Cortistatin-29 (rat)
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Cortistatin-29 (rat)

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Cortistatin-29 is a neuropeptide that has structurally similarity to somatostatin-28. It is produced by cleavage of preprocortistatin to procortistatin, which is cleaved at dibasic amino acids to form cortistatin-29 and cortistatin-14 as well as other partial cleavage products.

Category
Peptide APIs
Catalog number
BAT-015362
CAS number
1815618-17-7
Molecular Formula
C161H240N46O41S2
Molecular Weight
3540.05
Cortistatin-29 (rat)
IUPAC Name
(2S)-6-amino-2-[[(4R,7S,10S,13S,16S,19S,22S,25S,28S,31S,34S,37R)-37-[[(2S)-1-[(2S)-6-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-1-[(2S)-5-amino-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-1-[(2S)-1-[(2S)-5-carbamimidamido-2-[[(2S)-4-carboxy-2-[[(2S)-5-oxopyrrolidine-2-carbonyl]amino]butanoyl]amino]pentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-5-oxopentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]hexanoyl]pyrrolidine-2-carbonyl]amino]-19,34-bis(4-aminobutyl)-31-(2-amino-2-oxoethyl)-13,25,28-tribenzyl-16-[(1R)-1-hydroxyethyl]-7,10-bis(hydroxymethyl)-22-(1H-indol-3-ylmethyl)-6,9,12,15,18,21,24,27,30,33,36-undecaoxo-1,2-dithia-5,8,11,14,17,20,23,26,29,32,35-undecazacyclooctatriacontane-4-carbonyl]amino]hexanoic acid
Synonyms
Pyr-Glu-Arg-Pro-Pro-Leu-Gln-Gln-Pro-Pro-His-Arg-Asp-Lys-Lys-Pro-Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Ser-Ser-Cys-Lys-OH (Disulfide bridge: Cys17-Cys28); 5-oxo-L-prolyl-L-α-glutamyl-L-arginyl-L-prolyl-L-prolyl-L-leucyl-L-glutaminyl-L-glutaminyl-L-prolyl-L-prolyl-L-histidyl-L-arginyl-L-α-aspartyl-L-lysyl-L-lysyl-L-prolyl-L-cysteinyl-L-lysyl-L-asparaginyl-L-phenylalanyl-L-phenylalanyl-L-tryptophyl-L-lysyl-L-threonyl-L-phenylalanyl-L-seryl-L-seryl-L-cysteinyl-L-lysine, cyclic (17→28)-disulfide; L-pyroglutamyl-L-alpha-glutamyl-L-arginyl-L-prolyl-L-prolyl-L-leucyl-L-glutaminyl-L-glutaminyl-L-prolyl-L-prolyl-L-histidyl-L-arginyl-L-alpha-aspartyl-L-lysyl-L-lysyl-L-prolyl-D-cysteinyl-D-lysyl-L-asparagyl-L-phenylalanyl-L-phenylalanyl-D-tryptophyl-L-lysyl-L-threonyl-D-phenylalanyl-D-seryl-L-seryl-L-cysteinyl-L-lysine (17->28)-disulfide
Appearance
Lyophilized Powder
Purity
≥95%
Density
1.54±0.1 g/cm3
Sequence
pEERPPLQQPPHRDKKPCKNFFWKTFSSCK (Disulfide bridge: Cys17-Cys28)
Storage
Store at -20°C
Solubility
Soluble in Water
InChI
InChI=1S/C161H240N46O41S2/c1-87(2)72-107(195-150(238)120-48-28-68-204(120)157(245)122-50-30-70-206(122)155(243)104(46-26-66-176-161(172)173)187-136(224)102(55-59-128(215)216)184-134(222)100-54-58-127(214)179-100)138(226)185-101(52-56-124(167)211)135(223)188-105(53-57-125(168)212)156(244)207-71-31-51-123(207)158(246)205-69-29-49-121(205)151(239)196-112(77-93-81-174-86-178-93)143(231)182-99(45-25-65-175-160(170)171)133(221)194-114(79-129(217)218)145(233)180-96(40-15-20-60-162)131(219)186-103(43-18-23-63-165)154(242)203-67-27-47-119(203)152(240)201-118-85-250-249-84-117(149(237)189-106(159(247)248)44-19-24-64-166)200-147(235)116(83-209)199-146(234)115(82-208)198-141(229)110(75-91-36-11-6-12-37-91)197-153(241)130(88(3)210)202-137(225)98(42-17-22-62-164)181-142(230)111(76-92-80-177-95-39-14-13-38-94(92)95)192-140(228)109(74-90-34-9-5-10-35-90)190-139(227)108(73-89-32-7-4-8-33-89)191-144(232)113(78-126(169)213)193-132(220)97(183-148(118)236)41-16-21-61-163/h4-14,32-39,80-81,86-88,96-123,130,177,208-210H,15-31,40-79,82-85,162-166H2,1-3H3,(H2,167,211)(H2,168,212)(H2,169,213)(H,174,178)(H,179,214)(H,180,233)(H,181,230)(H,182,231)(H,183,236)(H,184,222)(H,185,226)(H,186,219)(H,187,224)(H,188,223)(H,189,237)(H,190,227)(H,191,232)(H,192,228)(H,193,220)(H,194,221)(H,195,238)(H,196,239)(H,197,241)(H,198,229)(H,199,234)(H,200,235)(H,201,240)(H,202,225)(H,215,216)(H,217,218)(H,247,248)(H4,170,171,175)(H4,172,173,176)/t88-,96+,97+,98+,99+,100+,101+,102+,103+,104+,105+,106+,107+,108+,109+,110+,111+,112+,113+,114+,115+,116+,117+,118+,119+,120+,121+,122+,123+,130+/m1/s1
InChI Key
GQJOQLQAIUKBOS-IOHUZKHFSA-N
Canonical SMILES
CC(C)CC(C(=O)NC(CCC(=O)N)C(=O)NC(CCC(=O)N)C(=O)N1CCCC1C(=O)N2CCCC2C(=O)NC(CC3=CN=CN3)C(=O)NC(CCCNC(=N)N)C(=O)NC(CC(=O)O)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)N4CCCC4C(=O)NC5CSSCC(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC5=O)CCCCN)CC(=O)N)CC6=CC=CC=C6)CC7=CC=CC=C7)CC8=CNC9=CC=CC=C98)CCCCN)C(C)O)CC1=CC=CC=C1)CO)CO)C(=O)NC(CCCCN)C(=O)O)NC(=O)C1CCCN1C(=O)C1CCCN1C(=O)C(CCCNC(=N)N)NC(=O)C(CCC(=O)O)NC(=O)C1CCC(=O)N1
1. Rat models of skin wound healing: a review
Wanda A Dorsett-Martin Wound Repair Regen . 2004 Nov-Dec;12(6):591-9. doi: 10.1111/j.1067-1927.2004.12601.x.
