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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Octreotide acetate (Sandostatin) is an octapeptide congener of native somatostatin, inhibits the secretion of insulin and glucagon. It reduces production of IGF-1 and IGF-2 by the liver by modulation of growth-hormone secretion from the pituitary gland. [1] The insulin-like growth factors IGF-1 and IGF-2, endogenously produced polypeptide hormones and potent stimulators of cell proliferation, are under investigation as clinical targets in prostate cancer. Octreotide acetate decreased the urinary excretion of uric acid as well as the plasma concentrations of glucagon and insulin. Octreotide acetate decreased the urinary excretion of sodium and chloride without significiant influence on creatinine clearance, while the concentrations of lactic acid, pyruvic acid in blood, and cyclic AMP in plasma were not changed. [1]References:[1] Tetsuya yamamoto, Yuji moriwaki et al. Effect of Octreotide acetate on the Plasma Concentration and Urinary Excretion of Uridine and Purine Bases. Endocrine Journal 2002, 49(2),139-144.
Cell lines
Human HUV-EC-C endothelial cells
Preparation method
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
Reaction Conditions
1 μM, 72 hours
Applications
Octreotide 1 nM produced a maximum 45.8% reduction of cell proliferation as compared to control cultures, from 9.7 to 4.4 x l03 cells/well. To assess the influence of medium supplements on the inhibition of HUV-EC-C cell growth. Octreotide was tested against graded concentrations of ECGF and heparin in the culture medium. Overall, these changes did not significantly affect the growth-inhibitory activity of octreotide as compared to baseline conditions.
Animal models
Male Sprague-Dawley rats
Dosage form
Subcutaneous injection, 1 μg/kg, 10 μg/kg and 200 μg/kg
NREMS and SWA were normal after 1 μg/kg octreotide. REMS, however, enhanced significantly during the light period. The increases in REMS started 2–3 h postinjection and persisted during the rest of the day, although they were very small when the individual hours were considered. In response to 10 μg/kg octreotide, NREMS was significantly suppressed in hour 1 postinjection. Calculated for the 12-h light period, NREMS or SWA did not differ between the baseline and the octreotide days.
Other notes
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
References:
[1] Danesi R, Agen C, Benelli U, et al. Inhibition of experimental angiogenesis by the somatostatin analogue octreotide acetate (SMS 201-995). Clinical Cancer Research, 1997, 3(2): 265-272.
[2] Beranek L, Obal Jr F, Taishi P, et al. Changes in rat sleep after single and repeated injections of the long-acting somatostatin analog octreotide. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 1997, 273(4): R1484-R1491.