IntermedineCAS# 10285-06-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 10285-06-0 | SDF | Download SDF |
| PubChem ID | 114843 | Appearance | White-beige powder |
| Formula | C15H25NO5 | M.Wt | 299.36 |
| Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
| Solubility | Soluble in chloroform | ||
| Chemical Name | [(7R,8R)-7-hydroxy-5,6,7,8-tetrahydro-3H-pyrrolizin-1-yl]methyl (2S)-2-hydroxy-2-[(1R)-1-hydroxyethyl]-3-methylbutanoate | ||
| SMILES | CC(C)C(C(C)O)(C(=O)OCC1=CCN2C1C(CC2)O)O | ||
| Standard InChIKey | SFVVQRJOGUKCEG-OPQSFPLASA-N | ||
| Standard InChI | InChI=1S/C15H25NO5/c1-9(2)15(20,10(3)17)14(19)21-8-11-4-6-16-7-5-12(18)13(11)16/h4,9-10,12-13,17-18,20H,5-8H2,1-3H3/t10-,12-,13-,15+/m1/s1 | ||
| 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 | 1. Intermedin (IMD), a multi-functional peptide, plays important roles in cardiovascular protection, the endogenous IMD and its receptor complexes are induced in hypertrophic cardiomyocytes and proposed to play an important role in the pathogenesis of cardiac hypertrophy. 2. Intermedin can decrease the melanin content of the skin of Rana pipiens. |
| Targets | PI3K | PKA | MAPK | ERK | cAMP |
Intermedine Dilution Calculator
Intermedine Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.3405 mL | 16.7023 mL | 33.4046 mL | 66.8092 mL | 83.5115 mL |
| 5 mM | 0.6681 mL | 3.3405 mL | 6.6809 mL | 13.3618 mL | 16.7023 mL |
| 10 mM | 0.334 mL | 1.6702 mL | 3.3405 mL | 6.6809 mL | 8.3511 mL |
| 50 mM | 0.0668 mL | 0.334 mL | 0.6681 mL | 1.3362 mL | 1.6702 mL |
| 100 mM | 0.0334 mL | 0.167 mL | 0.334 mL | 0.6681 mL | 0.8351 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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Intermedin suppresses pressure overload cardiac hypertrophy through activation of autophagy.[Pubmed:23737997]
PLoS One. 2013 May 29;8(5):e64757.
Left ventricular hypertrophy is a maladaptive response to pressure overload and an important risk factor for heart failure. Intermedin (IMD), a multi-functional peptide, plays important roles in cardiovascular protection. In this study, we revealed an autophagy-dependent mechanism involved in IMD's protection against cardiac remodeling and cardiomyocyte death in heart hypertrophy. We observed that transverse aortic contraction (TAC) induction, Ang II or ISO exposure induced remarkable increase in the expression of endogenous IMD and its receptor components, CRLR, RAMP1 and RAMP3, in mouse hearts and H9c2 cell cultures, respectively. Furthermore, the heart size, heart weight/body weight ratios, cardiomyocyte size and apoptosis, interstitial collagen, hypertrophic markers including ANP and BNP expression were also significantly increased, which were effectively suppressed by IMD supplementation. In addition, IMD induced capillary angiogenesis and improved functions in hypertrophic hearts. We further observed that IMD induced strong autophagy in hypertrophic hearts and cultured cells, which was paralleling with the decrease in cardiomyocyte size and apoptosis. Furthermore, an autophagy inhibitor, 3-MA, was used to block the IMD-augmented autophagy level, and then the protection of IMD on cardiomyocyte hypertrophy and apoptosis was almost abrogated. We also observed that IMD supplementation stirred intracellular cAMP production, and augmented the ERK1/2 phosphorylation induced by Ang II/ISO exposure in H9c2 cells. In addition, we inhibited PI3K, PKA and MAPK/ERK1/2 signaling pathways by using wortamannin, H89 and PD98059, respectively, in H9c2 cells co-incubating with both IMD and Ang II or ISO, and observed that these inhibitors effectively reduced IMD-augmented autophagy level, but only H89 and PD98059 pre-incubation abrogated the anti-apoptotic action of IMD. These results indicate that the endogenous IMD and its receptor complexes are induced in hypertrophic cardiomyocytes and proposed to play an important role in the pathogenesis of cardiac hypertrophy, and the autophagy stirred by IMD supplementation is involved in its protection against cardiomyocyte hypertrophy and apoptosis through the activation of both cAMP/PKA and MAPK/ERK1/2 pathways.
