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β-Amyloid (1-15) is a fragment of β-Amyloid peptide. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
β-Amyloid (1-16) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
β-Amyloid (1-28) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
MW108 (MW01-11-108SRM) hydrochloride is a selective and CNS-penetrant p38αMAPK inhibitor with a Ki of 114 nM. MW108 hydrochloride ameliorates beta-amyloid induced synaptic and cognitive dysfunction .
β Amyloid(17-28) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid(17-28) human enhances aggregation of full-length β Amyloid40, producing toxic aggregates in Alzheimer's disease (AD) .
β Amyloid(28-35) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid oligomers are neurotoxic, and β Amyloid(28-35) human can interact with neuronal membranes, regulate secondary structure and neurotoxicity, and cause Alzheimer's disease. β Amyloid(28-35) human has anisotropic effects on the acidic phospholipid DPH, resulting in enhanced internal fluidity of lipid membrane bilayers .
β-Amyloid (1-16) rat is a β-amyloid peptide (Abeta), a metal-binding domain fragment of amyloid. Three amino acid substitutions in β-Amyloid (1-16) rat that differ from humans render rats and mice less susceptible to AD-like neurodegeneration .
β-Amyloid (1-9), an N-terminal fragment of beta amyloid, consists of amino acid residues 1 to 9. β-Amyloid (1-9) contains a B cell epitope, but it does not include T cell epitopes. Omission of residues 1 to 9 from the full-length Alzheimer'sβ-Amyloid peptide 1 to 40 does not prevent the peptide from forming amyloid fibrils or eliminate fibril polymorphism .
β Amyloid (1-14), human is a peptide fragment of β-amyloid protein (Aβ), which is obtained by hydrolysis of Aβ1-40 peptide by catalytic antibody light chain #7TR. β Amyloid (1-14), human can be used for Alzheimer's disease research .
β-Amyloid (1-40) (rat) is a rat form of the amyloidβ-peptide, which accumulates as an insoluble extracellular deposit around neurons, giving rise to the senile plaques associated with Alzheimer's disease (AD). β-Amyloid (1-40) (rat) increases 45Ca 2+ influx, induces neurodegeneration in the rat hippocampal neurons of the CA1 subfield. β-Amyloid (1-40) (rat) induces apoptosis. β-Amyloid (1-40) (rat) can be used for the research of Alzheimer's disease .
β-Amyloid (1-37) (human) correlates moderately with Mini-Mental State Examination (MMSE) scores in Alzheimer disease. β-Amyloid (1-37) (human) possesses an added diagnostic value .
Biotin-β-Amyloid (17-40) is a N-terminal-labelled biotinylated amyloid-?-(1-40) peptide. β-Amyloid (17-40) is a 24-residue fragment of the Aβ protein via?post-translational processing of amyloid precursor protein (APP) .
β-Amyloid (1-43)(human) is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
β-Amyloid (1-43)(human) TFA is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) TFA shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) TFA could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
β-Amyloid 22-35 (Amyloidβ-Protein 22-35), the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
β-Amyloid peptide(16-20) is a amino acid sequences (KLVFF) of Amyloid-β (Abeta). β-Amyloid peptide(16-20) is an effective inhibitor of Abeta fibril formation, with RG-/-GR-NH2 residues added at N- and C-terminal ends to aid solubility) .
β-Amyloid (12-28) (Amyloidβ-Protein (12-28)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) shows aggregation properties. β-Amyloid (12-28) has the potential for Alzheimer’s disease research .
β-Amyloid 22-35 (Amyloidβ-Protein 22-35) TFA, the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 TFA forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
β-Amyloid (17-40) (Aβ(17-40)) is a fragment of Amyloid-β peptide that has shown neurotoxic activities in SH-SY5Y and IMR-32 cells. β-Amyloid (17-40) can be used for the research of neurological disease .
β-Amyloid (10-35), amide is composed of 26 aa (10-35 residues of the Aβ peptide) and is the primary component of the amyloid plaques of Alzheimer’s disease.
β-Amyloid/A4 Protein Precusor (319-335) (APP (319-335)) is a peptide fragment of β-Amyloid/A4 protein precursor (APP). β-Amyloid/A4 Protein Precusor (319-335) can recognize the heparinase-insensitive site that contains the neuritotropic activity of APP .
β-Amyloid (12-28) (TFA) (Amyloidβ-Protein (12-28) (TFA)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) (TFA) shows aggregation properties. β-Amyloid (12-28) (TFA) has the potential for Alzheimer’s disease research .
β-Amyloid (42-1), human is the inactive form of Amyloidβ Peptide (1-42). Its active form, β-Amyloid (1-42), may play a key role in the pathogenesis of Alzheimer's disease .
Talatisamine, a aconitum alkaloid, is specific K + channel blocker. Talatisamine attenuates beta-amyloid oligomers induced neurotoxicity in cultured cortical neurons .
β-Amyloid (1-38), mouse, rat is composed of 38 aa (1-38 residues of the Aβ peptide) and is the primary component of the amyloid plaques of Alzheimer’s disease .
β-Amyloid (42-1), human TFA is the inactive form of Amyloidβ Peptide (1-42). β-Amyloid (42-1), human TFA is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
Biotin-β-Amyloid (1-42), human TFA (Biotin-Amyloidβ-Peptide (1-42) (human) TFA) is the botin labeled β-Amyloid (1-42), human TFA (HY-P1363). β-Amyloid (1-42), human TFA is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
β-Amyloid (25-35) (Amyloidbeta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloidβ-peptide, has shown neurotoxic activities in cultured cells .
