From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
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.
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 (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 (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 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 (42-1), human is the inactive form of Amyloidβ Peptide (1-42). β-Amyloid (42-1), human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer 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 .
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 .
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- 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 (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.
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 .
βAmyloid(17-28) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. βAmyloid(17-28) human enhances aggregation of full-length βAmyloid40, producing toxic aggregates in Alzheimer's disease (AD) .
βAmyloid(28-35) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. βAmyloid oligomers are neurotoxic, and βAmyloid(28-35) human can interact with neuronal membranes, regulate secondary structure and neurotoxicity, and cause Alzheimer's disease. βAmyloid(28-35) human has anisotropic effects on the acidic phospholipid DPH, resulting in enhanced internal fluidity of lipid membrane bilayers .
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 .
JLK-6 markedly reduce the production of amyloidβ-peptide (Aβ) by amyloid-β Precursor protein (APP) expressing HEK293 cells by affecting the γ-secretase cleavage of APP, with no effect on the cleavage of the Notch receptor .
Biotin-β-Amyloid (17-40) is a N-terminal-labelled biotinylated amyloid-ß-(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 (1-16) 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 betaamyloid, 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 .
(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 .
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 .
(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 .
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 .
(Pyr3)-Amyloidβ-Protein (3-42) is the predominant amyloidβ-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloidβ-Protein (3-42) is suggested to accumulate in the brain and to trigger the formation of insoluble amyloidβ-peptide deposits .
(Glu20)-Amyloidβ-Protein (1-42) is a slower fibrillizing variant of amyloidβ-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's 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.
(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 .
(Pyr3)-Amyloidβ-Protein (3-42) TFA is the predominant amyloidβ-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloidβ-Protein (3-42) TFA is suggested to accumulate in the brain and to trigger the formation of insoluble amyloidβ-peptide deposits .
(Met(O)35)-Amyloidβ-Protein (1-42) is the oxidation form of Met35 in Aβ42. (Met(O)35)-Amyloidβ-Protein (1-42) can yield an oligomer size distribution characteristic of Aβ40. (Met(O)35)-Amyloidβ-Protein (1-42) can be used in the research of Alzheimer’s disease (AD) .
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 .
Biotinyl-Amyloidβ-Protein (1-42) ammonium is a biotinylated Amyloidβ-Protein (1-42) (HY-P1363). Biotinyl-Amyloidβ-Protein (1-42) ammonium can be used for the research of Aβ1-42 converts to Aβ1-40 in brain .
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 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 (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 .
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 (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 .
Cys-Gly-Lys-Arg-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Cys-Gly-Lys-Arg-Amyloidβ-Protein (1-42) can be used in research of Alzheimer's disease .
Acetyl-Amyloidβ-Protein (1-6) amide is a hexapeptide that contains a potential copper(II) binding site. Acetyl-Amyloidβ-Protein (1-6) amide can be used for research of Alzheimer's disease and related disorders .
FITC-β-Ala-Amyloidβ-Protein (1-42) ammonium is a FITC tagged Aβ1-42 monomer peptide. Aβ1-42 plays a key role in the pathogenesis of Alzheimer’s disease .
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) .
Glp-Amyloid-β (3-40) Peptide (human) (AβpE3-40) is a minor amounts of pyroglutamate-modified Aβ isolated from from 24-month-old Amyloid precursor protein (APP) transgenic Mice .
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 .
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)
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 .
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 .
Kaempferol-3,7-di-O-β-glucoside (Kaempferol 3,7-diglucoside), a flavonol, possesses enzyme inhibition property towards α-amylase, α-glucosidase and Acetylcholinesterase. Kaempferol-3,7-di-O-β-glucoside protects differentiating neuronal cells, SH-SY5Y from Amyloidβ peptide-induced injury. Kaempferol-3,7-di-O-β-glucoside has the potential for Alzheimer's research .
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 .
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 .
Gantenerumab is a fully human anti-amyloid-β (Aβ) IgG1 monoclonal antibody demonstrates sustained cerebral amyloid-β binding. Gantenerumab can be used for Alzheimer's disease research .
Latrepirdine dihydrochloride is a neuroactive compound with antagonist activity at histaminergic, α-adrenergic, and serotonergic receptors. Latrepirdine stimulates amyloid precursor protein (APP) catabolism and amyloid-β (Aβ) secretion.
AZD4694 Precursor (AZ13040214) is the precursor of [ 18F] AZD4694 for the synthesis of [ 18F] AZD4694, an amyloid-β imaging ligand with high affinity for amyloid-β plaques .
Amyloid 17-42 (Aβ(17-42)) is a major constituent of diffuse plaques in Alzheimer's disease and cerebellar pre-amyloid in Down's syndrome, derived by alpha- and gamma-secretase cleavage of the amyloid precursor protein (APP). Amyloid 17-42 can induce neuronal apoptosis via a Fas-like/caspase-8 activation pathway .
Aβ/tau aggregation-IN-3 is a potent amyloid protein aggregation inhibitor with an IC50 of 0.85 μM by Aβ-Thioflavin T (Aβ-ThT) functional aggregation assay. Aβ/tau aggregation-IN-3 has anti-amyloid activity .
Scyllo-Inositol, an amyloid inhibitor, potentialy inhibits α-synuclein aggregation. Scyllo-Inositol stabilizes a non-fibrillar non-toxic form of amyloid-β peptide (Aβ42) in vitro, reverses cognitive deficits, and reduces synaptic toxicity and lowers amyloid plaques in an Alzheimer's disease mouse model .
Remternetug is a human immunoglobulin G1-kappa, anti-APP (amyloidbeta A4 precursor protein) Aβ42 N3pGlu peptide monoclonal antibody. Remternetug recognizes a pyroglutamated form of Aβ that aggregates into amyloid plaques .
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 .
Cu(II)GTSM, a cell-permeable Cu-complex, significantly inhibits GSK3β. Cu(II)GTSM inhibits Amyloid-β oligomers (AβOs) and decreases tau phosphorylation. Cu(II)GTSM also decreases the abundance of Amyloid-β trimers. Cu(II)GTSM is a potential anticancer and antimicrobial agent .
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.
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 .
(R)-(+)-Anatabine is an less active R-enantiomer of Anatabine. Anatabine is a potent α4β2 nAChR agonist . Anatabine inhibits NF-κB activation lower amyloid-β (Aβ) production by preventing the β-cleavage of amyloid precursor protein (APP). Anatabine has anti-inflammatory effects and has the potential for neurodegenerative disorders treatment .
AChE-IN-58 (Compound 3) is an acetylcholinesterase (AChE) inhibitor. AChE-IN-58 can extend the mean lifespan, delay the Aβ1-42-induced paralysis, enhanc the locomotion, and alleviate glutamic acid (Glu)-induced neurotoxicity of CL4176 worms .
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-
β-Amyrin, an ingredient of Celastrus hindsii, blocks amyloidβ (Aβ)-induced long-term potentiation (LTP) impairment. β-amyrin is a promising candidate of treatment for AD .
BACE1-IN-5 (Compound 15) is a β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor with an IC50 of 9.1 nM, and also inhibits cellular amyloid-β (Aβ) with an IC50 of 0.82 nM. BACE1-IN-5 has a medicinal chemistry that improves hERG inhibition and P-gp efflux .
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 .
Anatabine dicitrate is a tobacco alkaloid that can cross the blood-brain barrier. Anatabine dicitrate is a potent α4β2 nAChR agonist. Anatabine dicitrate inhibits NF-κB activation lower amyloid-β (Aβ) production by preventing the β-cleavage of amyloid precursor protein (APP). Anatabine dicitrate has anti-inflammatory effects and has the potential for neurodegenerative disorders treatment .
Methoxy-X04 is a fluorescent dye that crosses the blood-brain barrier and selectively binds to beta-pleated sheets found in dense core amyloid Aβ plaques. Methoxy-X04 retains in vitro binding affinity for amyloid b (Ab) fibrils (Ki= 26.8 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity .
Aleplasinin is an orally active, potent, BBB-penetrated and selectiveSERPINE1 (PAI-1, Plasminogen activator inhibitor-1) inhibitor. Aleplasinin increases amyloid-β (Aβ) catabolism and ameliorates amyloid-related pathology. Aleplasinin improves memory deficiency. Aleplasinin can be used for Alzheimer's disease research .
Aducanumab (BIIB037) is a human monoclonal antibody that selectively targets aggregated amyloid-beta (Aβ). Aducanumab shows brain penetration, and can be used for Alzheimer's disease (AD) research .
NIAD-4 is a fluorophore for optical imaging of amyloid-β (Aβ) in the central nervous system (CNS) for Alzheimer’s disease (AD). NIAD-4 binds to the same Aβ site with the binding affinity (Ki) of 10 nM .
BChE-IN-31 (Compound 14d) is a selective BChE inhibitor with an IC50 of 65 nM. BChE-IN-31 inhibits the self-induced aggregation of neurotoxic amyloid-β (Aβ) peptide .
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 .
Donanemab (LY3002813) is a humanized IgG1 monoclonal antibody directed at an N‐terminal pyroglutamate amyloidbeta (Aβ) epitope. Donanemab has the potential for early Alzheimer's disease research .
Begacestat (GSI-953) is a selective thiophene sulfonamide inhibitor of amyloid precursor protein gamma-secretase (IC50Aβ40=15 nM) for the treatment of Alzheimer's disease .
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) .
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.
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 .
Saikosaponin C is a bioactive component found in radix bupleuri, targets amyloidbeta and tau in Alzheimer's disease. Saikosaponin C inhibits the secretion of both Aβ1-40 and Aβ1-42, and suppresses abnormal tau phosphorylation, but shows no effect on BACE1 activity and expression .
(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.
Aβ42-IN-5 (Compound 0152) is an oral active amyloid precursor protein (APP) degrader that can reduce Aβ42 in Alzheimer's disease iPSC neurons. Aβ42-IN-5 can bind CAPRIN1 and APP and enhance the protein-protein interaction .
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.
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 .
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 .
Aβ-IN-4 (compound 12) is a potent amyloidβ (Aβ) inhibitor. Aβ-IN-4 inhibits Aβ42 aggregation. However, Aβ-IN-4 can not alleviate the neurotoxicity of Aβ42 in SH-SY5Y cells. Aβ-IN-4 can not change the aggregation state of Aβ42 into a nontoxic one .
Aβ-IN-3 (compound 1) is a potent amyloidβ (Aβ) inhibitor. Aβ-IN-3 inhibits Aβ42 aggregation. However, Aβ-IN-3 can not alleviate the neurotoxicity of Aβ42 in SH-SY5Y cells. Aβ-IN-3 can not change the aggregation state of Aβ42 into a nontoxic one .
BMS 299897 is a sulfonamide γ-secretase inhibitor with an IC50 of 7 nM for Aβ production inhibition in HEK293 cells stably overexpressing amyloid precursor protein (APP).
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 .
2-O-Acetyl-20-hydroxyecdysone, an ecdysterones in insects and terrestrial plants, inhibits amyloid-β42 (Aβ42)-induced cytotoxicity. 2-O-Acetyl-20-hydroxyecdysone could decrease Aβ oligomer formation through promotion of fibrogenesis, transforming Aβ oligomers to the low-toxicity fibrils .
Artanin is a coumarin, has biological activities related to Alzheimer’s disease. Artanin exerts function including AChE inhibitory and AChE- and self-induced amyloidbeta (Aβ) aggregation inhibitory activities, with IC50s of 51 μM, 98 μM, and 124 μM, respectively .
Semilicoisoflavone B, an isoflavone, mainly derived from Glycyrrhiza uralensis Fisch.. Semilicoisoflavone B reduces amyloidβ (Aβ) secretion by inhibiting β-secretase-1 (BACE1) expression and activity. Semilicoisoflavone B decreases BACE1 expression mainly through increasing PPARγ expression and inhibiting STAT3 phosphorylation .
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.
PF-06751979 is a potent, brain penetrant, β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor with an IC50 of 7.3 nM in BACE1 binding assay.
γ-Secretase modulator 13 (compound 4) is a gamma-secretase modulator (GSMs) that inhibits the production of the aggregated amyloidβ-peptide Aβ42 with an IC50 value of 163 nM. γ-Secretase modulator 13 can be used in the study of Alzheimer's disease .
