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Human neutrophil peptide-1

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Human neutrophil peptide-1 is an antimicrobial peptide found in Homo sapiens (Human). It belongs to the alpha-defensin family and has antimicrobial activity against gram-negative bacteria, gram-positive bacteria and Fungi.

Category

Functional Peptides

Catalog number

BAT-006220

CAS number

99287-08-8

Molecular Formula

C150H222N44O38S6

Molecular Weight

3442.03

Size	Price	Stock	Quantity
1 mg	$1099	In stock

Specification
Reference Reading

IUPAC Name

(1R,4S,7S,13S,16S,19R,22S,25S,31S,34S,37S,40S,46S,49R,52S,55S,58S,64S,67S,70S,73S,76S,79R,82R,87R,90S)-58-(3-amino-3-oxopropyl)-87-[[(2S)-2-aminopropanoyl]amino]-76-benzyl-7,22,52-tris[(2S)-butan-2-yl]-4,34,37,64-tetrakis(3-carbamimidamidopropyl)-31-(2-carboxyethyl)-46-[(1R)-1-hydroxyethyl]-40,55,90-tris[(4-hydroxyphenyl)methyl]-70-(1H-indol-3-ylmethyl)-16,25,73-trimethyl-67-(2-methylpropyl)-2,5,8,14,17,20,23,26,29,32,35,38,41,44,47,50,53,56,59,62,65,68,71,74,77,80,88,91-octacosaoxo-84,85,94,95,98,99-hexathia-3,6,9,15,18,21,24,27,30,33,36,39,42,45,48,51,54,57,60,63,66,69,72,75,78,81,89,92-octacosazatetracyclo[47.43.4.419,79.09,13]hectane-82-carboxylic acid

Alternative CAS

148093-65-6

Synonyms

H-Ala-Cys(1)-Tyr-Cys(2)-Arg-Ile-Pro-Ala-Cys(3)-Ile-Ala-Gly-Glu-Arg-Arg-Tyr-Gly-Thr-Cys(2)-Ile-Tyr-Gln-Gly-Arg-Leu-Trp-Ala-Phe-Cys(3)-Cys(1)-OH; L-alanyl-L-cysteinyl-L-tyrosyl-L-cysteinyl-L-arginyl-L-isoleucyl-L-prolyl-L-alanyl-L-cysteinyl-L-isoleucyl-L-alanyl-glycyl-L-alpha-glutamyl-L-arginyl-L-arginyl-L-tyrosyl-glycyl-L-threonyl-L-cysteinyl-L-isoleucyl-L-tyrosyl-L-glutaminyl-glycyl-L-arginyl-L-leucyl-L-tryptophyl-L-alanyl-L-phenylalanyl-L-cysteinyl-L-cysteine (2->30),(4->19),(9->29)-tris(disulfide); Human Defensin NP-1; alpha-Defensin-1; Defensin HNP-1 (human); HNP-1; Defensin human neutrophil peptide-1

Purity

>95%

Density

1.5±0.1 g/cm3

Sequence

ACYCRIPACIAGERRYGTCIYQGRLWAFCC (Disulfide bridge: Cys2-Cys30, Cys4-Cys19, Cys9-Cys29)

