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.
Biological Activity
Description
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. Further protocols information, click here.
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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.
In Vivo
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.
Protocols
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Scratch/Wound-Healing Migration Assay
The scratch/wound-healing migration assay measures collective migration of adherent cells into an experimentally created cell-free gap in a confluent monolayer. The readout is generated by imaging the gap immediately after scratching and at later time points, then quantifying reduction in wound area, wound width, or percentage closure as cells move into the denuded region. Gap closure reflects cell migration but may also include cell proliferation, so interpretation should distinguish migration-focused conditions from proliferation-driven closure when possible, such as by using short assay windows, serum-controlled conditions, cell counting, or proliferation controls reported in published protocols.
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Mitochondrial membrane-potential fluorescent assay
Mitochondrial membrane potential fluorescent assays estimate ΔΨm in living cells using lipophilic cationic dyes such as TMRM, TMRE, rhodamine 123, and JC-1, which accumulate in mitochondria according to membrane polarization; loss of signal after FCCP or CCCP treatment is interpreted as mitochondrial depolarization. TMRM/TMRE and rhodamine 123 are commonly used for semi-quantitative live-cell microscopy or flow cytometry, while JC-1 can report a shift from red aggregate fluorescence to green monomer fluorescence during depolarization; interpretation requires controls because dye concentration, quenching mode, cell type, dye efflux, and mitochondrial mass can affect fluorescence independently of ΔΨm.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Chemotaxis Gradient Chamber Assay 1
The chemotaxis gradient chamber assay is based on the principle of observing directional cell migration in response to a stable, linear or quasi-linear concentration gradient of a chemoattractant formed between two fluid reservoirs separated by a narrow observation chamber. Cells placed within the chamber respond to the gradient by polarized movement toward higher chemoattractant concentrations, allowing quantification of chemotactic behavior in real time under microscopy. The classic Zigmond chamber design enables simultaneous visualization of gradient formation and individual cell trajectories, making it suitable for studying leukocyte chemotaxis and other motile cell types in vitro.
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Under-Agarose Cell Migration Assay
The under-agarose cell migration assay is a classical in vitro chemotaxis method designed to evaluate directed cell movement through a semi-solid agarose matrix toward soluble chemoattractant gradients, enabling visualization and quantification of leukocyte or motile cell migration in a confined 2D-like environment. In this system, cells and chemoattractants are placed in separate wells cut into an agarose gel, allowing diffusion-driven gradient formation that guides directional migration, which is typically assessed by measuring migration distance, cell morphology changes, and accumulation toward the chemoattractant source. This assay has been widely used to study neutrophil and leukocyte chemotaxis as a simple alternative to filter-based migration systems and allows direct microscopic observation of migrating cells under near-physiological confinement conditions.
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Neural Crest/Neuronal Cell Migration Explant Assay
Neural crest (NC) and neuronal cell migration explant assays are in vitro systems in which neural tube-derived tissues are cultured to allow premigratory or newly emigrated neural crest cells to undergo epithelial-to-mesenchymal transition (EMT), migrate away from the explant, and form a measurable radial outgrowth that reflects migratory capacity and environmental responsiveness. These assays typically quantify migration by measuring the expansion of cell outgrowth from neural tube or neural plate border explants over time, often comparing early and later timepoints to derive a migration index such as a radius ratio, which reflects net cell dispersal from the explant core. Neural tube explant cultures preserve key aspects of neural crest behavior, including EMT, migration, and early differentiation, making them suitable for assessing intrinsic migratory ability and extrinsic cue dependence. However, studies emphasize that migratory outgrowth from neural tube explants may include non-n
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Human pluripotent stem cell midbrain dopaminergic neuron differentiation
Human pluripotent stem cells are directed toward midbrain dopaminergic neurons by first inducing a neural floor-plate-like progenitor state, then patterning cells with ventralizing SHH signaling and midbrain/WNT-FGF cues, and finally maturing progenitors into neurons expressing dopaminergic markers such as TH, NURR1/NR4A2, PITX3, DAT/SLC6A3, VMAT2/SLC18A2, GIRK2/KCNJ6, FOXA2, LMX1A, and EN1. The main readouts are loss of pluripotency, acquisition of FOXA2+/LMX1A+ midbrain floor-plate progenitors, emergence of βIII-tubulin+/MAP2+ neurons, and production of TH+ dopaminergic neurons with molecular, dopamine-release, and electrophysiological features of midbrain dopaminergic identity.