LY2389575 hydrochloride is a selective and noncompetitive mGlu3 negative allosteric modulator (NAM), with an IC50 value of 190 nM. LY2389575 hydrochloride induces an increase in Mrc1 levels. LY2389575 hydrochloride also independently amplifies Amyloidbeta (Aβ) toxicity and can be used in study of Alzheimer's disease .
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 .
Chrysamine G, a carboxylic acid analogue of Congo Red, can be used as a probe of amyloid deposition in Alzheimer's disease. Chrysamine G also can inhibit Aβ-induced toxicity in PC12 cells .
2',3'-Dihydroxy-4',6'-dimethoxychalcone (compound 1) can inhibit Amyloidβ-protein (Aβ42) fibrillization and aggregation. 2',3'-Dihydroxy-4',6'-dimethoxychalcone has oral activity and can be detected in the brain .
AChE/Aβ-IN-3 (compound AM5) is a dual inhibitor of AChE and Amyloid-β aggregation with IC50<.sub> values of 1.29 and 4.93 μM, respectively. AChE/Aβ-IN-3 has antioxidant properties that scavenge ROS and restore their normal levels. AChE/Aβ-IN-3 can be used in the study of neurological diseases, such as Alzheimer's disease .
gamma-secretase modulator 5 (compound 22d) is a brain-penetrant gamma-secretase modulator (GSMs) that inhibits the production of the aggregated amyloidβ-peptide Aβ42 with an IC50 value of 60 nM. gamma-secretase modulator 5 can be used in the study of Alzheimer's disease .
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.
Thiethylperazine, a phenothiazine derivate, is an orally active and potent dopamine D2-receptor and histamine H1-receptor antagonist. Thiethylperazine is also a selective ABCC1activator that reduces amyloid-β (Aβ) load in mice. Thiethylperazine has anti-emetic, antipsychotic and antimicrobial effects .
E 2012 is a potent gamma (γ) secretase modulator without affecting Notch processing. E 2012 inhibits 3β-hydroxysterol Δ24-reductase (DHCR24) at the final step in the cholesterol biosynthesis. E 2012 aims at Alzheimer's disease by reduction of amyloidβ-42, and induces cataract following repeated doses in the rat .
(-)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) .
6’-Methyl paeonol is a paeonol derivative, which inihibits abnormal depolarizations and reduces the Amyloidβ-induced ERK phosphorylation. 6’-Methyl paeonol exhibits alleviating activity against Alzheimer’s Disease .
Dihydroergocristine mesylate (DHEC mesylate) is a inhibitor of γ-secretase (GSI), reduces the production of the Alzheimer's disease amyloid-β peptides, binds directly to γ-secretase and Nicastrin with equilibrium dissociation constants (Kd) of 25.7 nM and 9.8 μM, respectively .
BSB is a Congo red-derived fluorescent probe. BSB binds not only to extracellular amyloidβ protein, but also many intracellular lesions composed of abnormal tau and synuclein proteins. BSB acts as a prototype imaging agent for Alzheimer's disease .
Anti-Aβ agent 1A (compound M15) has potent activity against amyloid-β. Anti-Aβ agent 1A possesses can significantly inhibit LPS-induced levels of IL-1β, IL-6 and TNF-α, and reduces the apoptosis of SH-SY5Y induced by H2O2 through mitochondria pathway. Anti-Aβ agent 1A possesses antioxidant, anti-inflammatory, anti-Aβ toxicity and neuroprotective activities. Anti-Aβ agent 1A can be used for researching Alzheimer’s disease (AD) .
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 .
NB-360 is a potent, brain penetrable, and orally bioavailable dual BACE1/BACE2 inhibitor (IC50: mouse and human BACE1=5 nM; BACE2=6 nM). NB-360 shows a superior pharmacological profile and robust reduction of amyloid-β and neuroinflammation in amyloid precursor protein(APP) transgenic mice. NB-360 can completely block the progression of Aβ deposition in the brains of APP transgenic mice. NB-360 shows excellent selectivity over the related aspartyl proteases pepsin, cathepsin D and cathepsin E .
DAPT (GSI-IX) is a potent and orally active γ-secretase inhibitor with IC50s of 115 nM and 200 nM for total amyloid-β (Aβ) and Aβ42, respectively. DAPT inhibits the activation of Notch 1 signaling and induces cell differentiation. DAPT also induces autophagy and apoptosis. DAPT has neuroprotection activity and has the potential for autoimmune and lymphoproliferative diseases, degenerative disease and cancers treatment .
Atabecestat (JNJ-54861911) is a potent brain-penetrant and orally active β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor, achieves robust and high CSF Aβ reduction. Atabecestat s tolerated and displays a sustained pharmacokinetic (PK) and pharmacodynamic (PD) characteristics. Atabecestat has the potential for Alzheimer's Disease treatment .
Thiethylperazine dimaleate, a phenothiazine derivate, is an orally active and potent dopamine D2-receptor and histamine H1-receptor antagonist. Thiethylperazine dimaleate is also a selective ABCC1activator that reduces amyloid-β (Aβ) load in mice. Thiethylperazine dimaleate has anti-emetic, antipsychotic and antimicrobial effects .
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 .
Ponezumab (PF-04360365) is a humanised anti-amyloidIgG2 monoclonal antibody. Ponezumab reduces Aβ levels in the central nervous system and improves performance in mice in various models of learning and memory. Ponezumab can be used in study of 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 .
Trontinemab is a bispecific and humanizedized IgG1-κ antibody, targeting to amyloidbeta A4 precursor protein (APP) and transferrin receptor, p90, CD71 (TFRC). Trontinemab can be used for research on Alzheimer disease (AD) .
Santacruzamate A (CAY-10683, STA) is a potent and selective HDAC2 inhibitor with an IC50 of 119 pM. STA also exerts neuroprotective property against amyloid-β protein fragment 25–35. STA can be used for cancer and neurological disease research .
BACE-IN-1 (Compound 13) is a substituted lmidazo[1 ,2-a]pyridine derivative which can inhibit β-site amyloid precursor protein-cleaving enzyme (BACE) and that may be useful in the treatment of diseases in which BACE is involved, such as Alzheimer's disease.
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 .
