| ln Vitro |
KAFDITYVRLKF (100 μg/mL; 5 h) significantly promoted the migration of B16-F10 mouse melanoma cells in the Boyden chamber assay [1]. KAFDITYVRLKF (2–20 μg/mL; 16 h) dose-dependently promoted the secretion of MMP-9 from B16-F10 mouse melanoma cells, with an approximately 8-fold increase in MMP-9 secretion levels after 16 hours of treatment at a concentration of 20 μg/mL, but had no effect on MMP-2 production [1]. KAFDITYVRLKF selectively binds to αvβ3 and inhibits the migration of monocytes through endothelial cells [2].
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| ln Vivo |
KAFDITYVRLK (0.2 mg; intravenous injection; single dose) significantly enhanced experimental lung metastasis of B16-F10 melanoma cells in female C57BL6/N mice, increasing the average number of lung metastases to 481, which was three times that of the control group [1]. KAFDITYVRLKF (2 mg/100 g; intravenous injection; once daily for 14 days) protected dopaminergic and γ-aminobutyric acid-producing neurons, reduced neuroinflammation and blood-brain barrier disruption, and improved motor and cognitive function in MPTP-induced Parkinson's disease mice [2]. KAFDITYVRLKF (2 mg/100 g; intravenous injection; once daily for 14 days) protected dopaminergic and γ-aminobutyric acid-producing neurons, reduced neuroinflammation and blood-brain barrier disruption, and improved motor and cognitive function in 6-OHDA-induced Parkinson's disease rats [2].
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| Cell Assay |
Cell migration assay [1]
Cell Types: B16-F10 mouse melanoma cells Tested Concentrations: 100 μg/mL Incubation Duration: 5 hours Experimental Results: Stimulated B16-F10 cell migration, enhancing activity most strongly among all tested peptides. Activity was comparable to peptide A-13. |
| Animal Protocol |
Animal/Disease Models:Sprague-Dawley rats (male, 200-250 g, 6-OHDA-induced dopaminergic neuronal degeneration) [2]
Doses: 2 mg/100 g Route of Administration: Intravenous injection; once daily for 14 days Experimental Results: Improved motor impairment in open field test (increased total distance and average speed compared to carrier-treated 6-OHDA rats). Improved motor coordination in rotarod test (increased time spent on the rotarod compared to carrier-treated 6-OHDA rats). Improved spatial cognitive impairment in new object recognition test (increased discrimination score compared to carrier-treated 6-OHDA rats). Reduced synchronous contraction of hindlimb muscles of agonist and antagonist muscles compared to carrier-treated 6-OHDA rats. Reduced serum IL-6 and ROS levels compared to carrier-treated 6-OHDA rats. Reduced inflammatory cell infiltration in the central nervous system. Microglial activation was inhibited (fewer Iba-1+ cells in the striatum and substantia nigra compared to the vector group). Astrocyte activation was reduced (fewer GFAP+ cells compared to the vector group). Compared to the vector group, the expression of pro-inflammatory mediators NF-κB and COX-2 in the striatum and substantia nigra was downregulated. Vascular leakage and blood-brain barrier permeability were decreased compared to vector-treated 6-OHDA rats. Tight junction protein ZO-1 expression was increased compared to the vector group. NG2+ pericyte area density was increased compared to the vector group. The survival rate of TH+ dopaminergic neurons in the striatum and substantia nigra was increased compared to the vector group. The number of GABA transporter-positive neurons in the striatum returned to normal compared to the vector group. The number of CHAT-positive neurons in the striatum and substantia nigra returned to normal compared to the vector group. The expression of the neuronal apoptosis marker caspase-3 was decreased compared to the vector group. The expression of the synaptic protein syn was restored to normal compared to the vector group. Compared with the vector group, the expression of pS129-α-syn, a marker of Parkinson's disease progression, was decreased. The expression of cFos, a marker of neuronal activation, was upregulated compared with the vector group. The upregulation of phosphorylated DARPP-32 was inhibited compared with the vector group. The downregulation of pro-dynorphin and the upregulation of pro-endorphin were both reversed compared with the vector group. |
| References |
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| CAS # |
208116-26-1
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|---|---|
| Sequence |
Lys-Ala-Phe-Asp-Ile-Thr-Tyr-Val-Arg-Leu-Lys-PheKAFDITYVRLKF
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| SequenceShortening |
KAFDITYVRLKF
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| Appearance |
Typically exists as solids at room temperature
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 :Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400  (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.