1. GPCR/G Protein Neuronal Signaling Anti-infection NF-κB Apoptosis Immunology/Inflammation
  2. Melanocortin Receptor Bacterial NF-κB Apoptosis Interleukin Related
  3. α-MSH (11-13)

α-MSH (11-13)  (Synonyms: ACTH-(11-13); Lys-Pro-Val; H-Lys-Pro-Val-OH)

Cat. No.: HY-129724
Handling Instructions Technical Support

α-MSH (11-13) (ACTH-(11-13)) is a C-terminal tripeptide of α-MSH that can cross the blood-brain barrier. α-MSH (11-13) exhibits antipyretic, anti-inflammatory, and antibacterial activities. α-MSH (11-13) also exerts neuroprotective effects after traumatic brain injury by inhibiting excessive activation of microglia and reducing neuronal apoptosis. α-MSH (11-13) can be used in research related to traumatic brain injury, fever, and bacterial infections.

For research use only. We do not sell to patients.

Custom Peptide Synthesis

α-MSH (11-13)

α-MSH (11-13) Chemical Structure

CAS No. : 67727-97-3

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Other In-stock Forms of α-MSH (11-13):

Other Forms of α-MSH (11-13):

Top Publications Citing Use of Products

View All Melanocortin Receptor Isoform Specific Products:

View All NF-κB Isoform Specific Products:

View All Interleukin Related Isoform Specific Products:

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

α-MSH (11-13) (ACTH-(11-13)) is a C-terminal tripeptide of α-MSH that can cross the blood-brain barrier. α-MSH (11-13) exhibits antipyretic, anti-inflammatory, and antibacterial activities. α-MSH (11-13) also exerts neuroprotective effects after traumatic brain injury by inhibiting excessive activation of microglia and reducing neuronal apoptosis. α-MSH (11-13) can be used in research related to traumatic brain injury, fever, and bacterial infections[1][2][3].

In Vitro

α-MSH (11-13) induces MC1R-dependent calcium signaling and inhibits TNF-α-stimulated NF-κB activation in MC1R-transfected CHO-K1 cells[1].
α-MSH (11-13) inhibits the production of TNF-α, IL-6, and nitric oxide in LPS (HY-D1056)-stimulated mouse microglial cell cultures[1].
α-MSH (11-13) (0-0.1 mM; 2 h) significantly inhibits colony formation of clinical methicillin-resistant Staphylococcus aureus/Candida albicans isolates[3].
α-MSH (11-13) (1 μM; 3 min) significantly increases the level of cAMP accumulation in permeabilized Candida albicans[3].
α-MSH (11-13) (0-0.1 mM; 2 h) enhances the killing activity of human neutrophils against clinical isolates of methicillin-resistant Staphylococcus aureus and Candida albicans[3].

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

In Vivo

α-MSH (11-13) (1 mg/kg; i.p.; single administration) reduces the volume of secondary cerebral contusion, alleviates microglial activation, and decreases neuronal apoptosis in a mouse model of traumatic brain injury[1].
α-MSH (11-13) (0.5-200 mg; intracerebroventricular injection, intravenous injection; single administration) dose-dependently reduces leukocytic pyrogen-induced fever in rabbits after central or peripheral administration[2].

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

Animal Model: C57Bl/6N (2-month-old male, 21-35 g, traumatic brain injury induced via controlled cortical impact)[1]
Dosage: 1 mg/kg
Administration: i.p.; single dose
Result: Reduced secondary brain contusion volume by 24%.
Decreased microglial activation.
Lowered number of apoptotic neurons.
Did not significantly change neurological severity score.
Animal Model: New Zealand white (adult)[2]
Dosage: 0.5 mg (i.c.v.); 1.0 mg (i.c.v.); 2.0 mg (i.c.v.); 2 mg (i.v.); 20 mg (i.v.); 200 mg (i.v.)
Administration: i.c.v.; single dose; i.v.; single dose
Result: Produced average percent reductions of the area under the control fever curve (over 1.5 hr) of 24% (0.5 mg i.c.v.), 31% (1.0 mg i.c.v.), and 48% (2.0 mg i.c.v.), with each dose significantly more antipyretic than lower doses.
Produced average percent reductions of the area under the control fever curve (over 1.5 hr) of 34% (2 mg i.v.), 27% (20 mg i.v.), and 67% (200 mg i.v.).
Had no effect on body temperature when 200 mg i.v.
dose was administered to afebrile rabbits.
Molecular Weight

342.43

Formula

C16H30N4O4

CAS No.
Sequence

Lys-Pro-Val

Sequence Shortening

KPV

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Purity & Documentation
References
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.
  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

 

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

     

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
α-MSH (11-13)
Cat. No.:
HY-129724
Quantity:
MCE Japan Authorized Agent: