in LPS-stimulated HUVECs and in lung tissue from CLP mice. H2 enhanced HO-1 expression and activity in vitro and in vivo. HO-1 inhibition reversed the regulatory effects of H2 on cell adhesion molecules and inflammatory factors. H2 regulated endothelial injury and the inflammatory response via Nrf2-mediated HO-1 levels. These results suggest that H2 could suppress excessive inflammatory responses and endothelial injury via an Nrf2/HO-1 pathway. /Hydrogen-rich media/
PMID:26253656 Chen H et al; Int Immunopharmacol 28 (1): 643-54 (2015)
ABOUT THIS PAGE
