Gastric H+,K+-ATPase, with an IC50 of 0.1 μM in ion - leaky vesicles and 0.19 μM in isolated gastric glands, a Ki of 6.4 nM, and a Kd of 26.4 nM [1]

Soraprazan is a highly potent, reversible, and fast - acting inhibitor of gastric H+,K+-ATPase. It can immediately inhibit acid secretion in various in vitro models. It shows more than 2000 - fold selectivity for H+,K+-ATPase over Na+,K+- and Ca+-ATPases [1]
Remofuscin can increase the expression levels of genes related to xenobiotic metabolism in Caenorhabditis elegans, such as cyp35a subfamily genes, gst - 5, and gst - 28. It also up - regulates the expression of genes related to lysosomal lipases (lip l - 1), long - chain fatty acid transporters (lbp - 8), and fatty acid beta - oxidation (ech - 9). And it can increase the levels of nuclear hormone receptor genes nhr - 210 and nhr - 234. Through loss - of - function mutants experiments, it is proved that Remofuscin extends the lifespan of Caenorhabditis elegans by regulating genes related to lipid metabolism and xenobiotic detoxification [3]

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Soraprazan (BYK61359) is a strong gastric H,K-ATPase inhibitor with an IC50 of 0.1 μM when evaluated in the presence of 1 mM potassium in ion-leaking vesicles. Soraprazan (BYK61359) also significantly suppresses dibutyryl cAMP-stimulated [14C]AP accumulation in isolated stomach glands with an IC50 of 0.19 μM (geometric mean of n=6, 0.09-0.40 μM, 95% confidence limit) [1].

Soraprazan can inhibit gastric acid secretion in vivo. In cynomolgus monkeys, oral administration of 6, 12 and 24 mg/kg/day for 52 weeks can play a role in inhibiting gastric acid secretion [1]
Remofuscin can extend the lifespan of Caenorhabditis elegans. It is speculated that it may be achieved by preventing lipofuscin accumulation, and the specific mechanism is related to the lysosome - to - nucleus signaling pathway [3]
Dogs' stomach acid secretion is quickly and persistently inhibited by soraprazan (1–27 μmol/kg; oral) [1].

For Soraprazan, use ion - leaky vesicles or isolated gastric glands as the reaction system. Add different concentrations of Soraprazan to the system, and then detect the activity of gastric H+,K+-ATPase. According to the change of enzyme activity with the drug concentration, calculate the IC50, Ki and Kd values of Soraprazan on gastric H+,K+-ATPase [1]
- Cell Assay：There is no relevant content about cell assay in the two literatures.

Soraprazan is dissolved in an appropriate solvent and orally administered to cynomolgus monkeys at doses of 6, 12 and 24 mg/kg/day, once a day for 52 weeks [1]

[1]. Soraprazan: setting new standards in inhibition of gastric acid secretion. J Pharmacol Exp Ther. 2007 Jun;321(3):866-74.

[2]. Remofuscin induces xenobiotic detoxification via a lysosome-to-nucleus signaling pathway to extend the Caenorhabditis elegans lifespan. Sci Rep. 2022 May 3;12(1):7161.

Soraprasin is a potassium-competitive acid blocker with potential applications in the treatment of diseases related to excessive gastric acid secretion [1]. Remofocin is a small molecule compound whose mechanism of action is related to the induction of exogenous substance detoxification through the lysosomal-to-nucleus signaling pathway, and has a certain effect on prolonging the lifespan of Caenorhabditis elegans [3]. Soraprasin is a potent and reversible proton pump inhibitor of gastric H+/K+ ATPase with potassium-competitive acid blocker (P-CAB) activity. Soraprasin can specifically, competitively, and reversibly bind to the potassium-binding site of the proton pump hydrogen potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting the activity of the pump and inhibiting the secretion of H+ ions into the gastric lumen by parietal cells, which is the last step in the production of gastric acid. Lipofuscin is a representative biomarker of aging and is produced naturally over time. Remofuscin (soraprazan) improves age-related eye diseases by clearing lipofuscin from retinal pigment epithelial (RPE) cells. This study investigated the effects of remofusin on the lifespan of C. elegans and its potential mechanisms. Results showed that remofusin significantly prolonged the lifespan of C. elegans (N2) compared to the negative control group (p < 0.05). Senescence biomarkers in remofusin-treated nematodes were also improved. In nematodes treated with remofusin, the expression levels of genes associated with lysosomes (lipl-1 and lp-8), nuclear hormone receptors (nhr-234), fatty acid β-oxidation (ech-9), and exogenous substance detoxification (cyp-34A1, cyp-35A1, cyp-35A2, cyp-35A3, cyp-35A4, cyp-35A5, cyp-35C1, gst-28, and gst-5) were increased. Furthermore, remofuran failed to prolong the lifespan of C. elegans carrying loss-of-function mutations (lipl-1, lbp-8, nhr-234, nhr-49, nhr-8, cyp-35A1, cyp-35A2, cyp-35A3, cyp-35A5, and gst-5), suggesting that these genes are associated with the lifespan extension of C. elegans treated with remofuran. In summary, remofuran activates the lysosomal-nuclear pathway in C. elegans, thereby increasing the expression levels of xenobiotic detoxification genes and ultimately prolonging its lifespan. [2]

C21H25N3O3

367.4415

367.19

C, 68.64; H, 6.86; N, 11.44; O, 13.06

261944-46-1

213054

Light yellow to yellow solid powder

3.32

2

5

5

27

487

3

CC1=C(N2C=CC3=C(C2=N1)N[C@@H]([C@H]([C@@H]3OCCOC)O)C4=CC=CC=C4)C

PWILYDZRJORZDR-MISYRCLQSA-N

InChI=1S/C21H25N3O3/c1-13-14(2)24-10-9-16-18(21(24)22-13)23-17(15-7-5-4-6-8-15)19(25)20(16)27-12-11-26-3/h4-10,17,19-20,23,25H,11-12H2,1-3H3/t17-,19-,20-/m1/s1

(7R,8R,9R)-7-(2-methoxyethoxy)-2,3-dimethyl-9-phenyl-7,8,9,10-tetrahydroimidazo[1,2-h][1,7]naphthyridin-8-ol

Soraprazan; 261944-46-1; BYK61359; 5XB3671655; BYK-61359; (7R,8R,9R)-7-(2-Methoxyethoxy)-2,3-dimethyl-9-phenyl-7,8,9,10-tetrahydroimidazo(1,2-h)(1,7)naphtyridin-8-ol; soraprazanum; (7r,8r,9r)-7-(2-methoxyethoxy)-2,3-dimethyl-9-phenyl-7,8,9,10-tetrahydroimidazo[1,2-h][1,7]naphthyridin-8-ol;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~200 mg/mL (~544.31 mM)

Solubility in Formulation 1: ≥ 5 mg/mL (13.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 + to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)