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Transwell/Boyden Chamber Migration Assay
The Transwell/Boyden chamber migration assay measures cell movement through a porous membrane separating an upper and lower chamber, usually after a chemoattractant gradient is established by placing cells in the upper chamber and chemoattractant-containing medium in the lower chamber. The readout is generated by quantifying cells that traverse the membrane and appear on the lower membrane surface or in the lower chamber, depending on whether the cell type is adherent or non-adherent. This assay reflects chemotactic or haptotactic migration rather than matrix invasion unless an extracellular-matrix barrier is added to the membrane.
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Mitochondrial membrane-potential and mitochondrial mass staining
Mitochondrial membrane potential staining measures the electrochemical polarization across the mitochondrial inner membrane in live cells using lipophilic cationic fluorescent probes; early rhodamine-based work showed that selective mitochondrial dye accumulation is lost when the mitochondrial transmembrane potential is dissipated. JC-1 reports mitochondrial polarization by shifting from green monomer fluorescence to red J-aggregate fluorescence as dye concentration increases within energized mitochondria; therefore, the red/green fluorescence ratio is used as a relative readout of mitochondrial membrane potential. TMRE or TMRM staining provides a single-channel relative readout because these cationic rhodamine esters accumulate in polarized mitochondria, and lower fluorescence indicates reduced mitochondrial polarization when acquisition and dye-loading conditions are controlled. Mitochondrial mass staining is commonly performed with MitoTracker Green FM or related MitoTracker dyes as
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3D Collagen/Hydrogel Matrix Migration Assay
The 3D collagen/hydrogel matrix migration assay is based on embedding cells within or on top of a fibrillar collagen type I-rich three-dimensional matrix to model in vivo-like extracellular matrix (ECM) architecture, enabling analysis of cell migration through a physically and biochemically relevant scaffold. In contrast to 2D migration systems, cells in 3D matrices interact with fibrillar collagen networks, requiring coordinated adhesion remodeling and proteolytic or non-proteolytic deformation mechanisms to move through confined spaces, thereby providing a more physiologically relevant readout of invasive and migratory behavior in tissue-like environments. Cell movement in 3D collagen matrices is typically quantified by tracking single-cell trajectories, invasion depth, or matrix penetration over time, reflecting combined effects of cytoskeletal dynamics, cell-ECM adhesion turnover, and ECM remodeling. These systems are widely used to study tumor cell invasion and stromal cell motili
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Cell-Exclusion Zone Migration Assay
The Cell-Exclusion Zone (CEZ) migration assay is an in vitro 2D cell migration method in which a defined cell-free area is created using removable physical barriers such as silicone stoppers, allowing cells to be seeded around the barrier and subsequently migrate into the cleared zone after barrier removal. This approach enables quantification of collective cell migration by monitoring repopulation of the initially cell-free region over time using microscopy-based imaging. Compared with scratch-based wound healing assays, barrier-based exclusion methods are designed to avoid mechanical damage to the extracellular matrix and reduce injury-induced effects on boundary cells, thereby improving interpretability of migration behavior in vitro. The assay readout is typically the progressive reduction in the cell-free area or the number of cells invading the exclusion zone, reflecting coordinated cell motility relevant to physiological processes such as wound healing, epithelial repair, and ca
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Chemotaxis Gradient Chamber Assay 2
Chemotaxis gradient chamber assays measure directional cell migration in response to a soluble chemical gradient by imaging cells as they move across a defined observation region; the readout is generated from time-lapse cell trajectories, displacement toward the gradient, forward migration index, trajectory plots, rose/polar plots, and statistical tests of non-random directionality. The Dunn chamber is a direct-viewing glass chamber in which cells migrate across a bridge between control and chemoattractant wells, allowing observation of cells in a linear concentration gradient; related direct-viewing formats include the Insall chamber, which supports defined unidirectional gradients and high numerical-aperture microscopy, and the μ-Slide Chemotaxis chamber, which supports long-term live-cell imaging and gradient characterization with fluorescent dye.
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)