Panamycin 607CAS# 100905-89-3 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 100905-89-3 | SDF | Download SDF |
PubChem ID | 127712 | Appearance | Powder |
Formula | C35H61NO7 | M.Wt | 607.86 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
SMILES | CCCC1CC2CCC(O2)C(C(=O)OC(C(C3CCC(O3)C(C(=O)O1)C)C)C(C)C4CCC(O4)CC(CCC)N(C)C)C | ||
Standard InChIKey | AHOIPAFUOXGGQB-YSWOBQKZSA-N | ||
Standard InChI | InChI=1S/C35H61NO7/c1-9-11-25(36(7)8)19-27-13-15-29(39-27)21(3)33-22(4)30-17-18-32(42-30)24(6)34(37)41-26(12-10-2)20-28-14-16-31(40-28)23(5)35(38)43-33/h21-33H,9-20H2,1-8H3/t21-,22-,23+,24-,25?,26+,27+,28+,29-,30+,31-,32-,33+/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. |
Structure Identification | Journal of the Agricultural Chemical Society of Japan, 2005, 69(2):315-320.Biosynthetic origin of the carbon skeleton and nitrogen atom of pamamycin-607, a nitrogen-containing polyketide.[Reference: WebLink]
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Panamycin 607 Dilution Calculator
Panamycin 607 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.6451 mL | 8.2256 mL | 16.4512 mL | 32.9023 mL | 41.1279 mL |
5 mM | 0.329 mL | 1.6451 mL | 3.2902 mL | 6.5805 mL | 8.2256 mL |
10 mM | 0.1645 mL | 0.8226 mL | 1.6451 mL | 3.2902 mL | 4.1128 mL |
50 mM | 0.0329 mL | 0.1645 mL | 0.329 mL | 0.658 mL | 0.8226 mL |
100 mM | 0.0165 mL | 0.0823 mL | 0.1645 mL | 0.329 mL | 0.4113 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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Genetic polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 promoter may not be associated with development of hepatocellular carcinoma.[Pubmed:28000712]
Sci Rep. 2016 Dec 21;6:39404.
This study meta-analyzed the literature on possible association of polymorphisms -137 (rs187238) and -607 (rs1946518) in the interleukin-18 (IL-18) promoter with risk of hepatocellular carcinoma (HCC). The analysis included 8 case-control studies on the -137 polymorphism (1,318 cases, 2,254 controls) and 7 case-control studies on the -607 polymorphism (1,262 cases, 1,696 controls). None of the five genetic models suggested a significant association between the -137 polymorphism and HCC risk: allelic model, OR 0.99, 95% CI 0.74-1.34, P = 0.97; recessive model, OR 0.98, 95% CI 0.65-1.46, P = 0.91; dominant model, OR 1.35, 95% CI 0.73-2.52, P = 0.34; homozygous model, OR 0.99, 95% CI 0.65-1.49, P = 0.95; heterozygous model, OR 0.99, 95% CI 0.66-1.48, P = 0.94. Similar results were obtained in subgroup analyses of Asian patients, Chinese patients, or patients with hepatitis B virus (HBV)-related HCC. Similar results were also obtained for the -607 polymorphism across the entire study population as well as in the three subgroups. The available evidence suggests no significant association of the -137 or -607 polymorphisms with risk of HCC in general or specifically of HBV-related HCC. These conclusions should be verified in large, well-designed studies.
[Clinical manifestation and cytogenetic analysis of 607 patients with Turner syndrome].[Pubmed:28186596]
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2017 Feb 10;34(1):61-64.