Scrambled β-amyloid (1-40) is a biological active peptide. (Aβ (1-40) together with Aβ (1-42) are two major C-terminal variants of the Aβ protein constituting the majority of Aβs. These undergo post-secretory aggregation and deposition in the Alzheimer’s disease brain. This peptide is the scrambled sequence of Abeta 1-40 HY-P0265)
β-Amyloid- 15N (1-42), human (TFA) is the 15N-labledβ-Amyloid (1-42) (TFA). β-Amyloid (1-42), human TFA (Amyloidβ-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease[1].
5-Methoxyflavone, belonged to Flavonoid family, is a DNA polymerase-beta inhibitor and neuroprotective agent against beta-amyloid toxicity. possess central nervous system (CNS) depressant effect mediated through the ionotropic GABAA receptors.
β-Amyloid- 15N (1-40) (TFA) is the 15N-labledβ-Amyloid (1-40) (TFA). β-Amyloid (1-40) is a primary protein in plaques found in the brains of patients with Alzheimer's disease[1].
β-Amyloid (1-42), (rat/mouse) TFA is a 42-aa peptide, shows cytotoxic effect on acute hippocampal slices, and used in the research of Alzheimer's disease.
β-Amyloid (1-42), human TFA (Amyloidβ-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
(Rac)-AZD3839 is an orally active beta-amyloid precursor protein cleaving enzyme (BACE1) inhibitor that is blood-brain barrier-permeable. (Rac)-AZD3839 has an affinity for the human ether-a-go-go related gene (hERG) ion channel. (Rac)-AZD3839 can be used in the research of Alzheimer's disease .
Compound E is a γ-secretase inhibitor. Compound E bloks β-amyloid(40), β-amyloid(42), and Notch γ-secretase cleavage with IC50s of 0.24, 0.37, 0.32 nM, respectively.
Phenserine ((-)-Eseroline phenylcarbamate) is a derivative of Physostigmine and is a potent, noncompetitive, long-acting and selective AChE inhibitor. Phenserine reduces β-amyloid precursor protein (APP) and β-amyloid peptide (Aβ) formation. Phenserine improves cognitive performance and attenuates the progression of Alzheimer's disease .
Phenserine tartrate ((-)-Eseroline phenylcarbamate) is a derivative of Physostigmine and is a potent, noncompetitive, long-acting and selective AChE inhibitor. Phenserine tartrate reduces β-amyloid precursor protein (APP) and β-amyloid peptide (Aβ) formation. Phenserine tartrate improves cognitive performance and attenuates the progression of Alzheimer's disease .
TML-6-d3 is the deuterium labeled TML-6. TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-
TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-oxidative Nrf2 gene. TML-6 has the potential for Alzheimer’s disease (AD) research .
Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels .
(1R,3S)-Compound E is the isomer of Compound E (HY-14176), and can be used as an experimental control. Compound E is a γ-secretase inhibitor. Compound E bloks β-amyloid(40), β-amyloid(42), and Notch γ-secretase cleavage with IC50s of 0.24, 0.37, 0.32 nM, respectively.
Cys-Gly-Lys-Lys-Gly-Amyloidβ-Protein (36-42) is the 36-42 fragment of Amyloidβ-Protein. β-amyloid, a polypeptide made up of 36-43 amino acids, is the main component of amyloid plaques found in the brains of people with Alzheimer's disease. β-amyloid oligomers (Aβos) plays A key role in the progression of Alzheimer's disease (AD) by inducing neuronal damage and cognitive impairment .
Citrullinated amyloid-β (1-40) peptide (human) (Citrullinated Aβ (1-40)) is a modified form of β-Amyloid (1-40) (HY-P0265) with a citrullination at the Arg5 site. Citrullinated amyloid-β (1-40) peptide (human) exhibits increased transient formation of soluble oligomers and insoluble aggregates composed of distorted parallel β-sheets compared with unmodified β-Amyloid (1-40) .
Citrullinated amyloid-β (1-42) peptide (human) (Citrullinated Aβ (1-42)) is a modified form of β-Amyloid (1-42) (HY-P1363) with a citrullination at the Arg5 site. Compared to the unmodified β-Amyloid (1-42), its formation of soluble low-molecular-weight oligomers is enhanced, the rate of fibril formation is reduced, and like unmodified Aβ42, it forms protofibrils comprised of parallel β-sheets .
Hibifolin, a flavonol glycoside, is a potential inhibitor of adenosine deaminase (ADA), with a Ki of 49.92 μM. Hibifolin protects neurons against beta-amyloid-induced neurotoxicity .
AZD-3289 is a potent BACE1 inhibitor with potential Alzheimer's disease inhibitory activity. The application of AZD-3289 is intended to slow the pathological progression of Alzheimer's disease by inhibiting the production of β-amyloid protein. The development of AZD-3289 responds to the need to reduce neurodegenerative changes associated with Alzheimer's disease. As a BACE1 inhibitor, AZD-3289 can effectively reduce the accumulation of β-amyloid peptide in the brain, which may improve cognitive function .
4-(6-Bromo-2-benzothiazolyl)benzenamine is a β-amyloid PET (positron emission tomography) tracer that can be used in the diagnosis of neurological diseases, such as Alzheimer's and Down's syndrome.
Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
(D-Asp1)-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .
α-Secretase Substrate II, Fluorogenic is an internally quenched fluorogenic peptide substrate for α-Secretase that contains the α-secretase cleavage site of β-Amyloid precursor protein (APP) .Ex/Em = 340/490 nm
Z-FF-FMK is a selective cathepsin-L inhibitor. Z-FF-FMK can prevent β-amyloid to induce apoptotic changes such as activation of caspase-3, cleavage of the DNA repair enzyme, poly-ADP ribose polymerase, and DNA fragmentation .