(Rac)-BIIB042 (Compound 10) is an modulator of γ-Secretase. (Rac)-BIIB042 reduces Amyloid-β 42 level with an EC50 value of 0.39 µM. (Rac)-BIIB042 can be used for the study of Alzheimer's disease .
Crocetin monomethyl ester, isolated from Crocus sativus, possesses anti-inflammatory, neuroprotective and antioxidant activity . Crocetin monomethyl ester promotes clearance of amyloid-β by inducing autophagy via the STK11/LKB1-mediated AMPK pathway .
[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-IN-47 (compound g17) is a AChE inhibitor with the IC50 of 0.24 μM. AChE-IN-47 inhibits amyloidβ peptides self-aggregation. AChE-IN-47 displays neuroprotective effects and effectively suppresses the intracellular accumulation of reactive oxygen species .
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 .
AChE-IN-51 (compound 8C) is an orally active, non-competitive inhibitor of AChE and BChE (IC50: 84 nM, 97 nM). It also inhibits MMP-2 and amyloid Aβ1-42 aggregates (IC50: 724 nM, 302 nM). AChE-IN-51 has low cytotoxicity and in silico predicted blood-brain barrier permeability. Can be used for research on diseases such as Alzheimer's disease (AD) .
Umibecestat (CNP520) is a beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1) inhibitor with IC50s of 11 nM and 10 nM for human BACE-1 and mouse BACE-1, respectively . Umibecestat can be used for the research of alzheimer's disease.
γ-Secretase modulator 12 (Compound 1a) is a γ-secretase modulator that can selectively decrease amyloid-β42 (Aβ42) levels (IC50 of 0.39 µM). γ-Secretase modulator 12 can be used for Alzheimer’s disease research. γ-Secretase modulator 12 has a good brain/plasma ratio (Kp, brain = 0.72) in mice .
Ro 90-7501 is an amyloidβ42 (Aβ42) fibril assembly inhibitor that reduces Aβ42-induced cytotoxicity (EC50 of 2 μM). Ro 90-7501 inhibits ATM phosphorylation and DNA repair. RO 90-7501 selectively enhances toll-like receptor 3 (TLR3) and RIG-I-like receptor (RLR) ligand-induced IFN-β gene expression and antiviral response . Ro 90-7501 also inhibits protein phosphatase 5 (PP5) in a TPR-dependent manner . Ro 90-7501 has significant radiosensitizing effects on cervical cancer cells .
Dihydroergocristine (mesylate) (Standard) is the analytical standard of Dihydroergocristine (mesylate). This product is intended for research and analytical applications. Dihydroergocristine mesylate (DHEC mesylate) is a inhibitor of γ-secretase (GSI), reduces the production of the Alzheimer's disease amyloid-β peptides, binds directly to γ-secretase and Nicastrin with equilibrium dissociation constants (Kd) of 25.7 nM and 9.8 μM, respectively .
AChE/BChE-IN-9 (Compound 7a) is a potent, orally active AChE and BChE inhibitor with IC50 values of 5.74 μM and 14.05 μM against hAChE and eqBChE, respectively. AChE/BChE-IN-9 is also an efficacious antioxidant with an IC50 of 57.35 μM. AChE/BChE-IN-9 is able to chelate iron and modulates aggregation of amyloidβ1-42. AChE-IN-16 can cross the BBB .
Multitarget AD inhibitor-1 is a selective and reversible butyrylcholinesterase (BuChE) inhibitor with IC50s of 7.22 μM and 1.55 μM for hBuChE and eqBuChE (BuChE from equine serum), respectively. Multitarget AD inhibitor-1 inhibits β-secretase (IC50hBACE-1=41.60 μM), amyloidβ aggregation (IC50Aβ=3.09 μM), tau aggregation. Multitarget AD inhibitor-1, a diphenylpropylamine derivative, has the potential for multifunctional disease-modifying anti-Alzheimer’s research .
Ethyl ferulate, a naturally lipophilic derivative of ferulic acid originally derived from Rhizoma Chuanxiong, induces heme oxygenase-1 (HO-1) and protects rat neurons against oxidative stress . Ethyl ferulate also protects neurons against amyloidβ peptide (1-42)-induced oxidative stress and neurotoxicity .
WRW4, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloidbeta42 (Abeta42) peptide, and F peptide .
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 .
AChE/BChE-IN-12 (compound 10b), a 3,5-dimethoxy analogue, is a potent AChE, BChE, and β-secretase-1 (BACE-1) inhibitor, with IC50 values of 2.57, 3.26, and 10.65 μM, respectively. AChE/BChE-IN-12 crosses the blood-brain barrier via passive diffusion and inhibits the self-aggregation of amyloid-β monomers. AChE/BChE-IN-12 can be used for Alzheimer’s disease (AD) research .
Mca-SEVNLDAEFK(Dnp) is a Beta-secretase 1 (BACE-1) peptide FRET substrate, containing the 'Swedish' Lys-Met/Asn-Leu mutation of the amyloid precursor protein (APP) β-secretase cleavage site. Cleavage at -Leu-Asp- of Mca-SEVNLDAEFK(Dnp) liberates the highly fluorescent 7-methoxycoumarin (Mca) fragment from the proximity quenching effect of the 2,4-dinitrophenyl (Dnp) internal quencher resulting in a large and easily detectable increase in fluorescence intensity.
Stavudine (d4T) is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Stavudine has activity against HIV-1 and HIV-2. Stavudine also inhibits the replication of mitochondrial DNA (mtDNA). Stavudine reduces NLRP3 inflammasome activation and modulates Amyloid-β autophagy. Stavudine induces apoptosis .
Stavudine (d4T) sodium is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Stavudine sodium has activity against HIV-1 and HIV-2. Stavudine sodium also inhibits the replication of mitochondrial DNA (mtDNA). Stavudine sodium reduces NLRP3 inflammasome activation and modulates Amyloid-β autophagy. Stavudine sodium induces apoptosis .
WRW4 TFA, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 TFA specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloidbeta42 (Abeta42) peptide, and F peptide .
JNK3 inhibitor-5 (Compound 22b) is a potent and selective JNK3 inhibitor with an IC50 of 0.379 nM. JNK3 inhibitor-5 effectively protects the neuronal cells against amyloidbeta-induced apoptosis. JNK3 inhibitor-5 has a high cell permeability and is predicted as BBB permeable .
