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Antipain

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Antipain, a protease inhibitor isolated from Actinomycetes, inhibits N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced transformation and increases chromosomal aberration. It restricts DNA synthesis and function of mice uterus.

Category
Peptide Inhibitors
Catalog number
BAT-015121
CAS number
37691-11-5
Molecular Formula
C27H44N10O6
Molecular Weight
604.70
Antipain
IUPAC Name
(2S)-2-[[(2S)-5-(diaminomethylideneamino)-1-[[(2S)-1-[[5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxopentan-2-yl]carbamoylamino]-3-phenylpropanoic acid
Synonyms
[(S)-1-Carboxy-2-phenylethyl]carbamoyl-L-arginyl-L-valyl-argininal; L-valinamide, N2-[[((1S)-1-carboxy-2-phenylethyl)amino]carbonyl]-L-arginyl-N-[4-[(aminoiminomethyl)amino]-1-formylbutyl]-; Phe-CO-Arg-Val-L-Arg-H; N2-{[(1S)-1-Carboxy-2-phenylethyl]carbamoyl}-N5-(diaminomethylene)-L-ornithyl-N-{5-[(diaminomethylene)amino]-1-oxo-2-pentanyl}-L-valinamide
Related CAS
37682-72-7 (dihydrochloride)
Appearance
Yellow powder
Purity
95%
Density
1.38 g/cm3
Storage
Store at -20°C
InChI
InChI=1S/C27H44N10O6/c1-16(2)21(23(40)34-18(15-38)10-6-12-32-25(28)29)37-22(39)19(11-7-13-33-26(30)31)35-27(43)36-20(24(41)42)14-17-8-4-3-5-9-17/h3-5,8-9,15-16,18-21H,6-7,10-14H2,1-2H3,(H,34,40)(H,37,39)(H,41,42)(H4,28,29,32)(H4,30,31,33)(H2,35,36,43)/t18?,19-,20-,21-/m0/s1
InChI Key
SDNYTAYICBFYFH-KTYMLHDXSA-N
Canonical SMILES
CC(C)C(C(=O)NC(CCCN=C(N)N)C=O)NC(=O)C(CCCN=C(N)N)NC(=O)NC(CC1=CC=CC=C1)C(=O)O
1. [The necessity and possibilities of the antipain help organization in multyprofile clinics]
O I Zagorul'ko, A V Gnezdilov, L A Medvedeva, N V Samoĭlova Khirurgiia (Mosk). 2013;(1):13-6.
The personal work experience of the department of pain syndrome and analysis of foreign algologic service clearly demonstrated the necessity of similar adequate hierarchical medical service for treatment of chronic pain. The following principles should build the backbone of the service: multidisciplinary approach, usage of both traditional and alternative medicine, availability of help and stable feedback with tertiary hospitals. The algologic service should perform diagnostic, advisory and expert functions. The antipain center should obtain not only hospital facilities but also research laboratories and teaching centers.
2. Antipain inhibits N-methyl-N'-nitro-N-nitrosoguanidine-induced transformation and increases chromosomal aberrations
J A DiPaolo, S C Amsbaugh, N C Popescu Proc Natl Acad Sci U S A. 1980 Nov;77(11):6649-53. doi: 10.1073/pnas.77.11.6649.
The morphologic transformation induced in Syrian hamster embryo cells by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (0.25 microgram/ml of medium) is inhibited by posttreatment with antipain (6-600 microgram/ml), a protease inhibitor, but is unaffected by pretreatment. DNA replication relative to untreated controls is not affected by MNNG, antipain, or the combination of the two; no synergistic lethality of antipain and MNNG occurred as reflected in the cloning efficiency. Antipain was ineffective in influencing MNNG-induced sister chromatid exchanges, but it increased frequencies of chromosomal aberration (per metaphase) at 10, 26, and 40 hr when cells were treated with MNNG at 0.25 microgram/ml of medium followed by antipain 10 min later, the procedure used in the transformation studies. Antipain also increased the average number of aberrations at the second mitosis (34 hr) when the MNNG concentration was doubled. Chromatid exchanges increased 26 hr posttreatment with the combination of MNNG and antipain used for transformation. No difference in MNNG-induced aberrations was observed when antipain preceded MNNG by 24 hr. Although the mode of actin of antipain is unknown, antipain does not inhibit transformation by suppressing chromosomal rearrangements that could convert recessive mutations to the homozygous state.
3. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data
Loren Pickart, Anna Margolina Int J Mol Sci. 2018 Jul 7;19(7):1987. doi: 10.3390/ijms19071987.
The human peptide GHK (glycyl-l-histidyl-l-lysine) has multiple biological actions, all of which, according to our current knowledge, appear to be health positive. It stimulates blood vessel and nerve outgrowth, increases collagen, elastin, and glycosaminoglycan synthesis, as well as supports the function of dermal fibroblasts. GHK's ability to improve tissue repair has been demonstrated for skin, lung connective tissue, boney tissue, liver, and stomach lining. GHK has also been found to possess powerful cell protective actions, such as multiple anti-cancer activities and anti-inflammatory actions, lung protection and restoration of chronic obstructive pulmonary disease (COPD) fibroblasts, suppression of molecules thought to accelerate the diseases of aging such as NFκB, anti-anxiety, anti-pain and anti-aggression activities, DNA repair, and activation of cell cleansing via the proteasome system. Recent genetic data may explain such diverse protective and healing actions of one molecule, revealing multiple biochemical pathways regulated by GHK.
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