| Size | Price | Stock | Qty |
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| 1mg |
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| Other Sizes |
| Targets |
beta-Amyloid (1-42), human, Ala(13C3,15N) TFA targets the same biological pathways as the unlabeled Abeta1-42, but as a labeled standard it is primarily a tool for quantification rather than a modulator. Abeta1-42 binds to multiple neuronal receptors including the cellular prion protein (PrPc), metabotropic glutamate receptor 5 (mGluR5), N-methyl-D-aspartate (NMDA) receptors, and the receptor for advanced glycation end products (RAGE). These interactions trigger oxidative stress, calcium dysregulation, synaptic dysfunction, and neuroinflammation, ultimately leading to neuronal death in Alzheimer‘s disease. The labeled peptide is used as a tracer to study these interactions by mass spectrometry, enabling precise measurement of Abeta concentrations in various experimental contexts. It can also be used in receptor binding assays to compete with unlabeled Abeta for receptor occupancy, with detection via MS rather than radiolabels.
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| ln Vitro |
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Studies involving the human use of drugs labeled with deuterium suggest that these compounds may offer some advantages when compared with their nondeuterated counterparts. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs. Deutetrabenazine is the first deuterated drug to receive Food and Drug Administration approval. This deuterated form of the drug tetrabenazine is indicated for the treatment of chorea associated with Huntington's disease as well as tardive dyskinesia. Ongoing clinical trials suggest that a number of other deuterated compounds are being evaluated for the treatment of human diseases and not merely as research tools.
In vitro, beta-Amyloid (1-42), human, Ala(13C3,15N) TFA exhibits the same aggregation properties as the unlabeled peptide. When freshly prepared as a monomer (dissolved in HFIP or NaOH, then diluted in PBS to 10-50 microM), the peptide remains monomeric initially. Over time at 37degC, it forms soluble oligomers (within 4-24 hours) and eventually insoluble fibrils (72+ hours). The isotope labeling does not alter the peptide's aggregation kinetics or secondary structure (predominantly beta-sheet in aggregated forms). The labeled peptide can be used as an internal standard to accurately quantify unlabeled Abeta1-42 in cell culture supernatants or lysates by LC-MS/MS. In neurotoxicity assays, the unlabeled Abeta1-42 (5-20 microM) induces neuronal cell death in primary cortical neurons or SH-SY5Y cells with an IC50 of 5-10 microM after 48 hours, as measured by MTT or LDH release. The labeled version is biologically identical. |
| ln Vivo |
Deuterated compounds may, in some cases, offer advantages over nondeuterated forms, often through alterations in clearance. Deuteration may also redirect metabolic pathways in directions that reduce toxicities. The approval of additional deuterated compounds may soon follow. Clinicians will need to be familiar with the dosing, efficacy, potential side effects, and unique metabolic profiles of these new entities.
In vivo, beta-Amyloid (1-42), human, Ala(13C3,15N) TFA is administered to animals as a tracer for metabolic studies, not as a therapeutic. In rodent models of Alzheimer's disease (e.g., wild-type mice or APP/PS1 transgenic mice), injection of the labeled Abeta peptide (typically 1-10 microg, intracerebroventricularly or intrahippocampally) allows quantification of its clearance rate from brain to blood and cerebrospinal fluid. Using LC-MS/MS, the labeled peptide can be distinguished from endogenous Abeta, enabling precise measurement of half-life and distribution. Studies have shown that injected Abeta1-42 is cleared from mouse brain with a half-life of approximately 1-2 hours. The labeled peptide can also be used to assess the efficacy of anti-Abeta antibodies or beta-secretase inhibitors in reducing Abeta levels. It does not cause the full pathological phenotype of Alzheimer's disease when injected acutely due to the lack of chronic accumulation. |
| Enzyme Assay |
General protocol for in vitro enzyme/receptor binding (non-cellular): For receptor binding studies, perform a competitive binding assay using radiolabeled Abeta or a labeled tracer. Coat a 96-well plate with recombinant PrPc or mGluR5 protein (1 microg/well) overnight at 4degC. Block with 5% BSA in PBS for 1 hour. Add increasing concentrations of unlabeled Abeta1-42 (0.1-10 microM) mixed with a fixed concentration of beta-Amyloid (1-42), human, Ala(13C3,15N) TFA (0.1 microM, used as an MS-detectable tracer) to each well. Incubate for 2 hours at room temperature. Wash wells three times with PBS-0.05% Tween-20. Elute bound peptides with 0.1% formic acid in 50% acetonitrile. Analyze eluates by LC-MS/MS, monitoring the mass transitions of the labeled peptide (m/z for 13C3,15N-Ala) versus unlabeled peptide. Calculate specific binding as percentage of total added tracer that is recovered from each well. Determine IC50 and Ki values using non-linear regression of displacement curves. This approach avoids radioactivity while maintaining sensitivity.
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| Cell Assay |
General protocol for in vitro cell-based experiments: For Abeta production and clearance studies, culture SH-SY5Y neuroblastoma cells stably expressing human APP (amyloid precursor protein) or primary mouse cortical neurons in Neurobasal medium with B27 supplement. Treat cells with gamma-secretase inhibitor (e.g., DAPT, 1 microM) to block endogenous Abeta production, if measuring clearance. Add beta-Amyloid (1-42), human, Ala(13C3,15N) TFA (100 nM to 1 microM) to the culture medium. Incubate for 2-48 hours. Collect culture supernatants at various time points. For intracellular Abeta measurement, wash cells with PBS, lyse in RIPA buffer with protease inhibitors. Add a known amount of internal standard (e.g., Abeta1-40, 13C-labeled) to each sample. Precipitate proteins with cold acetonitrile (1:3 v/v), centrifuge, and dry supernatant under vacuum. Reconstitute in 0.1% formic acid in water. Analyze by LC-MS/MS using a C18 column and a gradient of water/acetonitrile with 0.1% formic acid. Quantify labeled and unlabeled Abeta by multiple reaction monitoring (MRM) of specific peptide fragments (e.g., the N-terminal fragment). Calculate clearance rate as disappearance of labeled Abeta over time.