Memoquin is an anti-amyloid and anti-oxidant multi-target-directed ligand. Memoquin is an orally active inhibitor of BACE-1 and AChE with IC50 values of 108 and 1.55 nM, respectively. Memoquin is a cognitive enhancer that prevents the Aβ-induced neurotoxicity mediated by oxidative stress. Memoquin can be used for the research of Alzheimer’s disease (AD) .
(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 .
MAO-B-IN-9 (compound 16) is a potent, selective, BBB-penetrated, irreversible and time-dependent MAO-B (monoamine oxidase B) inhibitor, with an IC50 of 0.18 μM. MAO-B-IN-9 prevents Aβ1-42-induced neuronal cell death. MAO-B-IN-9 shows neuroprotective effects, which may be the result of its Aβ1-42 anti-aggregation effects . MAO-B-IN-9 is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
(R)-DRF053 dihydrochloride is a potent casein kinases 1 (CK1), CDK1/cyclin B and CDK5/p25 inhibitor with IC50s of 14 nM, 220 nM and 80 nM, respectively. (R)-DRF053 dihydrochloride prevents the CK1-dependent production of amyloid-beta in a cell model .
Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloidβ (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) is a potent amyloidβ (Aβ) inhibitor. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases the expression of acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) decreases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) can be used for Alzheimer's disease research .
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 .
Stavudine-d4 is the deuterium labeled Stavudine. Stavudine (d4T) is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Stavudine has activity against HIV-1 and HIV-2. Stavudine also inhibits the replication of mitochondrial DNA (mtDNA). Stavudine reduces NLRP3 inflammasome activation and modulates Amyloid-β autophagy. Stavudine induces apoptosis[1][2][3][4].
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 .
LY2886721 is a potent, selective and orally active beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor with an IC50 of 20.3 nM for recombinant human BACE1. LY2886721 is selectivity against cathepsin D, pepsin, and renin, but lacking selectivity against BACE2 (IC50 of 10.2 nM). LY2886721 can across blood-brain barrier and has the potential for Alzheimer's disease treatment .
Emrusolmin (Anle138b), an oligomeric aggregation inhibitor, blocks the formation of pathological aggregates of prion protein (PrPSc) and of α-synuclein (α-syn). Emrusolmin strongly inhibits oligomer accumulation, neuronal degeneration, and disease progression in vivo. Emrusolmin has low toxicity and an excellent oral bioavailability and blood-brain-barrier penetration. Emrusolmin blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology .
SAK3 is a potent T-type voltage-gated Ca 2+ channels (T-VGCCs) enhancer. SAK3 enhances Cav3.1 and Cav3.3 T-type Ca 2+ channel currents. Acute SAK3 administration improves memory deficits in olfactory-bulbectomized mice . SAK3 inhibits amyloidβ plaque formation in APP-KI mice by activating the proteasome activity .
LY2886721 hydrochloride is a potent, selective and orally active beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor with an IC50 of 20.3 nM for recombinant human BACE1. LY2886721 hydrochloride is selectivity against cathepsin D, pepsin, and renin, but lacking selectivity against BACE2 (IC50 of 10.2 nM). LY2886721 hydrochloride can across blood-brain barrier and has the potential for Alzheimer's disease treatment .
AM-6494 is a potent and orally active BACE1 (efficacious β-site amyloid precursor protein cleaving enzyme 1) inhibitor (IC50=0.4 nM) with in vivo selectivity over BACE2 (IC50=18.6 nM) . AM-6494 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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 .
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].
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 βamyloid and reduce Alzheimer's-associated neurodegeneration. hAChE-IN-3 has the potential for the research of Alzheimer's disease .
L-685458 is a potent transition state analog (TSA) γ-secretase inhibitor (GSI). L-685458 inhibits amyloidβ-protein precursor γ-secretase activity with IC50 of 17 nM, shows greater than 50-100-fold selectivity over other aspartyl proteases tested. L685458 inhibits γ-secretase-mediated cleavage of APP-C99 and Notch-100 with IC50s of 301.3 nM and 351.3 nM, respectively. L-685458 can be used for the research of alzheimer’s disease (AD) and cancers .
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 .
Alzheimer’s Disease (AD) is a progressive degenerative brain disease which causes mental and physical decline, gradually resulting in death. Despite the significant public health issue that it poses, only few medical treatments have been approved for Alzheimer’s Disease (AD) and these act to control symptoms rather than alter the course of the disease. Discovery of new therapeutic approaches depends on the study of pathology of AD. Recent research findings have led to greater understanding of disease neurobiology in Alzheimer's Disease (AD) and identification of unique targets for drug development. Several important mechanisms have been proposed to explain the underlying pathology of AD, such as Amyloid cascade hypothesis, Tau hypothesis and Cholinergic hypothesis, etc.
MCE offers a unique collection of 1374 compounds with anti-Alzheimer’s Disease activities or targeting the unique targets of AD. MCE Anti-Alzheimer’s Disease Compound Library is a useful tool for exploring the mechanism of AD and discovering new drugs for AD.
Neurodegenerative diseases are incurable and life-threatening conditions that result in progressive degeneration and/or death of nerve cells. Some common neurodegenerative diseases include Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Motor Neuron Disease (MND), Huntington’s Disease (HD), Spino-Cerebellar Ataxia (SCA), Spinal Muscular Atrophy (SMA), and Amyotrophic Lateral Sclerosis (ALS). Because the pathophysiology of neurodegenerative disorders is generally poorly understood, it is difficult to identify promising molecular targets and validate them. At the same time, about 85% of the drugs fail in clinical trials. Therefore, validating new targets and discovering new drugs to mitigate neurodegenerative disorders is need of the hour.
MCE offers a unique collection of 2228 compounds with anti-Neurodegenerative Diseases activities or targeting the unique targets of neurodegenerative diseases. MCE Neurodegenerative Disease-related Compound Library is a useful tool for exploring the mechanism of neurodegenerative diseases and discovering new drugs for neurodegenerative diseases.
Methoxy-X04 is a fluorescent dye that crosses the blood-brain barrier and selectively binds to beta-pleated sheets found in dense core amyloid Aβ plaques. Methoxy-X04 retains in vitro binding affinity for amyloid b (Ab) fibrils (Ki= 26.8 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity .
NIAD-4 is a fluorophore for optical imaging of amyloid-β (Aβ) in the central nervous system (CNS) for Alzheimer’s disease (AD). NIAD-4 binds to the same Aβ site with the binding affinity (Ki) of 10 nM .
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 .
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 .
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.
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 (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 (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 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 (42-1), human is the inactive form of Amyloidβ Peptide (1-42). β-Amyloid (42-1), human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer 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 .
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 .
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- 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].
Amyloidβ-Protein (3-42) is the precursor of Pyr peptide. Pyroglutamate-modified Aβ (pEAβ) (3-42) is the core of the amyloid template block in Alzheimer's disease. pEAβ(3-42) accelerated the aggregation of Aβ(1-42), while Aβ(1-42) significantly slowed the primary and secondary nucleation of pEAβ(3-42) .
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.
Amyloidβ-Protein (1-24) is a polypeptide that can be found by peptide screening. Peptide screening is a research tool that pools active peptides primarily by immunoassay. Peptide screening can be used for protein interaction, functional analysis, epitope screening, especially in the field of agent research and development .
Amyloidβ-Protein (1-12) is a polypeptide that can be found by peptide screening. Peptide screening is a research tool that pools active peptides primarily by immunoassay. Peptide screening can be used for protein interaction, functional analysis, epitope screening, especially in the field of agent research and development .
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 .
βAmyloid(17-28) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. βAmyloid(17-28) human enhances aggregation of full-length βAmyloid40, producing toxic aggregates in Alzheimer's disease (AD) .
βAmyloid(28-35) human is a β-amyloid peptide (Abeta), a lipid-induced amyloid core fragment. βAmyloid oligomers are neurotoxic, and βAmyloid(28-35) human can interact with neuronal membranes, regulate secondary structure and neurotoxicity, and cause Alzheimer's disease. βAmyloid(28-35) human has anisotropic effects on the acidic phospholipid DPH, resulting in enhanced internal fluidity of lipid membrane bilayers .
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 .
Biotin-β-Amyloid (17-40) is a N-terminal-labelled biotinylated amyloid-ß-(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 (1-16) 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 betaamyloid, 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 .
Acetly-βAmyloid (15-20), Amide is a peptides fragment. Acetly-βAmyloid (15-20), Amide inhibits the β-sheet formation and stabilizes structure of Aβ (1–40) peptide. Acetly-βAmyloid (15-20), Amide can be used in study 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 .
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 .
(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 .
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 .
(Pyr3)-Amyloidβ-Protein (3-42) is the predominant amyloidβ-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloidβ-Protein (3-42) is suggested to accumulate in the brain and to trigger the formation of insoluble amyloidβ-peptide deposits .
(Glu20)-Amyloidβ-Protein (1-42) is a slower fibrillizing variant of amyloidβ-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloidβ-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's 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.
(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 .
(Pyr3)-Amyloidβ-Protein (3-42) TFA is the predominant amyloidβ-peptide structure deposited in human brain of Alzheimer's disease and Down's syndrome patients. (Pyr3)-Amyloidβ-Protein (3-42) TFA is suggested to accumulate in the brain and to trigger the formation of insoluble amyloidβ-peptide deposits .
(Met(O)35)-Amyloidβ-Protein (1-42) is the oxidation form of Met35 in Aβ42. (Met(O)35)-Amyloidβ-Protein (1-42) can yield an oligomer size distribution characteristic of Aβ40. (Met(O)35)-Amyloidβ-Protein (1-42) can be used in the research of Alzheimer’s disease (AD) .
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 .
Biotinyl-Amyloidβ-Protein (1-42) ammonium is a biotinylated Amyloidβ-Protein (1-42) (HY-P1363). Biotinyl-Amyloidβ-Protein (1-42) ammonium can be used for the research of Aβ1-42 converts to Aβ1-40 in brain .
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 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 (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 .
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 (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 .
(Gly22)-amyloidbeta-protein(1-40) (Arctic variant Ab40ARC (E22G)) is a peptide. (Gly22)-amyloidbeta-protein(1-40) can be used for the research of Alzheimer's disease .
Cys-Gly-Lys-Arg-Amyloidβ-Protein (1-42) is a peptide fragment of amyloidβ-protein (Aβ). Cys-Gly-Lys-Arg-Amyloidβ-Protein (1-42) can be used in research of Alzheimer's disease .
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 .
(Gln22,Asn23)-Amyloidβ-Protein (1-40) is a peptide. (Gln22,Asn23)-Amyloidβ-Protein (1-40) can be used for the research of Cerebral Amyloid Angiopathy Mutations .
[Asn23]-beta-Amyloid (1-42), iowa mutation is a biological active peptide. (Several mutations in the betaamyloid 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 betaamyloid 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.)
Acetyl-Amyloidβ-Protein (1-6) amide is a hexapeptide that contains a potential copper(II) binding site. Acetyl-Amyloidβ-Protein (1-6) amide can be used for research of Alzheimer's disease and related disorders .
[Arg6]-β-Amyloid (1-42), england mutation is a biological active peptide. (Several mutations in the betaamyloid precursor gene cause autosomal dominant Alzheimer's Disease in a number of kindreds.Tthe English (H6R) mutation will disrupt H6 interactions.)
FITC-β-Ala-Amyloidβ-Protein (1-42) ammonium is a FITC tagged Aβ1-42 monomer peptide. Aβ1-42 plays a key role in the pathogenesis of Alzheimer’s disease .
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) .
Glp-Amyloid-β (3-40) Peptide (human) (AβpE3-40) is a minor amounts of pyroglutamate-modified Aβ isolated from from 24-month-old Amyloid precursor protein (APP) transgenic Mice .
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 .
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)
[Arg6]-β-Amyloid (1-40), england mutation is a biological active peptide. (Several mutations in the betaamyloid 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.)
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 .
FITC-β-Ala-Amyloidβ-Protein (1-42) is a polypeptide that can be found by peptide screening. Peptide screening is a research tool that pools active peptides primarily by immunoassay. Peptide screening can be used for protein interaction, functional analysis, epitope screening, especially in the field of agent research and development .