Hibifolin (Standard) is the analytical standard of Hibifolin. This product is intended for research and analytical applications. Hibifolin, a flavonol glycoside, is a potential inhibitor of adenosine deaminase (ADA), with a Ki of 49.92 μM. Hibifolin protects neurons against beta-amyloid-induced neurotoxicity .
Benzothiazole is a natural occurring heterocyclic nuclei. Benzothiazole nucleus possesses a number of biological activities such as anticancer, antimicrobial, antidiabetic, anti-inflammatory, antileishmanial, and antiviral. Furthermore, Benzothiazole nucleus can function as an efficacious β-amyloid imaging agent [1][2][3][4].
CypD-IN-29 (compound 29) is an inhibitor of the Alzheimer's disease target CypD (KD=88.2 nM). CypD is a mitochondrial-specific cyclophilin that can bind to β-amyloid protein in brain mitochondria and promote the formation of mitochondrial permeability transition pore (mPTP).
PE154 (Compound 13) is a potent fluorescent inhibitor of human acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) (IC50s=280 pM and 16 nM, respectively) . PE154 can label β-amyloid plaques in histochemical analysis .
DSS30 is a P25/CDK5 inhibitor that reduces β-amyloid (Aβ) secretion by inhibiting amyloid precursor protein lyase 1 (BACEl) phosphorylation. DSS30 can be used in the study of neurodegenerative diseases such as Alzheimer's disease .
Bacoside A3 is a triterpenoid saponin isolated from Bacopa monnieri. Bacoside A3 has neuroprotective activity, downregulating β-amyloid-induced inflammatory responses and inhibiting neuronal apoptosis. Bacoside A3 can be used in the study of Alzheimer's disease .
[D-Arg25]-Neuropeptide Y (human) ([D-Arg25] NPY) is a Y1 receptor selective agonist. Neuropeptide Y (human) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity .
AChE/Aβ-IN-5 (compound AV-2) is a bifunctional inhibitor that targets AChE and auto-induced Aβ (Amyloid-β) aggregation. AChE/Aβ-IN-5 can significantly improve scopolamine- and Aβ-induced cognitive impairment in mice .
Solanezumab is a humanized monoclonal IgG1 antibody directed against the mid-domain of the amyloid-β (Aβ) peptide. Solanezumab has the potential for the research of Alzheimer’s disease .
β-Sheet Breaker Peptide iAβ5 is a potent degrader of cerebral amyloid-beta (Abeta). Abeta deposition is associatied with the Alzheimer disease (AD), due to its related toxicity linked to its beta-sheet conformation and/or aggregation. β-Sheet Breaker Peptide iAβ5 reproducibly induces in vivo disassembly of fibrillar amyloid deposits. Thus, β-Sheet Breaker Peptide iAβ5 prevents and/or reverses neuronal shrinkage caused by Abeta, and reduces the extent of interleukin-1beta positive microglia-like cells that surround the Abeta deposits. β-Sheet Breaker Peptide iAβ5 reduces the size and/or number of cerebral amyloid plaques in AD. β-Sheet Breaker Peptide iAβ5 labeled by hydrophobic benzyl alcohol (HBA) tag, can be used for quantitative assay by showing vivid blue color under acidic conditions .
Ginsenoside Re (Standard) is the analytical standard of Ginsenoside Re. This product is intended for research and analytical applications. Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
Semagacestat is a γ-secretase inhibitor, inhibits β-amyloid (Aβ42), Aβ38 and Aβ40 with IC50s of 10.9, 12 and 12.1 nM, respectively; also inhibits Notch signaling with IC50 of 14.1 nM. Semagacestat can be used for the research of alzheimer's?disease .
(Gly22)-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease. Mutation of Glu22 to Gly22 in Aβ can increase aggregation .
(Gln22)-Amyloidβ-Protein (1-42) is a Dutch mutation (E22Q) form of β-Amyloid (1-42) (HY-P1363). (Gln22)-Amyloidβ-Protein (1-42) exhibits enhanced fibrillogenic and pathogenic properties .
AChE/Aβ-IN-4 is a dual inhibitor of acetylcholinesterase (AChE) and β-amyloid (Aβ) aggregation, with the IC50 values of 1.72 ± 0.18 μM and 1.42 ± 0.3 μM, respectively. AChE/Aβ-IN-4 plays an impotant role in neurological disorders, such as Alzheimer’s disease .
Carnosine conjugated hyalyronate is a hyaluronic acid derivative functionalized with the dipeptide carnosine (Carnosine, Car) and has the ability to resist Aβ amyloid aggregation. Carnosine conjugated hyalyronate dissolves amyloid fibrils and reduces Aβ-induced toxicity in vitro. The effectiveness of Carnosine conjugated hyalyronate against amyloid aggregation is directly proportional to the Carnosine loading .
ALZ-801 is a potent and orally available small-molecule β-amyloid (Aβ) anti-oligomer and aggregation inhibitor, valine-conjugated proagent of Tramiprosate with substantially improved PK properties and gastrointestinal tolerability compared with the parent compound . ALZ-801 is an advanced and markedly improved candidate for the treatment of alzheimer’s disease .
CGP52411 (DAPH) is a high selective, potent, orally active and ATP-competitive EGFR inhibitor with an IC50 of 0.3 μM. CGP52411 blocks the toxic influx of Ca 2+ ions into neuronal cells, and dramatic inhibits and reverses the formation of β-amyloid (Aβ42) fibril aggregates associated with Alzheimer's disease .
OAB-14, is a Bexarotene (HY-14171) derivative, improves Alzheimer's disease-related pathologies and cognitive impairments by increasing β-amyloid clearance in APP/PS1 mice. OAB-14 effectively ameliorates the dysfunction of the endosomal-autophagic-lysosomal pathway in APP/PS1 transgenic mice .
