HE4-1 leech peptide
HE4-1 leech peptide is a p38 MAPK inhibitor with an additional c-Jun N-terminal kinase (JNK) inhibitory role. HE4-1 leech peptide suppresses macrophage migration, and does not significantly affect macrophage immunological activities including phagocytic ability, lysozyme activity, and expression levels of most inflammatory factors. HE4-1 leech peptide can be used for the research of atherosclerosis.
For research use only. We do not sell to patients.
- CAS No.: 2531396-44-6
- Formula: C59H96N16O25
- Molecular Weight:1429.49
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
HE4-1 leech peptide (200-800 μg/mL; 24 h after 2 h LPS pretreatment) inhibits LPS-induced migration of RAW264.7 macrophages through p38 MAPK and JNK signaling pathways, and downregulates transcription of MEKK4 and ASK2[1].
HE4-1 leech peptide (200-800 μg/mL; 24 h after 2 h LPS pretreatment) does not significantly affect phagocytic ability, lysozyme activity, or secretion of IL-1β, IL-6, or IL-12 in RAW264.7 macrophages at concentrations up to 800 μg/mL, but increases TNF-α secretion at 400 and 800 μg/mL[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:RAW264.7 cells
-
Concentration:200-800 μg/mL
-
Incubation Time:24 h (after 2 h LPS pretreatment)
-
Result:Inhibited LPS-induced migration of RAW264.7 cells; reduced LPS-induced macrophage migration by 15.2% at 800 μg/mL.\nInhibited LPS-induced migration of RAW264.7 macrophages by 14.9% at 800 μg/mL, similar to the effect of HE4-1.
-
Cell Line:RAW264.7 cells
-
Concentration:200-800 μg/mL
-
Incubation Time:24 h (after 2 h LPS pretreatment)
-
Result:Did not alter total JNK or p38 protein levels; significantly inhibited LPS-induced phosphorylation of JNK and p38 at 800 μg/mL.
Chemical Information
-
CAS No. 2531396-44-6
-
Molecular Weight 1429.49
-
Formula C59H96N16O25
-
Sequence
Glu-Ala-Gly-Ser-Ala-Lys-Glu-Leu-Glu-Gly-Asp-Pro-Val-Ala-Gly
-
Sequence Shortening
EAGSAKELEGDPVAG
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
-
Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
-
Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)