(Val2)-Amyloidβ-Protein (1-6) is a polypeptide that can be found by peptide screening. Peptide screening is a research tool that pools active peptides primarily by immunoassay. Peptide screening can be used for protein interaction, functional analysis, epitope screening, especially in the field of agent research and development .
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 .
Amyloid 17-42 (Aβ(17-42)) is a major constituent of diffuse plaques in Alzheimer's disease and cerebellar pre-amyloid in Down's syndrome, derived by alpha- and gamma-secretase cleavage of the amyloid precursor protein (APP). Amyloid 17-42 can induce neuronal apoptosis via a Fas-like/caspase-8 activation pathway .
Amylin (20-29) (human) is the fragment of human islet amyloid polypeptide (hIAPP) or Amylin. Amylin is a 37-residue hormone. Amylin (20-29) (human) is responsible for the amyloidogenic propensities of the full length protein. Amylin (20-29) (human) can be transformed into its corresponding peptoid and retropeptoid sequences, to obtain beta-sheet breaker peptides as amyloid inhibitors .
Mca-SEVKMDAEFRK(Dnp)RR-NH2, containing the wild-type amyloid precursor protein (APP) beta-secretase cleavage site, is the substrate of thimet oligopeptidase (TOP). It is used for Alzheimer's disease research .
Amyloid-Forming peptide GNNQQNY is a biological active peptide. (This is a heptapeptide from the N-terminal prion-determining domain of the yeast protein Sup35 that forms amyloid fibrils. The availability of its detailed atomic oligomeric structure makes it a good model for studying the early stage of aggregation. The GNNQQNY dimer forms three stable sheet structures. in-register parallel, off-register parallel, and anti-parallel. The in-register parallel dimer, which is close to the amyloidbeta-sheet structure, has few interpeptide hydrogen bonds, making hydrophobic interactions more important and increasing the conformational entropy compared to the anti-parallel sheet.)
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 .
F(N-Me)GA(N-Me)IL is a biological active peptide. (Double N-methylated derivatives of amyloidogenic and cytotoxic partial IAPP sequence were found to be devoid of β-sheet structure, amyloidogenicity and cytotoxicity, The derivatives were able to interact with the native sequences and inhibit amyloid formation)
WRW4, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloidbeta42 (Abeta42) peptide, and F peptide .
Mca-SEVNLDAEFK(Dnp) is a Beta-secretase 1 (BACE-1) peptide FRET substrate, containing the 'Swedish' Lys-Met/Asn-Leu mutation of the amyloid precursor protein (APP) β-secretase cleavage site. Cleavage at -Leu-Asp- of Mca-SEVNLDAEFK(Dnp) liberates the highly fluorescent 7-methoxycoumarin (Mca) fragment from the proximity quenching effect of the 2,4-dinitrophenyl (Dnp) internal quencher resulting in a large and easily detectable increase in fluorescence intensity.
WRW4 TFA, a specific formyl peptide receptor-like 1 (FPRL1) antagonist, inhibits WKYMVm binding to FPRL1 with an IC50 of 0.23 μM. WRW4 TFA specifically inhibits the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloidbeta42 (Abeta42) peptide, and F peptide .
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 .
Gantenerumab is a fully human anti-amyloid-β (Aβ) IgG1 monoclonal antibody demonstrates sustained cerebral amyloid-β binding. Gantenerumab can be used for Alzheimer's disease research .
Remternetug is a human immunoglobulin G1-kappa, anti-APP (amyloidbeta A4 precursor protein) Aβ42 N3pGlu peptide monoclonal antibody. Remternetug recognizes a pyroglutamated form of Aβ that aggregates into amyloid plaques .
Aducanumab (BIIB037) is a human monoclonal antibody that selectively targets aggregated amyloid-beta (Aβ). Aducanumab shows brain penetration, and can be used for Alzheimer's disease (AD) research .
Donanemab (LY3002813) is a humanized IgG1 monoclonal antibody directed at an N‐terminal pyroglutamate amyloidbeta (Aβ) epitope. Donanemab has the potential for early Alzheimer's disease research .
Oloctinebart is a humanized immunoglobulin G4-kappa, anti-LGALS3 monoclonal antibody. Oloctinebart is used for reduction of amyloidbeta oligomers formation .
Ponezumab (PF-04360365) is a humanised anti-amyloidIgG2 monoclonal antibody. Ponezumab reduces Aβ levels in the central nervous system and improves performance in mice in various models of learning and memory. Ponezumab can be used in study of Alzheimer's disease .
Trontinemab is a bispecific and humanizedized IgG1-κ antibody, targeting to amyloidbeta A4 precursor protein (APP) and transferrin receptor, p90, CD71 (TFRC). Trontinemab can be used for research on Alzheimer disease (AD) .
Scyllo-Inositol, an amyloid inhibitor, potentialy inhibits α-synuclein aggregation. Scyllo-Inositol stabilizes a non-fibrillar non-toxic form of amyloid-β peptide (Aβ42) in vitro, reverses cognitive deficits, and reduces synaptic toxicity and lowers amyloid plaques in an Alzheimer's disease mouse model .
β-Amyrin, an ingredient of Celastrus hindsii, blocks amyloidβ (Aβ)-induced long-term potentiation (LTP) impairment. β-amyrin is a promising candidate of treatment for AD .
Kaempferol-3,7-di-O-β-glucoside (Kaempferol 3,7-diglucoside), a flavonol, possesses enzyme inhibition property towards α-amylase, α-glucosidase and Acetylcholinesterase. Kaempferol-3,7-di-O-β-glucoside protects differentiating neuronal cells, SH-SY5Y from Amyloidβ peptide-induced injury. Kaempferol-3,7-di-O-β-glucoside has the potential for Alzheimer's research .
AChE-IN-58 (Compound 3) is an acetylcholinesterase (AChE) inhibitor. AChE-IN-58 can extend the mean lifespan, delay the Aβ1-42-induced paralysis, enhanc the locomotion, and alleviate glutamic acid (Glu)-induced neurotoxicity of CL4176 worms .
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.
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 .
Saikosaponin C is a bioactive component found in radix bupleuri, targets amyloidbeta and tau in Alzheimer's disease. Saikosaponin C inhibits the secretion of both Aβ1-40 and Aβ1-42, and suppresses abnormal tau phosphorylation, but shows no effect on BACE1 activity and expression .