Benzothiazole (Standard) is the analytical standard of Benzothiazole. This product is intended for research and analytical applications. Benzothiazole is a natural occurring heterocyclic nuclei. Benzothiazole nucleus possesses a number of biological activities such as anticancer, antimicrobial, antidiabetic, anti-inflammatory, antileishmanial, and antiviral. Furthermore, Benzothiazole nucleus can function as an efficacious β-amyloid imaging agent .
Lecanemab (Mouse IGG2a) is a monoclonal antibody that targets soluble β-amyloid and has the potential to reduce cognitive decline. The variable region of Lecanemab (Mouse IGG2a) is consistent with that of Lecanemab, while the constant region is of Mouse IGG2a sequence. Lecanemab (Mouse IGG2a) holds promise for research in the field of Alzheimer's disease .
SQ-3 is a quinoline analogue, displays moderate selectivity for α-syn aggregates (Ki=39.3 nM) over β-amyloid (Aβ) aggregates (Ki=230 nM). [ 18F]SQ3 has basic properties as a lead compound for the development of a useful α-syn imaging probe .
His-D-beta-Nal-Ala-Trp-D-Phe-Lys-NH2 TFA, is a growth hormone releasing peptide, as well as a metabolite of GHRP-1. GHRP-1, or Ala-His-D-beta Nal-Ala-Trp-D-Phe-Lys-NH2, has the effect of promoting the release of growth hormone (GH). GHRP-1 increases GH release and increases [Ca2+]i levels in static monolayer cells of rat pituitary gland, but does not affect cAMP levels .
YM-I-26 is a selective NLRP3 inflammasome inhibitor. YM-I-26 enhances the phagocytosis of β-amyloid protein by mouse microglial BV2 cells and inhibits the production of IL-1β and IL-10. YM-I-26 can be used to study the immunomodulatory activity associated with inflammation .
MAO-B-IN-10 (compound 4f) is a potent, selective, BBB-penetrated MAO-B (monoamine oxidase-B) inhibitor, with IC50 of 5.3 μM. MAO-B-IN-10 can inhibit (58.2%) and disaggregate (43.3%) self-mediated Aβ (amyloidβ) aggregation. MAO-B-IN-10 can be use for Alzheimer’s disease research .
RU-505 is an effective β-amyloid (Aβ)-fibrinogen interaction inhibitor with IC50s of 5.00 and 2.72 μM in fluorescence polarization (FP) and AlphaLISA assays, respectively. RU-505 is highly permeable to the BBB. RU-505 reduces cerebral amyloid angiopathy (CAA). RU-505 can be used for the research of Alzheimer’s disease (AD) .
DCDAPH (Compound 2c) is a novel smart NIRF probe for detection of β-amyloid (Aβ) plaques (λex/λem=597/665 nm in PBS). DCDAPH shows high affinity for Aβ aggregates (Ki=37 nM, Kd=27 nM). DCDAPH shows good blood brain barrier permeation and can meet most of the requirements for the detection of Aβ plaques both in vitro and in vivo .
ARN14494 is a potent and selective serine palmitoyltransferase (SPT) inhibitor, with an IC50 of 27.3 nM. ARN14494 affects the CNS in terms of anti-inflammation and neuroprotection. ARN14494 protects neurons from β-amyloid 1-42-induced neurotoxicity through a variety of mechanisms, including anti-oxidation, anti-apoptosis, and anti-inflammation. ARN14494 can be used for Alzheimer’s disease research .
AChE/BuChE-IN-2 (Compound 5f) is an orally active AChE and BuChE inhibitor with IC50 values of 0.72 μM and 0.16 μM, respectively. AChE/BuChE-IN-2 shows a non-competitive inhibition with AChE and shows potent self-induced β-amyloid (Aβ) aggregation inhibition with an IC50 of 62.52 μM. AChE/BuChE-IN-2 can cross the BBB .
(-)Clausenamide is an active alkaloid isolated from the leaves of Clausena lansium (Lour.) Skeels, and improves cognitive function in both normal physiological and pathological conditions. (-)Clausenamide inhibits β-amyloid (Aβ) toxicity, blocking neurofibrillary tangle formation by inhibiting the phosphorylation of tau protein. (-)Clausenamide exerts a significant neuroprotective activity against Aβ25-35. (-)Clausenamide can be used for researching Alzheimer's disease (AD) .
Dual AChE-MAO B-IN-5, indanone derivative, is a potent dual AChE/MAO-B inhibitior with IC50 values of 0.0224, 0.0412, and 0.1116 μM for AChE, MAO-B and MAO-A, respectively. Dual AChE-MAO B-IN-5 has antioxidant activity and prevents β-amyloid plaque aggregation. Dual AChE-MAO B-IN-5 can be used for Alzheimer’s disease (AD) research .
Caprospinol (SP-233) is a steroid compound candidate based on the structure of 22R-hydroxycholesterol. It has multiple mechanisms of neuroprotection, including binding to β-amyloid protein (Aβ(42)), interacting with the mitochondrial respiratory chain, clearing Aβ(42) monomers, and acting as a σ-1 receptor ligand. It can cross the blood-brain barrier in vivo and restore cognitive impairment, and has the potential to inhibit Alzheimer's disease.
hAChE-IN-3 (compounds 5c) is a potent and blood-brain barrier permeable AChE, BuChE， MAO-B-IN-1 and BACE-1 inhibitor, with IC50 values of 0.44, 0.08, 5.15 and 0.38 μM, respectively. hAChE-IN-3 has antioxidant activity and metal chelating ability. In addition, hAChE-IN-3 can bind to peripheral anion sites, and affect β amyloid and reduce Alzheimer's-associated neurodegeneration. hAChE-IN-3 has the potential for the research of Alzheimer's disease .
