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| Targets |
The primary target of the KLVFF peptide is the full-length amyloid-beta (Abeta) protein itself. KLVFF functions as a beta-sheet breaker or aggregation inhibitor by binding to the homologous central hydrophobic region (CHR) of Abeta via molecular recognition. This homotypic interaction disrupts the intermolecular beta-sheet formation that drives Abeta fibrillogenesis, preventing the assembly of Abeta into toxic oligomers and amyloid fibrils.
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| ln Vitro |
After 12 days of incubation at 37°C, β-Amyloid peptide(16–20) (-NH2) suppresses the development of Abeta fibrils at a dose of 1:2 molar ratio (Aβ40/peptide) [1].
In vitro, the KLVFF peptide (residues 16-20 of Abeta) binds to full-length Abeta peptides via homologous interaction with their central hydrophobic region. This binding inhibits Abeta aggregation in a concentration-dependent manner. KLVFF has been shown to block the formation of Abeta oligomers and fibrils, the primary neurotoxic species implicated in Alzheimer‘s disease. Modification of KLVFF (e.g., retro-inverso or multivalent dendrimer display) can enhance its proteolytic stability and inhibitory potency. |
| ln Vivo |
The KLVFF peptide has been studied in vivo in preclinical models of Alzheimer's disease. When administered systemically or intracerebrally in transgenic mouse models of AD, KLVFF-based peptidic inhibitors can reduce cerebral amyloid plaque burden, decrease levels of soluble Abeta oligomers, and improve cognitive function in behavioral tests (e.g., Morris water maze). The retro-inverso forms of KLVFF show enhanced stability against proteolytic degradation and greater efficacy in reducing Abeta toxicity.
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| Enzyme Assay |
A non-cellular assay for KLVFF peptide activity is the thioflavin T (ThT) aggregation assay. Synthetic Abeta1-42 or Abeta1-40 is incubated with varying concentrations of KLVFF (e.g., 0.1-100 uM) in PBS (pH 7.4) at 37degC with shaking. After 24-72 hours, Thioflavin T is added to the samples, and fluorescence intensity (excitation 440 nm, emission 485 nm) is measured. A reduction in ThT fluorescence compared to Abeta alone indicates inhibition of fibril formation by KLVFF.
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| Cell Assay |
For cellular assays, neuroblastoma cells (e.g., SH-SY5Y) or primary cortical neurons are exposed to pre-aggregated Abeta42 (5-20 uM) in the presence or absence of KLVFF peptide (e.g., 1-50 uM). After 24-72 hours of incubation, cell viability is assessed using MTT or LDH release assays. KLVFF should protect cells from Abeta-induced toxicity by preventing the formation of neurotoxic aggregates. Alternatively, co-incubation with KLVFF prior to Abeta addition enhances its inhibitory effects.
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| Animal Protocol |
In an in vivo animal protocol, transgenic mouse models of Alzheimer‘s disease (e.g., APP/PS1 or Tg2576 mice) are used. KLVFF peptide is administered via intracerebroventricular (ICV) injection (e.g., 10-50 ug per mouse) or via intraperitoneal (IP) injection if formulated for improved stability. After a treatment period of weeks, mice are sacrificed, and brain sections are stained with Congo red or Thioflavin S to assess amyloid plaque burden. Alternatively, solubilized brain Abeta levels are quantified by ELISA to measure treatment efficacy.
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| ADME/Pharmacokinetics |
No specific pharmacokinetic data is provided for KLVFF in these references. As a pentapeptide, KLVFF is susceptible to rapid proteolytic degradation by peptidases in the blood and tissues, leading to a short half-life in vivo. The peptide has poor oral bioavailability and limited ability to cross the blood-brain barrier (BBB). Chemical modifications (e.g., retro-inverso or D-amino acid substitution) are required to enhance its stability and brain penetration for in vivo efficacy studies.
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| Toxicity/Toxicokinetics |
No detailed toxicological data is provided for KLVFF. As a short peptide, it is generally considered to have low toxicity when used at standard research concentrations (1-100 uM) in vitro. In vivo studies using stabilized KLVFF derivatives at therapeutic doses report no significant adverse effects, though local injection (ICV) may cause minor inflammation at the injection site. Standard laboratory safety precautions for handling synthetic peptides should be followed.
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| References | |
| Additional Infomation |
The KLVFF pentapeptide is one of the most important tools in Alzheimer‘s disease research, representing the minimal self-recognition motif required for Abeta aggregation. Residues 16-20 (KLVFF) of the Abeta sequence are known to be essential for the nucleation-dependent polymerization of Abeta into amyloid fibrils. This sequence has been used extensively to develop peptidic and peptidomimetic inhibitors of Abeta aggregation, including retro-inverso peptides and multivalent dendrimer conjugates, which serve as lead compounds for therapeutic development. Unlabeled KLVFF is also used as a reference standard in mass spectrometry and HPLC methods for characterizing Abeta aggregation inhibitors.
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| Molecular Formula |
C35H52N6O6
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|---|---|
| Molecular Weight |
652.82
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| Exact Mass |
652.395
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| CAS # |
153247-40-6
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| PubChem CID |
9852568
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| Appearance |
White to off-white solid powder
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| LogP |
4.618
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| Hydrogen Bond Donor Count |
7
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| Hydrogen Bond Acceptor Count |
8
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| Rotatable Bond Count |
20
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| Heavy Atom Count |
47
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| Complexity |
995
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| Defined Atom Stereocenter Count |
5
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| SMILES |
CC(C)C[C@@H](C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N[C@@H](CC2=CC=CC=C2)C(=O)O)NC(=O)[C@H](CCCCN)N
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| InChi Key |
SICITCLFXRGKJW-IIZANFQQSA-N
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| InChi Code |
InChI=1S/C35H52N6O6/c1-22(2)19-27(38-31(42)26(37)17-11-12-18-36)33(44)41-30(23(3)4)34(45)39-28(20-24-13-7-5-8-14-24)32(43)40-29(35(46)47)21-25-15-9-6-10-16-25/h5-10,13-16,22-23,26-30H,11-12,17-21,36-37H2,1-4H3,(H,38,42)(H,39,45)(H,40,43)(H,41,44)(H,46,47)/t26-,27-,28-,29-,30-/m0/s1
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| Chemical Name |
(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2,6-diaminohexanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]-3-phenylpropanoyl]amino]-3-phenylpropanoic acid
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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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| 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) |
H2O: 33.33 mg/mL (51.06 mM)
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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.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.5318 mL | 7.6591 mL | 15.3182 mL | |
| 5 mM | 0.3064 mL | 1.5318 mL | 3.0636 mL | |
| 10 mM | 0.1532 mL | 0.7659 mL | 1.5318 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
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.
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