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 .
2-O-Acetyl-20-hydroxyecdysone, an ecdysterones in insects and terrestrial plants, inhibits amyloid-β42 (Aβ42)-induced cytotoxicity. 2-O-Acetyl-20-hydroxyecdysone could decrease Aβ oligomer formation through promotion of fibrogenesis, transforming Aβ oligomers to the low-toxicity fibrils .
Artanin is a coumarin, has biological activities related to Alzheimer’s disease. Artanin exerts function including AChE inhibitory and AChE- and self-induced amyloidbeta (Aβ) aggregation inhibitory activities, with IC50s of 51 μM, 98 μM, and 124 μM, respectively .
Semilicoisoflavone B, an isoflavone, mainly derived from Glycyrrhiza uralensis Fisch.. Semilicoisoflavone B reduces amyloidβ (Aβ) secretion by inhibiting β-secretase-1 (BACE1) expression and activity. Semilicoisoflavone B decreases BACE1 expression mainly through increasing PPARγ expression and inhibiting STAT3 phosphorylation .
2',3'-Dihydroxy-4',6'-dimethoxychalcone (compound 1) can inhibit Amyloidβ-protein (Aβ42) fibrillization and aggregation. 2',3'-Dihydroxy-4',6'-dimethoxychalcone has oral activity and can be detected in the brain .
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.
(-)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) .
Santacruzamate A (CAY-10683, STA) is a potent and selective HDAC2 inhibitor with an IC50 of 119 pM. STA also exerts neuroprotective property against amyloid-β protein fragment 25–35. STA can be used for cancer and neurological disease research .
Crocetin monomethyl ester, isolated from Crocus sativus, possesses anti-inflammatory, neuroprotective and antioxidant activity . Crocetin monomethyl ester promotes clearance of amyloid-β by inducing autophagy via the STK11/LKB1-mediated AMPK pathway .
Ethyl ferulate, a naturally lipophilic derivative of ferulic acid originally derived from Rhizoma Chuanxiong, induces heme oxygenase-1 (HO-1) and protects rat neurons against oxidative stress . Ethyl ferulate also protects neurons against amyloidβ peptide (1-42)-induced oxidative stress and neurotoxicity .
Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloidβ (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) is a potent amyloidβ (Aβ) inhibitor. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases the expression of acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) decreases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by Aβ (1-42). Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) increases muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity. Fustinis ((±)-Fustin; 3,7,3',4'-Tetrahydroxyflavanone) can be used for Alzheimer's disease research .
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 (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. 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.
SNCA proteins are critical for synaptic activity and regulate vesicle trafficking and neurotransmitter release. As a monomer, it enhances the vesicle exocytosis process. SNCA Protein, Mouse is the recombinant mouse-derived SNCA protein, expressed by E. coli , with tag free. The total length of SNCA Protein, Mouse is 140 a.a., with molecular weight of ~17.0 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.
Alpha-synuclein (SNCA) is a key neuronal protein that regulates synaptic activity, including vesicle transport and neurotransmitter release. As a monomer, it enhances vesicle exocytosis, promotes fusion and fusion pore expansion, and increases local Ca(2+) release. SNCA Protein, Human is the recombinant human-derived SNCA protein, expressed by E. coli , with tag free. The total length of SNCA Protein, Human is 140 a.a., with molecular weight of ~17.0 kDa.
APLP-1 protein is involved in postsynaptic function and synaptic processes. Its processing produces ALID1, which activates transcription through APBB1 binding. APLP-1 Protein, Mouse (HEK293, His) is the recombinant mouse-derived APLP-1 protein, expressed by HEK293 , with C-His labeled tag. The total length of APLP-1 Protein, Mouse (HEK293, His) is 584 a.a., with molecular weight of ~62.4 kDa.
Alpha-synuclein (SNCA) is a key neuronal protein that regulates synaptic activity, including vesicle transport and neurotransmitter release. As a monomer, it enhances vesicle exocytosis, promotes fusion and fusion pore expansion, and increases local Ca(2+) release. SNCA Protein, Human (His) is the recombinant human-derived SNCA protein, expressed by E. coli , with N-6*His labeled tag. The total length of SNCA Protein, Human (His) is 140 a.a., with molecular weight of ~18.0 kDa.
APBA3 Protein, Human (rHuAPBA3, His; Amyloid beta A4 precursor protein-binding family A member 3; APBA3) is an approximately 20.0 kDa APBA3 protein fused to His-tag. APBA3 Protein, Human (His) is an adapter protein that belongs to the X11 family and is involved in signal transduction processes.
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.
The TM2D1 protein may be involved in amyloid beta-induced apoptosis by interacting with beta-APP42, especially amyloid beta protein 42 (APP beta-APP42). This suggests a role in molecular pathways associated with amyloid-induced cell death. TM2D1 Protein, Human (HEK293, Fc) is the recombinant human-derived TM2D1 protein, expressed by HEK293 , with C-mFc labeled tag. The total length of TM2D1 Protein, Human (HEK293, Fc) is 81 a.a., with molecular weight of 45-60 KDa.
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- 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].
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-
Stavudine-d4 is the deuterium labeled Stavudine. Stavudine (d4T) is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Stavudine has activity against HIV-1 and HIV-2. Stavudine also inhibits the replication of mitochondrial DNA (mtDNA). Stavudine reduces NLRP3 inflammasome activation and modulates Amyloid-β autophagy. Stavudine induces apoptosis[1][2][3][4].
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].
MAO-B-IN-9 (compound 16) is a potent, selective, BBB-penetrated, irreversible and time-dependent MAO-B (monoamine oxidase B) inhibitor, with an IC50 of 0.18 μM. MAO-B-IN-9 prevents Aβ1-42-induced neuronal cell death. MAO-B-IN-9 shows neuroprotective effects, which may be the result of its Aβ1-42 anti-aggregation effects . MAO-B-IN-9 is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
AM-6494 is a potent and orally active BACE1 (efficacious β-site amyloid precursor protein cleaving enzyme 1) inhibitor (IC50=0.4 nM) with in vivo selectivity over BACE2 (IC50=18.6 nM) . AM-6494 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Inquiry Online
Your information is safe with us. * Required Fields.