BuChE-IN-11 (Compound 3b-1) is an selective BuChE inhibitor with an IC50 of 0.44 μM for hBuChE. BuChE-IN-11 has high blood-brain barrier permeability and exhibits strong antioxidant activity due to its free radical scavenging properties. BuChE-IN-11 interacts with the choline binding site, acetyl binding site, and peripheral anionic site, exhibiting submicromolar BuChE inhibitory activity and preventing β-amyloid (Aβ) self-aggregation. BuChE-IN-11 holds promise for research in the field of Alzheimer's disease .
Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
Punicic acid is a bioactive compound of pomegranate seed oil. Punicic acid is an isomer of conjugated α-linolenic acid and ω-5 polyunsaturated fatty acids. Punicic acid has anti-inflammatory and antioxidant activities and can inhibit the expression of inflammatory mediators such as tumor necrosis factor α (TNF-α). Punicic acid can also reduce the formation of β-amyloid deposits and hyperphosphorylation of tau by increasing the expression of GLUT4 protein and inhibiting the overactivation of calpain, and is used to prevent and treat neurodegenerative diseases. In addition, punicic acid also has breast cancer inhibitor properties that depend on lipid peroxidation and PKC pathways .
AChE/BChE/MAO-B-IN-4, an indan-1-one derivative, is a potent MAO-B inhibitor with an IC50 of 0.0393 μM for human MAO-B. AChE/BChE/MAO-B-IN-4 is a potent AChE and BChE enzyme inhibitor, with IC50s of 0.0458 μM and 0.075 μM for human AChE and BChE enzyme, respectively. AChE/BChE/MAO-B-IN-4 shows significant antioxidant activity and prevent β-amyloid plaque aggregation. AChE/BChE/MAO-B-IN-4 has the potential for Alzheimer's disease (AD) research .
Resveratrol (Standard) is the analytical standard of Resveratrol. This product is intended for research and analytical applications. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
Resveratrol- 13C6 is the 13C-labeled Resveratrol. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator[1][2][3][4]. Resveratrol is a potent pregnane X receptor (PXR) inhibitor[5]. Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model[6]. Resveratrol increases production of NO in endothelial cells[7].
Resveratrol-d4 is the deuterium labeled Resveratrol. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator[1][2][3][4]. Resveratrol is a potent pregnane X receptor (PXR) inhibitor[5]. Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model[6]. Resveratrol increases production of NO in endothelial cells[7].
Aβ42 agonist-1 (compound 7a) is a small molecule compound that can promote Aβ42 aggregation. Aβ42 agonist-1 can interact with Aβ42 oligomers and pentamers to promote nontoxic aggregate self-assembly and rapid fibril formation. Aβ42 agonist-1 prevents Aβ42-induced cytotoxicity in HT22 hippocampal neuronal cells .
Aβ42 agonist-2 (compound 7b) is a small molecule compound that can promote Aβ42 aggregation. Aβ42 agonist-2 can interact with Aβ42 oligomers and pentamers to promote nontoxic aggregate self-assembly and rapid fibril formation. Aβ42 agonist-2 prevents Aβ42-induced cytotoxicity in HT22 hippocampal neuronal cells .
PE154 (Compound 13) is a potent fluorescent inhibitor of human acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) (IC50s=280 pM and 16 nM, respectively) . PE154 can label β-amyloid plaques in histochemical analysis .
DCDAPH (Compound 2c) is a novel smart NIRF probe for detection of β-amyloid (Aβ) plaques (λex/λem=597/665 nm in PBS). DCDAPH shows high affinity for Aβ aggregates (Ki=37 nM, Kd=27 nM). DCDAPH shows good blood brain barrier permeation and can meet most of the requirements for the detection of Aβ plaques both in vitro and in vivo .
Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
β-Amyloid (1-15) is a fragment of β-Amyloid peptide. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
β-Amyloid (1-16) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
β-Amyloid (1-28) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
[Asn23]-beta-Amyloid (1-42), iowa mutation is a biological active peptide. (Several mutations in the beta amyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds. The Iowa mutation, where Asp 23 is replaced with Asn, is associated with severe cerebral amyloidbeta-protein angiopathy (CAA). The affected individuals share a missense mutation in APP at position 694. The mutated beta-amyloid peptide aggregates more rapidly and forms toxic fibrils.)
[Asn23] β-Amyloid (1-40), Iowa mutation is a biological active peptide. (Several mutations in the beta amyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds. The Iowa mutation, where Asp 23 is replaced with Asn, is associated with severe cerebral amyloidbeta-protein angiopathy (CAA). The affected individuals share a missense mutation in APP at position 694. The mutated beta-amyloid peptide aggregates more rapidly and forms toxic fibrils.)
β Amyloid(17-28) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid(17-28) human enhances aggregation of full-length β Amyloid40, producing toxic aggregates in Alzheimer's disease (AD) .
β Amyloid(28-35) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. β Amyloid oligomers are neurotoxic, and β Amyloid(28-35) human can interact with neuronal membranes, regulate secondary structure and neurotoxicity, and cause Alzheimer's disease. β Amyloid(28-35) human has anisotropic effects on the acidic phospholipid DPH, resulting in enhanced internal fluidity of lipid membrane bilayers .
β-Amyloid (1-16) rat is a β-amyloid peptide (Abeta), a metal-binding domain fragment of amyloid. Three amino acid substitutions in β-Amyloid (1-16) rat that differ from humans render rats and mice less susceptible to AD-like neurodegeneration .
