YS-49JNK/ROS inhibitor CAS# 132836-42-1 |
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Quality Control & MSDS
3D structure
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| Cas No. | 132836-42-1 | SDF | Download SDF |
| PubChem ID | 10249534 | Appearance | Powder |
| Formula | C20H20BrNO2 | M.Wt | 386.28 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 100 mg/mL (258.88 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 1-(naphthalen-1-ylmethyl)-1,2,3,4-tetrahydroisoquinoline-6,7-diol;hydrobromide | ||
| SMILES | C1CNC(C2=CC(=C(C=C21)O)O)CC3=CC=CC4=CC=CC=C43.Br | ||
| Standard InChIKey | JXFRKNGQHAAJKY-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C20H19NO2.BrH/c22-19-11-15-8-9-21-18(17(15)12-20(19)23)10-14-6-3-5-13-4-1-2-7-16(13)14;/h1-7,11-12,18,21-23H,8-10H2;1H | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | YS 49 inhibits Ang II-stimulated proliferation of VSMCs via induction of HO-1.
IC50 value:
Target: HO-1
YS-49 is a novel positive inotropic isoquinoline compound. YS-49 has potential as a therapeutic strategy for the pathogenesis of Ang II-related vascular diseases such as hypertension and atherosclerosis, via the induction of HO-1 gene activity. YS-49 induced HO-1 protein production in a dose-and time-dependent manner in VSMCs. Treatment with YS-49 significantly and dose-dependently inhibited Ang II-induced VSMC proliferation, ROS production, and phosphorylation of JNK, but not P38 MAP kinase or ERK1/2.YS-49(32.8 microM) exhibited much stronger inhibitory effects on TXA(2) formation. The higher inhibitory potencies of YS-49 (IC(50): 3.3microM) than higenamine (IC(50): 140 microM) on AA induced rat platelet aggregation was presumed to be the result of low inhibitory effect of higenamine than YS-49 on TXA(2) production from AA. The oral administration of YS-49 (50 mg/kg) increased the recovery rates from the acute thrombotic challenge in mice and lowered the weight of thrombus formed inside the AV shunt tube in rats. References: | |||||
YS-49 Dilution Calculator
YS-49 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5888 mL | 12.944 mL | 25.888 mL | 51.7759 mL | 64.7199 mL |
| 5 mM | 0.5178 mL | 2.5888 mL | 5.1776 mL | 10.3552 mL | 12.944 mL |
| 10 mM | 0.2589 mL | 1.2944 mL | 2.5888 mL | 5.1776 mL | 6.472 mL |
| 50 mM | 0.0518 mL | 0.2589 mL | 0.5178 mL | 1.0355 mL | 1.2944 mL |
| 100 mM | 0.0259 mL | 0.1294 mL | 0.2589 mL | 0.5178 mL | 0.6472 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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YS-49 is a novel positive inotropic isoquinoline compound. YS-49 has potential as a therapeutic strategy for the pathogenesis of Ang II-related vascular diseases such as hypertension and atherosclerosis, via the induction of HO-1 gene activity. YS-49 induced HO-1 protein production in a dose-and time-dependent manner in VSMCs. Treatment with YS-49 significantly and dose-dependently inhibited Ang II-induced VSMC proliferation, ROS production, and phosphorylation of JNK, but not P38 MAP kinase or ERK1/2.YS-49(32.8 microM) exhibited much stronger inhibitory effects on TXA(2) formation. The higher inhibitory potencies of YS-49 (IC(50): 3.3microM) than higenamine (IC(50): 140 microM) on AA induced rat platelet aggregation was presumed to be the result of low inhibitory effect of higenamine than YS-49 on TXA(2) production from AA. The oral administration of YS-49 (50 mg/kg) increased the recovery rates from the acute thrombotic challenge in mice and lowered the weight of thrombus formed inside the AV shunt tube in rats.
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Effects of two tetrahydroisoquinolines (YS-49 and YS-51) on experimental disseminated intravascular coagulation induced by lipopolysaccharide in rats.[Pubmed:15612611]
Arzneimittelforschung. 2004;54(11):705-10.
Disseminated intravascular coagulation (DIC) is a pathological syndrome, which occurs following the uncontrolled widespread activation of blood coagulation, resulting in the intravascular formation of fibrin, which may lead to thrombotic occlusion of small and midsize vessels. The effects of 1-(alpha-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (YS-49, CAS 132836-42-1) and 1-(beta-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetra-hydroisoquinoline (YS-51, CAS 213179-96-5) on the experimental DIC induced by lipopolysaccharide (LPS) in rats, were investigated. The oral administration of YS-49 and YS-51 (10 or 50 mg/kg) attenuated the dramatic increase of serum fibrinogen/fibrin degradation product (FDP) level, the decrease of plasma fibrinogen concentration and the number of platelets in blood and the prolongation of prothrombin time (PT) and activated partial thromboplastin time (aPTT) induced by LPS. The liver and kidney function parameters, aspartate amino-transferase (AST) and blood urea nitrogen (BUN), were also improved with YS-49 and YS-51. The above results suggest that YS-49 and YS-51 have therapeutic potential for DIC and/or accompanying multiple organ failure.