Storage

Store at -20°C

Solubility

Soluble in Water

InChI

InChI=1S/C150H222N44O38S6/c1-14-74(6)116-142(227)171-78(10)121(206)166-64-112(200)173-97(49-51-115(203)204)129(214)175-93(32-23-53-162-148(155)156)127(212)174-94(33-24-54-163-149(157)158)128(213)180-99(59-83-36-42-87(196)43-37-83)125(210)168-66-114(202)190-119(81(13)195)144(229)188-108-71-236-233-68-105-136(221)176-95(34-25-55-164-150(159)160)130(215)193-118(76(8)16-3)145(230)194-56-26-35-110(194)141(226)170-80(12)123(208)185-107(139(224)191-116)70-235-234-69-106(138(223)189-109(146(231)232)72-238-237-67-104(184-120(205)77(9)151)137(222)181-101(135(220)186-105)60-84-38-44-88(197)45-39-84)187-134(219)100(58-82-27-18-17-19-28-82)178-122(207)79(11)169-131(216)103(62-86-63-165-91-30-21-20-29-90(86)91)182-132(217)98(57-73(4)5)179-126(211)92(31-22-52-161-147(153)154)172-113(201)65-167-124(209)96(48-50-111(152)199)177-133(218)102(61-85-40-46-89(198)47-41-85)183-143(228)117(75(7)15-2)192-140(108)225/h17-21,27-30,36-47,63,73-81,92-110,116-119,165,195-198H,14-16,22-26,31-35,48-62,64-72,151H2,1-13H3,(H2,152,199)(H,166,206)(H,167,209)(H,168,210)(H,169,216)(H,170,226)(H,171,227)(H,172,201)(H,173,200)(H,174,212)(H,175,214)(H,176,221)(H,177,218)(H,178,207)(H,179,211)(H,180,213)(H,181,222)(H,182,217)(H,183,228)(H,184,205)(H,185,208)(H,186,220)(H,187,219)(H,188,229)(H,189,223)(H,190,202)(H,191,224)(H,192,225)(H,193,215)(H,203,204)(H,231,232)(H4,153,154,161)(H4,155,156,162)(H4,157,158,163)(H4,159,160,164)/t74-,75-,76-,77-,78-,79-,80-,81+,92-,93-,94-,95-,96-,97-,98-,99-,100-,101-,102-,103-,104-,105-,106-,107-,108-,109-,110-,116-,117-,118-,119-/m0/s1

InChI Key

KRJOFJHOZZPBKI-KSWODRSDSA-N

Canonical SMILES

CCC(C)C1C(=O)NC(C(=O)NCC(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NCC(=O)NC(C(=O)NC2CSSCC3C(=O)NC(C(=O)NC(C(=O)N4CCCC4C(=O)NC(C(=O)NC(CSSCC(C(=O)NC(CSSCC(C(=O)NC(C(=O)N3)CC5=CC=C(C=C5)O)NC(=O)C(C)N)C(=O)O)NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)CNC(=O)C(NC(=O)C(NC(=O)C(NC2=O)C(C)CC)CC6=CC=C(C=C6)O)CCC(=O)N)CCCNC(=N)N)CC(C)C)CC7=CNC8=CC=CC=C87)C)CC9=CC=CC=C9)C(=O)N1)C)C(C)CC)CCCNC(=N)N)C(C)O)CC1=CC=C(C=C1)O)CCCNC(=N)N)CCCNC(=N)N)CCC(=O)O)C

1. Human neutrophil peptide 1 promotes immune sterilization in vivo by reducing the virulence of multidrug-resistant Klebsiella pneumoniae and increasing the ability of macrophages

Tian He, Fan Tu, Subash C B Gopinath, Xiao-Chun Chen, Xiao-Hong Rui, Hui-Yun Wang, Zhi-Han Yan, Fu-Tao Cao Biotechnol Appl Biochem . 2022 Oct;69(5):2091-2101. doi: 10.1002/bab.2270.

By studying the expression in patients and cell modeling in vitro, antimicrobial peptides for Klebsiella were screened. Killing curve and membrane permeability experiments are used to study the antibacterial effect of antimicrobial peptides in vitro. Cytotoxicity-related indicators including lipopolysaccharide (LPS), capsule polysaccharide (CPS), and outer membrane protein expression were measured. Intranasal inoculation of pneumoconiosis was used to construct a mouse infection model, and the survival rate and cytokine expression level were tested. Human neutrophil peptide 1 (HNP-1) showed a significant antibacterial effect, which improved the permeability of the outer membrane of K. pneumoniae. Moreover, HNP-1 decreased LPS, CPS content, and outer membrane proteins. K. pneumoniae infection decreased antimicrobial peptide, oxidative stress, and autophagy-related genes, while HNP-1 increased these genes. After coculture with macrophages, the endocytosis of macrophages is enhanced and the bacterial load is greater in the K. pneumoniae + peptide group. Besides, higher levels of pp38 and pp65 in the K. pneumoniae + peptide group. HNP-1 rescued the cytotoxicity induced by K. pneumoniae. The survival rate is significantly improved after K. pneumoniae is treated by HNP-1. All cytokines in the peptide group were significantly higher. HNP-1 promotes immune sterilization by reducing the virulence of multidrug-resistant K. pneumoniae and increasing the ability of macrophages.

2. Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis

Tsutomu Tamai, Akihiko Ohshige, Akihiro Moriuchi, Hirohito Tsubouchi, Kotaro Kumagai, Seiichi Mawatari, Rie Ibusuki, Kazuaki Tabu, Shuji Kanmura, Kohei Oda, Akio Ido, Hirofumi Uto PLoS One . 2017 Apr 12;12(4):e0174913. doi: 10.1371/journal.pone.0174913.

Background and aims:Neutrophil infiltration of the liver is a typical feature of alcoholic liver injury. Human neutrophil peptide (HNP)-1 is an antimicrobial peptide secreted by neutrophils. The aim of this study was to determine if HNP-1 affects ethanol-induced liver injury and to examine the mechanism of liver injury induced by HNP-1.Methods:Transgenic (TG) mice expressing HNP-1 under the control of a β-actin-based promoter were established. Ethanol was orally administered to HNP-1 TG or wild-type C57BL/6N (WT) mice. SK-Hep1 hepatocellular carcinoma cells were used to investigate the effect of HNP-1 on hepatocytes in vitro.Results:After 24 weeks of ethanol intake, hepatic fibrosis and hepatocyte apoptosis were significantly more severe in TG mice than in WT mice. Levels of CD14, TLR4, and IL-6 in liver tissues were higher in TG mice than in WT mice. Apoptosis was accompanied by higher protein levels of caspase-3, caspase-8, and cleaved PARP in liver tissue. In addition, phosphorylated ASK1, ASK1, phosphorylated JNK, JNK1, JNK2, Bax, Bak and Bim were all more abundant in TG mice than in WT mice. In contrast, the level of anti-apoptotic Bcl2 in the liver was significantly lower in TG mice than in WT mice. Analysis of microRNAs in liver tissue showed that miR-34a-5p expression was significantly higher in TG mice than in WT mice. Furthermore, in the presence of ethanol, HNP-1 increased the apoptosis with the decreased level of Bcl2 in a concentration-dependent manner in vitro.Conclusions:HNP-1 secreted by neutrophils may exacerbate alcohol-induced hepatic fibrosis and hepatocyte apoptosis with a decrease in Bcl2 expression and an increase in miR-34a-5p expression.

3. Apoptotic human neutrophil peptide-1 anti-tumor activity revealed by cellular biomechanics

Miguel A R B Castanho, João T Barata, João M Freire, Diana Gaspar, Teresa R Pacheco Biochim Biophys Acta . 2015 Feb;1853(2):308-16. doi: 10.1016/j.bbamcr.2014.11.006.

Cancer remains a major cause of morbidity and mortality worldwide. Although progress has been made regarding chemotherapeutic agents, new therapies that combine increased selectivity and efficacy with low resistance are still needed. In the search for new anticancer agents, therapies based on biologically active peptides, in particular, antimicrobial peptides (AMPs), have attracted attention for their decreased resistance development and low cytotoxicity. Many AMPs have proved to be tumoricidal agents against human cancer cells, but their mode of action is still controversial. The existence of common properties shared by the membranes of bacteria and tumor cells points to similar lipid-targeting mechanisms in both cases. On the other hand, anticancer peptides (ACPs) also induce apoptosis and inhibit angiogenesis. Human neutrophil peptide-1 (HNP-1) is an endogenous AMP that has been implicated in different cellular phenomena such as tumor proliferation. The presence of HNP-1 in the serum/plasma of oncologic patients turns this peptide into a potential tumor biomarker. The present work reveals the different effects of HNP-1 on the biophysical and nanomechanical properties of solid and hematological tumor cells. Studies on cellular morphology, cellular stiffness, and membrane ultrastructure and charge using atomic force microscopy (AFM) and zeta potential measurements show a preferential binding of HNP-1 to solid tumor cells from human prostate adenocarcinoma when compared to human leukemia cells. AFM also reveals induction of apoptosis with cellular membrane defects at very low peptide concentrations. Understanding ACPs mode(s) of action will certainly open innovative pathways for drug development in cancer treatment.