β-Amyloid (1-9), an N-terminal fragment of beta amyloid, consists of amino acid residues 1 to 9. β-Amyloid (1-9) contains a B cell epitope, but it does not include T cell epitopes. Omission of residues 1 to 9 from the full-length Alzheimer'sβ-Amyloid peptide 1 to 40 does not prevent the peptide from forming amyloid fibrils or eliminate fibril polymorphism .
β Amyloid (1-14), human is a peptide fragment of β-amyloid protein (Aβ), which is obtained by hydrolysis of Aβ1-40 peptide by catalytic antibody light chain #7TR. β Amyloid (1-14), human can be used for Alzheimer's disease research .
Acetly-β Amyloid (15-20), Amide is a peptides fragment. Acetly-β Amyloid (15-20), Amide inhibits the β-sheet formation and stabilizes structure of Aβ (1–40) peptide. Acetly-β Amyloid (15-20), Amide can be used in study Alzheimer’s disease .
β-Amyloid (1-40) (rat) is a rat form of the amyloidβ-peptide, which accumulates as an insoluble extracellular deposit around neurons, giving rise to the senile plaques associated with Alzheimer's disease (AD). β-Amyloid (1-40) (rat) increases 45Ca 2+ influx, induces neurodegeneration in the rat hippocampal neurons of the CA1 subfield. β-Amyloid (1-40) (rat) induces apoptosis. β-Amyloid (1-40) (rat) can be used for the research of Alzheimer's disease .
β-Amyloid (1-37) (human) correlates moderately with Mini-Mental State Examination (MMSE) scores in Alzheimer disease. β-Amyloid (1-37) (human) possesses an added diagnostic value .
Biotin-β-Amyloid (17-40) is a N-terminal-labelled biotinylated amyloid-?-(1-40) peptide. β-Amyloid (17-40) is a 24-residue fragment of the Aβ protein via?post-translational processing of amyloid precursor protein (APP) .
β-Amyloid (1-43)(human) is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
β-Amyloid (1-43)(human) TFA is more prone to aggregation and has higher toxic properties than the long-known Aβ1-42. β-Amyloid (1-43)(human) TFA shows a correlation with both sAPPα and sAPPβ. β-Amyloid (1-43)(human) TFA could be considered an added Alzheimer's disease (AD) biomarker together with the others already in use .
β-Amyloid 22-35 (Amyloidβ-Protein 22-35), the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
β-Amyloid precursor protein (96-110), cyclized (human) is an amyloid precursor protein. β-Amyloid precursor protein (96-110), cyclized (human) can be used in study Alzheimer’s disease .
β-Amyloid peptide(16-20) is a amino acid sequences (KLVFF) of Amyloid-β (Abeta). β-Amyloid peptide(16-20) is an effective inhibitor of Abeta fibril formation, with RG-/-GR-NH2 residues added at N- and C-terminal ends to aid solubility) .
β-Amyloid (12-28) (Amyloidβ-Protein (12-28)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) shows aggregation properties. β-Amyloid (12-28) has the potential for Alzheimer’s disease research .
[Arg6]-β-Amyloid (1-42), england mutation is a biological active peptide. (Several mutations in the beta amyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds.Tthe English (H6R) mutation will disrupt H6 interactions.)
β-Amyloid 22-35 (Amyloidβ-Protein 22-35) TFA, the residues 22-35 fragment ofβ-amyloid protein, has a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. β-Amyloid 22-35 TFA forms aggregates and typical amyloid fibrils resembling those of the β-amyloid protein in neutral buffer solution) .
β-Amyloid (17-40) (Aβ(17-40)) is a fragment of Amyloid-β peptide that has shown neurotoxic activities in SH-SY5Y and IMR-32 cells. β-Amyloid (17-40) can be used for the research of neurological disease .
β-Amyloid (10-35), amide is composed of 26 aa (10-35 residues of the Aβ peptide) and is the primary component of the amyloid plaques of Alzheimer’s disease.
β-Amyloid/A4 Protein Precusor (319-335) (APP (319-335)) is a peptide fragment of β-Amyloid/A4 protein precursor (APP). β-Amyloid/A4 Protein Precusor (319-335) can recognize the heparinase-insensitive site that contains the neuritotropic activity of APP .
β-Amyloid (12-28) (TFA) (Amyloidβ-Protein (12-28) (TFA)) is a peptide fragment of β-amyloid protein (β1-42). β1-42, a 42 amino acid protein , is the major component of senile plaque cores. β-Amyloid (12-28) (TFA) shows aggregation properties. β-Amyloid (12-28) (TFA) has the potential for Alzheimer’s disease research .
[Arg6]-β-Amyloid (1-40), england mutation is a biological active peptide. (Several mutations in the beta amyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds. Among them, the English mutation, with His at position 6 replaced with Arg, was reported to accelerate the kinetics of oligomers formation which act as fibril seeds and are more toxic to cultured neuronal cells.)
β-Amyloid (42-1), human is the inactive form of Amyloidβ Peptide (1-42). Its active form, β-Amyloid (1-42), may play a key role in the pathogenesis of Alzheimer's disease .
β-Amyloid (1-38), mouse, rat is composed of 38 aa (1-38 residues of the Aβ peptide) and is the primary component of the amyloid plaques of Alzheimer’s disease .
β-Amyloid (42-1), human TFA is the inactive form of Amyloidβ Peptide (1-42). β-Amyloid (42-1), human TFA is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
Biotin-β-Amyloid (1-42), human TFA (Biotin-Amyloidβ-Peptide (1-42) (human) TFA) is the botin labeled β-Amyloid (1-42), human TFA (HY-P1363). β-Amyloid (1-42), human TFA is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
β-Amyloid (25-35) (Amyloidbeta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloidβ-peptide, has shown neurotoxic activities in cultured cells .