Antithrombotic effects of YS-49 and YS-51--1-naphthylmethyl analogs of higenamine.[Pubmed:11728526]
Thromb Res. 2001 Nov 15;104(4):249-55.
The antiplatelet and antithrombotic effects of YS-49 and YS-51--l-naphthylmethyl analogs of higenamine, which is a benzyl-tetrahydroisoquinoline alkaloid isolated from Aconitum japonicum (Ranunculaceae)--were investigated. YS-49 and YS-51 showed inhibitory activities to both human and rat platelet aggregation induced by ADP, collagen and epinephrine. They were more inhibitory to epinephrine-induced aggregation (IC(50); 3.4 and 1.7 microM of YS-49, and 6.0 and 6.3 microM of YS-51 to human and rat platelets, respectively) than ADP- or collagen-induced aggregation. The antithrombotic effects of YS-49 and YS-51 were also observed in both mouse acute thrombosis model and rat arterio-venous shunt (AV shunt) model. The oral administration of YS-49 and YS-51 (50 or 100 mg/kg) increased the recovery rates from the acute thrombotic challenge in mice and lowered the weight of thrombus formed inside the AV shunt tube in rats.
Effects of higenamine and its 1-naphthyl analogs, YS-49 and YS-51, on platelet TXA2 synthesis and aggregation.[Pubmed:17020781]
Thromb Res. 2007;120(1):81-6.
The effects of higenamine and its 1-naphthyl analogs, YS-49 and YS-51, on thromboxane A(2) (TXA(2)) formation from arachidonic acid (AA) and aggregation in platelets, were investigated. YS-49 and YS-51 (IC(50); 32.8 and 39.4 microM respectively) exhibited much stronger inhibitory effects on TXA(2) formation than higenamine (IC(50); 2.99 mM). The higher inhibitory potencies of YS-49 and YS-51 (IC(50): 3.3 and 5.7 microM respectively) than higenamine (IC(50): 140 microM) on AA induced rat platelet aggregation was presumed to be the result of low inhibitory effect of higenamine than YS-49 and YS-51 on TXA(2) production from AA. Among the present three compounds, the more hydrophobic naphthylmethyl groups were supposed to be more favorable than p-hydroxybenzyl moiety, at 1-position of the tetrahydroisoquinoline ring, to display the inhibitory effects on TXA(2) production and AA induced aggregation of platelets. In addition, higenamine, YS-49 and YS-51 were observed directly antagonistic on TXA(2) receptor (TP receptors) by displaying inhibitory effects to U46619 (TXA(2) mimetic) induced platelet aggregation, however all of the three compounds showed similar order of inhibitory potencies. The present results are suggestive that YS-49 and YS-51 exert their inhibitory effects on AA-induced platelet aggregation partly by inhibiting the production of TXA(2) from AA and partly by directly blocking the TP receptor, in addition to the previously reported effects on alpha(2)-adrenergic receptor. On the other hand, higenamine is supposed to antagonize AA-induced platelet aggregation by mostly directly blocking the TP receptor.
YS 49, 1-(alpha-naphtylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, regulates angiotensin II-stimulated ROS production, JNK phosphorylation and vascular smooth muscle cell proliferation via the induction of heme oxygenase-1.[Pubmed:18262205]
Life Sci. 2008 Mar 12;82(11-12):600-7.
Overexpression of the gene for heme oxygenase (HO)-1 leads to a reduction in pressor responsiveness to angiotensin II (Ang II) in experimental animals. Using rat vascular smooth muscle cells (VSMCs), we tested whether YS 49 [1-(alpha-naphtylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline] inhibits Ang II-stimulated proliferation of VSMCs via induction of HO-1. YS 49 induced HO-1 protein production in a dose-and time-dependent manner in VSMCs. Treatment with YS 49 significantly and dose-dependently inhibited Ang II-induced VSMC proliferation, ROS production, and phosphorylation of JNK, but not P38 MAP kinase or ERK1/2. The antiproliferation effect of YS 49 was reversed by pretreatment with the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX), or with hemoglobin, a carbon monoxide (CO) scavenger. Similarly, VSMC proliferation, ROS production and phosphorylation of JNK by Ang II were significantly inhibited in VSMCs transfected with the HO-1 gene. Thus, HO-1 and the HO-1 product CO play, at least in part, a crucial role in Ang II-stimulated VSMC proliferation through the regulation of ROS production and JNK phosphorylation. Therefore, YS 49 has potential as a therapeutic strategy for the pathogenesis of Ang II-related vascular diseases such as hypertension and atherosclerosis, via the induction of HO-1 gene activity.