Rats have been widely used in the study of skin wound healing and the efficacy of different treatment modalities. This particular animal species is often selected for its availability, low cost, and small size. To define the current use of rat skin wound healing models, this manuscript provides a review of articles published between 2000 and 2003 that chose rats as their research animals. Of the 55 articles reviewed, it was found that 38.2% of the studies used incisional models and 38.2% used excisional models, with some studies using combinations. The majority of the studies (78.2%) used the rat's dorsum as the wound location. Male Sprague Dawley in the 250-300 gram weight range were the most preferred rats. Sodium pentobarbital/pentobarbitone was the most commonly used anesthetic choice. Similarities and differences in the selected experimental conditions are noted and questions are raised with regard to comparability between studies and the ability to transfer the data from the animal model to the human clinical situation. Attempts to compare studies for the advancement of wound healing knowledge are being hampered by the differences found between the studies. Standardization in reporting could facilitate comparisons and may instigate additional research that favors the inevitable comparisons between the studies. Thus, universal reporting requirements need to be developed for animal wound healing studies.
2. Lessons from rat models of hypertension: from Goldblatt to genetic engineering
M Paul, Y M Pinto, D Ganten Cardiovasc Res . 1998 Jul;39(1):77-88. doi: 10.1016/s0008-6363(98)00077-7.
Over the past 50 years various animal models of hypertension have been developed, predominantly in the rat. In this review we discuss the use of the rat as a model of hypertension, and evaluate what these models have taught us. Interestingly, the spontaneously hypertensive rat (SHR) is by far the most widely used rat model, although it reflects only a rare subtype of human hypertension, i.e. primary hypertension that is inherited in a Mendelian fashion. Many other aspects of the etiology of hypertension are found in other rat models, but these models are less frequently employed. The widespread use of the SHR suggests that this rat model is often chosen without considering alternative (and possibly better suited) models. To illustrate the importance of the choice for a particular model, we compared the natural history and response to antihypertensive drugs in different rat models of hypertension (SHR, Dahl, deoxycorticosterone acetate (DOCA)-salt, two-kidney one-clip, transgenic TGR(mRen2)27. This revealed that the outcome of hypertension can be similar in some respects, as all models exhibit cardiac hypertrophy, and all demonstrate impaired endothelium-dependent relaxations. However, the more severe forms of end-organ damage such as heart failure, stroke and kidney failure, occur only in some models and then only in a subset of the hypertensive rats. The effects of antihypertensives varies even more in the different models: antihypertensive treatment only attenuates end-organ damage if it decreases blood pressure. Moreover, if a given antihypertensive is effective, it sometimes even attenuates end-organ damage in nonhypotensive doses. On the other hand, some agents do decrease blood pressure but do not prevent end-organ damage (e.g. hydralazine in SHR). Furthermore, not all classes of antihypertensives are equally effective in all rat models of hypertension: endothelin-receptor antagonists are not effective in SHR, but have beneficial effects in the DOCA-salt model. The comparison of models, and the comparison of treatment effects suggests that end-organ damage critically depends upon not only on the stress imposed by high blood pressure and its underlying biochemical disturbance, but also upon the ability of the organism to recruit adequate 'coping' mechanisms. These coping mechanisms deserve greater attention, as failure to recruit such mechanisms may indicate an increased risk. The current development of transgenic techniques will provide new opportunities, to develop specific models to address this balance between stress and coping.
3. Electrocardiography in rats: a comparison to human
P Konopelski, M Ufnal Physiol Res . 2016 Nov 23;65(5):717-725. doi: 10.33549/physiolres.933270.
Electrocardiography (ECG) in rats is a widely applied experimental method in basic cardiovascular research. The technique of ECG recordings is simple; however, the interpretation of electrocardiographic parameters is challenging. This is because the analysis may be biased by experimental settings, such as the type of anesthesia, the strain or age of animals. Here, we aimed to review electrocardiographic parameters in rats, their normal range, as well as the effect of experimental settings on the parameters variation. Furthermore, differences and similarities between rat and human ECG are discussed in the context of translational cardiovascular research.
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