Scrambled β-amyloid (1-40) is a biological active peptide. (Aβ (1-40) together with Aβ (1-42) are two major C-terminal variants of the Aβ protein constituting the majority of Aβs. These undergo post-secretory aggregation and deposition in the Alzheimer’s disease brain. This peptide is the scrambled sequence of Abeta 1-40 HY-P0265)
β-Amyloid- 15N (1-42), human (TFA) is the 15N-labledβ-Amyloid (1-42) (TFA). β-Amyloid (1-42), human TFA (Amyloidβ-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease[1].
β-Amyloid- 15N (1-40) (TFA) is the 15N-labledβ-Amyloid (1-40) (TFA). β-Amyloid (1-40) is a primary protein in plaques found in the brains of patients with Alzheimer's disease[1].
β-Amyloid (1-42), (rat/mouse) TFA is a 42-aa peptide, shows cytotoxic effect on acute hippocampal slices, and used in the research of Alzheimer's disease.
β-Amyloid (1-42), human TFA (Amyloidβ-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease .
Cys-Gly-Lys-Lys-Gly-Amyloidβ-Protein (36-42) is the 36-42 fragment of Amyloidβ-Protein. β-amyloid, a polypeptide made up of 36-43 amino acids, is the main component of amyloid plaques found in the brains of people with Alzheimer's disease. β-amyloid oligomers (Aβos) plays A key role in the progression of Alzheimer's disease (AD) by inducing neuronal damage and cognitive impairment .
Citrullinated amyloid-β (1-40) peptide (human) (Citrullinated Aβ (1-40)) is a modified form of β-Amyloid (1-40) (HY-P0265) with a citrullination at the Arg5 site. Citrullinated amyloid-β (1-40) peptide (human) exhibits increased transient formation of soluble oligomers and insoluble aggregates composed of distorted parallel β-sheets compared with unmodified β-Amyloid (1-40) .
Citrullinated amyloid-β (1-42) peptide (human) (Citrullinated Aβ (1-42)) is a modified form of β-Amyloid (1-42) (HY-P1363) with a citrullination at the Arg5 site. Compared to the unmodified β-Amyloid (1-42), its formation of soluble low-molecular-weight oligomers is enhanced, the rate of fibril formation is reduced, and like unmodified Aβ42, it forms protofibrils comprised of parallel β-sheets .
(D-Asp1)-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .
α-Secretase Substrate II, Fluorogenic is an internally quenched fluorogenic peptide substrate for α-Secretase that contains the α-secretase cleavage site of β-Amyloid precursor protein (APP) .Ex/Em = 340/490 nm
Z-FF-FMK is a selective cathepsin-L inhibitor. Z-FF-FMK can prevent β-amyloid to induce apoptotic changes such as activation of caspase-3, cleavage of the DNA repair enzyme, poly-ADP ribose polymerase, and DNA fragmentation .
[D-Arg25]-Neuropeptide Y (human) ([D-Arg25] NPY) is a Y1 receptor selective agonist. Neuropeptide Y (human) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity .
β-Sheet Breaker Peptide iAβ5 is a potent degrader of cerebral amyloid-beta (Abeta). Abeta deposition is associatied with the Alzheimer disease (AD), due to its related toxicity linked to its beta-sheet conformation and/or aggregation. β-Sheet Breaker Peptide iAβ5 reproducibly induces in vivo disassembly of fibrillar amyloid deposits. Thus, β-Sheet Breaker Peptide iAβ5 prevents and/or reverses neuronal shrinkage caused by Abeta, and reduces the extent of interleukin-1beta positive microglia-like cells that surround the Abeta deposits. β-Sheet Breaker Peptide iAβ5 reduces the size and/or number of cerebral amyloid plaques in AD. β-Sheet Breaker Peptide iAβ5 labeled by hydrophobic benzyl alcohol (HBA) tag, can be used for quantitative assay by showing vivid blue color under acidic conditions .
(Gly22)-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease. Mutation of Glu22 to Gly22 in Aβ can increase aggregation .
(Gln22)-Amyloidβ-Protein (1-42) is a Dutch mutation (E22Q) form of β-Amyloid (1-42) (HY-P1363). (Gln22)-Amyloidβ-Protein (1-42) exhibits enhanced fibrillogenic and pathogenic properties .
His-D-beta-Nal-Ala-Trp-D-Phe-Lys-NH2 TFA, is a growth hormone releasing peptide, as well as a metabolite of GHRP-1. GHRP-1, or Ala-His-D-beta Nal-Ala-Trp-D-Phe-Lys-NH2, has the effect of promoting the release of growth hormone (GH). GHRP-1 increases GH release and increases [Ca2+]i levels in static monolayer cells of rat pituitary gland, but does not affect cAMP levels .
Solanezumab is a humanized monoclonal IgG1 antibody directed against the mid-domain of the amyloid-β (Aβ) peptide. Solanezumab has the potential for the research of Alzheimer’s disease .
Lecanemab (Mouse IGG2a) is a monoclonal antibody that targets soluble β-amyloid and has the potential to reduce cognitive decline. The variable region of Lecanemab (Mouse IGG2a) is consistent with that of Lecanemab, while the constant region is of Mouse IGG2a sequence. Lecanemab (Mouse IGG2a) holds promise for research in the field of Alzheimer's disease .
Talatisamine, a aconitum alkaloid, is specific K + channel blocker. Talatisamine attenuates beta-amyloid oligomers induced neurotoxicity in cultured cortical neurons .
Pratensein, a flavonoid, ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels .
Hibifolin, a flavonol glycoside, is a potential inhibitor of adenosine deaminase (ADA), with a Ki of 49.92 μM. Hibifolin protects neurons against beta-amyloid-induced neurotoxicity .
Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
Benzothiazole is a natural occurring heterocyclic nuclei. Benzothiazole nucleus possesses a number of biological activities such as anticancer, antimicrobial, antidiabetic, anti-inflammatory, antileishmanial, and antiviral. Furthermore, Benzothiazole nucleus can function as an efficacious β-amyloid imaging agent [1][2][3][4].
Bacoside A3 is a triterpenoid saponin isolated from Bacopa monnieri. Bacoside A3 has neuroprotective activity, downregulating β-amyloid-induced inflammatory responses and inhibiting neuronal apoptosis. Bacoside A3 can be used in the study of Alzheimer's disease .
Hibifolin (Standard) is the analytical standard of Hibifolin. This product is intended for research and analytical applications. Hibifolin, a flavonol glycoside, is a potential inhibitor of adenosine deaminase (ADA), with a Ki of 49.92 μM. Hibifolin protects neurons against beta-amyloid-induced neurotoxicity .
Ginsenoside Re (Standard) is the analytical standard of Ginsenoside Re. This product is intended for research and analytical applications. Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
Benzothiazole (Standard) is the analytical standard of Benzothiazole. This product is intended for research and analytical applications. Benzothiazole is a natural occurring heterocyclic nuclei. Benzothiazole nucleus possesses a number of biological activities such as anticancer, antimicrobial, antidiabetic, anti-inflammatory, antileishmanial, and antiviral. Furthermore, Benzothiazole nucleus can function as an efficacious β-amyloid imaging agent .
(-)Clausenamide is an active alkaloid isolated from the leaves of Clausena lansium (Lour.) Skeels, and improves cognitive function in both normal physiological and pathological conditions. (-)Clausenamide inhibits β-amyloid (Aβ) toxicity, blocking neurofibrillary tangle formation by inhibiting the phosphorylation of tau protein. (-)Clausenamide exerts a significant neuroprotective activity against Aβ25-35. (-)Clausenamide can be used for researching Alzheimer's disease (AD) .
Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
Punicic acid is a bioactive compound of pomegranate seed oil. Punicic acid is an isomer of conjugated α-linolenic acid and ω-5 polyunsaturated fatty acids. Punicic acid has anti-inflammatory and antioxidant activities and can inhibit the expression of inflammatory mediators such as tumor necrosis factor α (TNF-α). Punicic acid can also reduce the formation of β-amyloid deposits and hyperphosphorylation of tau by increasing the expression of GLUT4 protein and inhibiting the overactivation of calpain, and is used to prevent and treat neurodegenerative diseases. In addition, punicic acid also has breast cancer inhibitor properties that depend on lipid peroxidation and PKC pathways .
Resveratrol (Standard) is the analytical standard of Resveratrol. This product is intended for research and analytical applications. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator . Resveratrol is a potent pregnane X receptor (PXR) inhibitor . Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model . Resveratrol increases production of NO in endothelial cells .
There is no specific Pubmed ID mentioned in the paragraph. APP/Protease Nexin-II Protein, Human (HEK293, Fc) is the recombinant human-derived APP/Protease Nexin-II protein, expressed by HEK293 , with C-hFc labeled tag. The total length of APP/Protease Nexin-II Protein, Human (HEK293, Fc) is 652 a.a., with molecular weight of 150-160 kDa.
There is no specific Pubmed ID mentioned in the paragraph. Amyloid Precursor/Beta-APP42 Protein, Human (His-GST) is the recombinant human-derived Amyloid Precursor/Beta-APP42 protein, expressed by E. coli , with N-His, N-GST labeled tag. The total length of Amyloid Precursor/Beta-APP42 Protein, Human (His-GST) is 42 a.a., with molecular weight of ~27-31 KDa.
There is no specific Pubmed ID mentioned in the paragraph. Amyloid Precursor/Beta-APP40 Protein, Human (His-GST) is the recombinant human-derived Amyloid Precursor/Beta-APP40 protein, expressed by E. coli , with N-His, N-GST labeled tag. The total length of Amyloid Precursor/Beta-APP40 Protein, Human (His-GST) is 40 a.a., with molecular weight of ~33 kDa.
Resveratrol-d4 is the deuterium labeled Resveratrol. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator[1][2][3][4]. Resveratrol is a potent pregnane X receptor (PXR) inhibitor[5]. Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model[6]. Resveratrol increases production of NO in endothelial cells[7].
β-Amyloid- 15N (1-42), human (TFA) is the 15N-labledβ-Amyloid (1-42) (TFA). β-Amyloid (1-42), human TFA (Amyloidβ-Peptide (1-42) (human) TFA) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease[1].
β-Amyloid- 15N (1-40) (TFA) is the 15N-labledβ-Amyloid (1-40) (TFA). β-Amyloid (1-40) is a primary protein in plaques found in the brains of patients with Alzheimer's disease[1].
TML-6-d3 is the deuterium labeled TML-6. TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-
Resveratrol- 13C6 is the 13C-labeled Resveratrol. Resveratrol (trans-Resveratrol; SRT501), a natural polyphenolic phytoalexin that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. Resveratrol (SRT 501) has a wide spectrum of targets including mTOR, JAK, β-amyloid, Adenylyl cyclase, IKKβ, DNA polymerase. Resveratrol also is a specific SIRT1 activator[1][2][3][4]. Resveratrol is a potent pregnane X receptor (PXR) inhibitor[5]. Resveratrol is an Nrf2 activator, ameliorates aging-related progressive renal injury in mice model[6]. Resveratrol increases production of NO in endothelial cells[7].
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