OBJECTIVE: To explore the correlation between cytogenetic findings and clinical manifestations of Turner syndrome. METHODS: 607 cases of cytogenetically diagnosed Turner syndrome, including those with a major manifestation of Turner syndrome, were analyzed with conventional G-banding. Correlation between the karyotypes and clinical features were analyzed. RESULTS: Among the 607 cases, there were 154 cases with monosomy X (25.37%). Mosaicism monosomy X was found in 240 patients (39.54%), which included 194 (80.83%) with a low proportion of 45,X (3 = the number of 45, X =5, while the normal cells >/= 30). Structural X chromosome abnormalities were found in 173 patients (28.50%). A supernumerary marker chromosome was found in 40 cases (6.59%). Most patients with typical manifestations of Turner syndrome were under 11 years of age and whose karyotypes were mainly 45,X. The karyotype of patients between 11 and 18 years old was mainly 45,X, 46,X,i(X)(q10) and mos45,X/46,X,i(X)(q10), which all had primary amenorrhea in addition to the typical clinical manifestations. The karyotype of patients over 18 years of age were mainly mosaicism with a low proportion of 45,X, whom all had primary infertility. 53 patients had a history of pregnancy, which included 48 with non-structural abnormalities of X chromosome and 5 with abnormal structure of X chromosome. CONCLUSION: Generally, the higher proportion of cells with an abnormal karyotype, the more severe were the clinical symptoms and the earlier clinical recognition. Karyotyping analysis can provide guidance for the early diagnosis of Turner syndrome, especially those with a low proportion of 45,X.
Preclinical safety evaluation of IQG-607 in rats: Acute and repeated dose toxicity studies.[Pubmed:28232042]
Regul Toxicol Pharmacol. 2017 Jun;86:11-17.
In the present study, we evaluated the safety and the possible toxic effects of IQG-607 after acute and 90-day repeated administrations in rats. Single oral administration of IQG-607 (300 or 2000 mg/kg) on female rats did not result in any mortality. No gross lesions were observed in the animals at necropsy. Ninety-day administration test resulted in 20% of deaths, in both male and female rats administered with the highest dose of IQG-607, 300 mg/kg. Repeated administration of the IQG 607 (25, 100 and 300 mg/kg) did not result in any significant body mass alteration, or changes in food and water consumption. The most important clinical sign observed was salivation in both sexes. Importantly, long-term treatment with IQG-607 did not induce alterations in any hematological (for both sex) and serum biochemical (for female) parameters evaluated, even at the highest dose tested. Treatment of male rats with 100 or 300 mg/kg of IQG-607 decreased total cholesterol levels, while animals treated with 100 mg/kg also presented reduction on triglyceride levels. Of note, no treatment induced significant histopathological alterations in tissues of all organs and glands analyzed, even in that group that received the highest dose of IQG-607.
The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27 607 patients.[Pubmed:28053261]
Bone Joint J. 2017 Jan;99-B(1):78-86.
AIMS: The aims of this study were to establish the incidence of acute Achilles tendon rupture (AATR) in a North American population, to select demographic subgroups and to examine trends in the management of this injury in the province of Ontario, Canada. PATIENTS AND METHODS: Patients >/= 18 years of age who presented with an AATR to an emergency department in Ontario, Canada between 1 January 2003 and 31 December 2013 were identified using administrative databases. The overall and annual incidence density rate (IDR) of AATR were calculated for all demographic subgroups. The annual rate of surgical repair was also calculated and compared between demographic subgroups. RESULTS: A total of 27 607 patients (median age, 44 years; interquartile range 26 to 62; 66.5% male) sustained an AATR. The annual IDR increased from 18.0 to 29.3 per 100 000 person-years between 2003 and 2013. The mean IDR was highest among men between the ages of 40 and 49 years (46.0/100 000 person-years). The annual rate of surgical repair dropped from 20.1 in 2003 to 9.2 per 100 AATRs in 2013. There was a noticeable decline after 2009. CONCLUSION: The incidence of AATR is increasing in Ontario, while the annual rate of surgical repair is decreasing. A sharp decline in the rate of surgical repair was noted after 2009. This coincided with the publication of several high-quality RCTs which showed similar outcomes for the 'functional' non-operative management and surgical repair. Cite this article: Bone Joint J 2017;99-B:78-86.