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| Animal Protocol |
General protocol for in vivo animal experiments: Use 8-10-week-old male C57BL/6 mice. Prepare beta-Amyloid (1-42), human, Ala(13C3,15N) TFA by dissolving in 0.1% NH4OH (to 1 mg/mL), then diluting to 0.2 mg/mL in PBS (final pH 7.4). Anesthetize mice with isoflurane and place in a stereotaxic frame. Inject 2 microL (400 ng) of labeled Abeta peptide into the right lateral ventricle (coordinates: AP -0.3 mm, ML +1.0 mm, DV -2.5 mm from bregma) or directly into the hippocampus (AP -2.0 mm, ML +/-1.5 mm, DV -1.8 mm). Allow 5 minutes for diffusion. At time points 0.5, 1, 2, 4, 8, 12, and 24 hours post-injection, euthanize mice (n=3-4 per time point). Collect cerebrospinal fluid (CSF) from cisterna magna, blood via cardiac puncture into EDTA tubes (centrifuge for plasma), and perfuse brain with PBS. Homogenize brain tissue in 1 mL PBS with protease inhibitors. Process CSF, plasma, and brain homogenates for LC-MS/MS analysis as described in the cell protocol. Calculate elimination half-life by fitting a one-phase decay model to the concentration-time data. Compare clearance rates in wild-type versus Alzheimer's model mice.
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| ADME/Pharmacokinetics |
General pharmacokinetic properties: For intracerebroventricularly (ICV) injected beta-Amyloid (1-42), human, Ala(13C3,15N) TFA in mice, the elimination half-life from brain is approximately 1-2 hours. Peak brain concentration occurs within 5 minutes after ICV injection, reaching approximately 20-50 ng/g tissue (depending on injection dose). The peptide rapidly effluxes from brain to blood via perivascular drainage and transport across the blood-brain barrier (BBB) mediated by LRP1 (low-density lipoprotein receptor-related protein 1). Within 1 hour, approximately 30-50% of the injected dose is found in plasma, with peak plasma concentration (Cmax) reached at 1-2 hours. Plasma half-life is short (<30 minutes) due to rapid proteolytic degradation and clearance by the liver and kidneys. Less than 1% of the injected dose is excreted unchanged in urine. The peptide is metabolized by various proteases including neprilysin, insulin-degrading enzyme (IDE), and matrix metalloproteinases. The labeled peptide is stable in frozen brain homogenates for months at -80degC.
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| Toxicity/Toxicokinetics |
General toxicity profile: beta-Amyloid (1-42), human, Ala(13C3,15N) TFA is not intended for therapeutic use; toxicity data are derived from acute administration studies in animals. When injected intracerebroventricularly in mice at doses up to 2 microg (common tracer dose), no acute behavioral changes or mortality are observed over 24-72 hours. Higher doses (10-50 microg) can cause seizures, neuronal apoptosis, and neuroinflammation, as unlabeled Abeta1-42 is known to be neurotoxic. The labeled version shares this neurotoxicity profile. In vitro, the peptide (10-50 microM) induces 50-80% cell death in cultured neurons after 48 hours (MTT assay), similar to unlabeled Abeta. The TFA salt is not systemically toxic at the low doses used in tracer studies. Standard safety precautions for working with neurotoxic peptides should be followed: wear gloves and lab coat, avoid generating aerosols, and dispose of as hazardous biological waste. The peptide is not classified as carcinogenic or mutagenic based on limited data.
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| References |
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| Additional Infomation |
beta-Amyloid (1-42), human, Ala(13C3,15N) TFA is a highly purified stable isotope-labeled peptide used as an internal standard for mass spectrometry. The peptide sequence is: Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala. The labeled alanine (Ala) residues at positions 2, 21, and/or 30 (depending on the product) contain 13C3 and 15N. Molecular weight of the labeled peptide is approximately 4518.01 Da, an increase of about 4 Da per labeled alanine compared to unlabeled. The peptide is supplied lyophilized, store at -20degC, protect from light. Before use, monomerize by dissolving in 1,1,1,3,3,3-hexafluoro-2-propanol (HFIP) to 1 mM, incubate at room temperature for 1 hour, aliquot, and dry under nitrogen; then redissolve in DMSO to 5 mM, and dilute into PBS for experiments. The product is for research use only, not for human diagnostic or therapeutic use.
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| Molecular Formula |
C20013C3H311N5415NO60S
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| Molecular Weight |
4518.01
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| Related CAS # |
β-Amyloid (1-42), human TFA; β-Amyloid (1-42), human; β-Amyloid-15N (1-42), human TFA
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| Sequence |
Asp-{Ala(13C3,15N)}-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-AlaD-{Ala(13C3,15N)}-EFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
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| Appearance |
white solid powder
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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, avoid exposure to moisture. |
| 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.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.2213 mL | 1.1067 mL | 2.2134 mL | |
| 5 mM | 0.0443 mL | 0.2213 mL | 0.4427 mL | |
| 10 mM | 0.0221 mL | 0.1107 mL | 0.2213 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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