2. Cytoskeleton Metabolic Enzyme/Protease
  3. Integrin MMP
  4. 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.

Custom Peptide Synthesis

KAFDITYVRLKF

KAFDITYVRLKF Chemical Structure

CAS No. : 208116-26-1

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KAFDITYVRLKF Related Antibodies

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αvβ1 αvβ3 αvβ5 αvβ6 αvβ8 α5β1 α1β1 α2β1 α4β1 α9β1 αIIbβ3 α4β7 αLβ2

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MMP-1 MMP-2 MMP-3 MMP-8 MMP-9 MMP-13 MMP-14 MMP-17 ADAM10 ADAM17 MMP-7 MMP-12 MMP-10 MMP ADAM8 MMP-19

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Description

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[1][2].

IC50 & Target[1]

MMP-9

 

αvβ3

 

In Vitro

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.

KAFDITYVRLKF Related Antibodies

Cell Migration Assay [1]

Cell Line: B16-F10 mouse melanoma cells
Concentration: 100 μg/mL
Incubation Time: 5 h
Result: Stimulated migration of B16-F10 cells, with the strongest enhancement activity among tested peptides.
Showed activity comparable to that of peptide A-13.
In Vivo

KAFDITYVRLK (0.2 mg; intravenous injection; single administration) significantly enhances experimental lung metastasis of B16-F10 melanoma cells in female C57BL6/N mice, increasing the average number of lung colonies to 481, which is a 3-fold increase compared with the control group[1].
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.

Animal Model: Sprague-Dawley (male, 200-250 g, 6-OHDA-induced dopaminergic neuron degeneration)[2]
Dosage: 2 mg/100 g
Administration: i.v.; once daily; 14 consecutive days
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.
Molecular Weight

1500.81

Formula

C73H113N17O17
CAS No.
Sequence

Lys-Ala-Phe-Asp-Ile-Thr-Tyr-Val-Arg-Leu-Lys-Phe
Sequence Shortening

KAFDITYVRLKF
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
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KAFDITYVRLKF Related Classifications

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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.

Keywords:

KAFDITYVRLKF208116-26-1IntegrinMMPMatrix metalloproteinasesParkinson's diseaseintegrin αvβ3neuronsB16-F10 mouse melanoma cellsendothelial cellsMMP-9melanomaLRRK2integrin α5β1monocytesInhibitorinhibitorinhibit

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