KAFDITYVRLKF
KAFDITYVRLKF is a selective, competitive integrin αvβ3 binder. KAFDITYVRLKF induces the production of MMP-9. KAFDITYVRLKF blocks monocyte migration, promotes melanoma cell migration, protects neurons, and improves motor and cognitive functions. KAFDITYVRLKF can be used in research related to melanoma and Parkinson's disease.
For research use only. We do not sell to patients.
- CAS No.: 208116-26-1
- Formula: C73H113N17O17
- Molecular Weight:1500.81
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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MMP-9 |
αvβ3 |
KAFDITYVRLKF (100 μg/mL; 5 h) strongly promotes the migration of B16-F10 mouse melanoma cells in Boyden chamber assays[1].
KAFDITYVRLKF (2-20 μg/mL; 16 h) dose-dependently promotes the secretion of MMP-9 by B16-F10 mouse melanoma cells, increasing the secretion level by approximately 8-fold after treatment at 20 μg/mL for 16 h, but exerts no effect on the production of MMP-2[1].
KAFDITYVRLKF selectively binds to αvβ3 and reduces the migration of monocytes across endothelial cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:B16-F10 mouse melanoma cells
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Concentration:100 μg/mL
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Incubation Time:5 h
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Result:Stimulated migration of B16-F10 cells, with the strongest enhancement activity among tested peptides.
Showed activity comparable to that of peptide A-13.
KAFDITYVRLKF (2 mg/100 g; intravenous injection; once daily for 14 consecutive days) protects dopaminergic and γ-aminobutyric acidergic neurons, alleviates neuroinflammation and blood-brain barrier disruption, and improves motor and cognitive functions in mice with MPTP (HY-W114750)-induced Parkinson's disease[2].
KAFDITYVRLKF (2 mg/100 g; intravenous injection; once daily for 14 consecutive days) protects dopaminergic and γ-aminobutyric acidergic neurons, alleviates neuroinflammation and blood-brain barrier disruption, and improves motor and cognitive functions in rats with Parkinson's disease induced by 6-OHDA (HY-B1081)[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (male, 200-250 g, 6-OHDA-induced dopaminergic neuron degeneration)[2]
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Dosage:2 mg/100 g
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Administration:i.v.; once daily; 14 consecutive days
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Result:Ameliorated locomotor impairment in the open field test (increased total traveled distance and mean velocity relative to vehicle-treated 6-OHDA rats).
Improved motor coordination in the rotarod test (increased time spent on the rotating device relative to vehicle-treated 6-OHDA rats).
Rescued spatial cognitive impairment in the novel object recognition test (increased discrimination score relative to vehicle-treated 6-OHDA rats).
Reduced synchronous contraction of agonist and antagonist hindlimb muscles relative to vehicle-treated 6-OHDA rats.
Reduced serum IL-6 and ROS levels relative to vehicle-treated 6-OHDA rats.
Reduced CNS inflammatory cell infiltration.
Suppressed microglial activation (reduced Iba-1+ cell count in striatum and substantia nigra relative to vehicle group).
Reduced astrocyte activation (reduced GFAP+ cell count relative to vehicle group).
Downregulated pro-inflammatory mediators NF-κB and COX-2 in striatal and nigral tissues relative to vehicle group.
Reduced blood vessel leakage and BBB permeability relative to vehicle-treated 6-OHDA rats.
Increased expression of tight junction protein ZO-1 relative to vehicle group.
Increased NG2+ pericyte area density relative to vehicle group.
Increased survival of TH+ dopaminergic neurons in the striatum and substantia nigra relative to vehicle group.
Restored GABA transporter-positive neuron count in the striatum relative to vehicle group.
Restored CHAT+ neuron count in striatal and nigral tissues relative to vehicle group.
Reduced expression of neuronal apoptosis marker active caspase-3 relative to vehicle group.
Restored expression of synapse-associated protein Syn relative to vehicle group.
Reduced expression of PD progression marker pS129-α-syn relative to vehicle group.
Upregulated expression of neuronal activation marker cFos relative to vehicle group.
Suppressed upregulation of phospho-DARPP-32 relative to vehicle group.
Reversed downregulation of prodynorphin and upregulation of preproenkephalin relative to vehicle group.
Chemical Information
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CAS No. 208116-26-1
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Molecular Weight 1500.81
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Formula C73H113N17O17
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Sequence
Lys-Ala-Phe-Asp-Ile-Thr-Tyr-Val-Arg-Leu-Lys-Phe
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Sequence Shortening
KAFDITYVRLKF
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Kuratomi Y, et al. Laminin gamma 1 chain peptide, C-16 (KAFDITYVRLKF), promotes migration, MMP-9 secretion, and pulmonary metastasis of B16-F10 mouse melanoma cells. Br J Cancer. 2002;86(7):1169-1173. [Content Brief]
[2]. Cai HY, et al. Adjusting vascular permeability, leukocyte infiltration, and microglial cell activation to rescue dopaminergic neurons in rodent models of Parkinson's disease. NPJ Parkinsons Dis. 2021;7(1):91. Published 2021 Oct 8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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