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.
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- CAS 番号: 208116-26-1
- 分子式: C73H113N17O17
- 分子量:1500.81
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
IC50 & Target
[1]|
MMP-9 |
αvβ3 |
体外実験
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.
体内実験
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.
- Scratch/Wound-Healing Migration Assay
- Mitochondrial membrane-potential fluorescent assay
- Cell migration
- Zigmond Chamber Chemotaxis Assay
- Under-Agarose Cell Migration Assay
- Neural Crest/Neuronal Cell Migration Explant Assay
- Human pluripotent stem cell midbrain dopaminergic neuron differentiation
- Transwell/Boyden Chamber Migration Assay
- Mitochondrial membrane-potential and mitochondrial mass staining
- 3D Collagen/Hydrogel Matrix Migration Assay
- Cell-Exclusion Zone Migration Assay
- Dunn/Insall Chamber Chemotaxis Assay
化学情報
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CAS 番号 208116-26-1
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分子量 1500.81
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分子式 C73H113N17O17
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配列
Lys-Ala-Phe-Asp-Ile-Thr-Tyr-Val-Arg-Leu-Lys-Phe
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シーケンスの短縮
KAFDITYVRLKF
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
[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
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
KAFDITYVRLKF 関連分類
HY-P11780 関連分類
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