Heart-homing peptide

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Heart-homing peptide is a heart-targeting peptide with the sequence CRPPR that mediates cardiac endothelial targeting and accumulates in cardiac tissues. Heart-homing peptide mediates the translocation of liposomal and exosomal cargos across cardiac endothelium into interstitial tissues, enhances the accumulation of exosomes in the heart, and inhibits the GP130-STAT3/ERK1/2/AKT pathway. Heart-homing peptide accumulates at sites of ischemia/reperfusion, myocardial infarction and hypertrophy in mice. Heart-homing peptide can be used for the research of cardiovascular diseases.

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Heart-homing peptide 화학구조

CAS No. : 876460-72-9

사이즈		재고
MOQ		Minimum order quantity
50 mg		견적 받기
100 mg		견적 받기
250 mg		견적 받기
Other size		견적 받기

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Other In-stock Forms of Heart-homing peptide:

Heart-homing peptide TFA

Other Forms of Heart-homing peptide:

Heart-homing peptide TFA In-stock

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•Related Small Molecules:

•Related Proteins:

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View All Isoforms

STAT3 STAT5 STAT6 STAT1

View All ERK Isoform Specific Products:

View All Isoforms

ERK ERK1 ERK2 ERK5 ERK8

View All Akt Isoform Specific Products:

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Akt Akt1 Akt2 Akt3

Biological Activity
순도&문서
References
고객리뷰

제품 설명

In Vivo

Heart-homing peptide-exposed liposomes (7-60 mg/kg; i.v.; single dose) deliver cargo across intact murine cardiac endothelium efficiently, with peak accumulation and transport observed at a 20 mg/kg single i.v. dose, resulting in a 47-fold increase in cardiac tissue fluorescence relative to non-targeted liposomes within 30 minutes^[1].
Exosomes displaying heart-homing peptide (4 mg/kg; i.v.; every third day; 7 doses total) preferentially accumulate in mouse hearts, significantly improve cardiac function, reduce left ventricular hypertrophy and fibrosis, and normalize hypertrophy signaling molecules in TAC-induced cardiac hypertrophy, with effects mediated via miRNA-148a-dependent suppression of the GP130-STAT3/ERK1/2/AKT pathway^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	FVB (2-month old, male, 20-25 g)^[1]
Dosage:	7 mg/kg; 20 mg/kg; 60 mg/kg
Administration:	i.v.; single dose
Result:	Achieved 47-fold greater fluorescence in cardiac tissue surrounding vascular lumens than non-targeted liposomes and 64-fold greater than free dye within 30 minutes of 20 mg/kg injection. Increased tissue, endothelial, and punctate fluorescence intensities from 7 mg/kg to 20 mg/kg, with no further increase at 60 mg/kg, indicating saturation of accumulation and trans-endothelial transport. Maintained cardiac fluorescence intensity at ~40% of the 30-minute value at 24 hours post-injection, which was significantly greater than control groups. Detected fluorescence above non-treated controls in 37.0% of endothelial (CD31+) cells, 0.63% of cardiomyocytes (MF20+), and 5.3% of fibroblasts (Thy1.1+) at 4 hours post-injection of 60 mg/kg liposomes. Detected fluorescence above non-treated controls in 29.1% of endothelial (CD31+) cells, 0.80% of cardiomyocytes (MF20+), and 4.0% of fibroblasts (Thy1.1+) at 12 hours post-injection of 60 mg/kg liposomes.

Animal Model:	C57BL/6 (10-week-old male, TAC-induced pressure overload)^[3]
Dosage:	4 mg/kg
Administration:	i.v.; every third day; 7 doses total
Result:	Accumulated at nearly double the mean fluorescence intensity in mouse hearts 24 hours post-single intravenous administration compared to non-targeted exosomes. Significantly ameliorated TAC-induced reductions in left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) at days 28 and 42 post-TAC, and significantly improved left ventricular end-systolic volume (LVV.s), diastolic left ventricular anterior wall thickness (LVAW.d), systolic left ventricular anterior wall thickness (LVAW.s), and left ventricular mass compared to PBS controls. Reversed TAC-induced mean arterial blood pressure elevation from 116.70 mmHg to 92.37 mmHg. Significantly reduced serum levels of angiotensin II (Ang II) and N-terminal pro B-type natriuretic peptide (NT-proBNP), and lung wet/dry weight ratio compared to PBS controls. Significantly reduced TAC-induced increases in heart/body weight ratio, heart weight/tibial length ratio, and relative cardiomyocyte surface area (increased by 30% in PBS-treated TAC mice). Significantly reduced TAC-induced upregulation of hypertrophic marker genes Acta1, Nppa, Nppb, and the Myh7/Myh6 ratio, and significantly decreased perivascular and myocardial interstitial fibrosis from 19.49% and 16.88% in PBS-treated TAC mice to 2.43% and 1.13%. Significantly reduced TAC-induced upregulation of hypertrophy-associated proteins β-MHC, BNP, GP130, p-ERK1/2, p-AKT, and p-STAT3 in ventricular tissues. Restored TAC-induced reduction in cardiac miRNA-148a levels to 252.30% of sham levels (vs. 66.83% in PBS-treated TAC mice).

분자량

627.76

화학식

C₂₅H₄₅N₁₁O₆S

CAS No.

876460-72-9

Sequence

Cys-Arg-Pro-Pro-Arg

Sequence Shortening

CRPPR

선적

Room temperature in continental US; may vary elsewhere.

보관

Please store the product under the recommended conditions in the Certificate of Analysis.

순도&문서

Handling Instructions (2659 KB)

References

[1]. Zhang H, et al. The cargo of CRPPR-conjugated liposomes crosses the intact murine cardiac endothelium. J Control Release. 2012;163(1):10-17. [Content Brief]

[2]. Rodríguez-Castejón J, et al. Targeting strategies with lipid vectors for nucleic acid supplementation therapy in Fabry disease: a systematic review. Drug Deliv Transl Res. 2024;14(10):2615-2628. [Content Brief]

[3]. Mao L, et al. Heart-targeting exosomes from human cardiosphere-derived cells improve the therapeutic effect on cardiac hypertrophy. J Nanobiotechnology. 2022;20(1):435. Published 2022 Oct 4.