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Amyloid beta (Aβ or Abeta) is a peptide of 36-C43 amino acids that is processed from the Amyloid precursor protein. Amyloid β-Peptide (1-42) human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease. Downregulates bcl-2 and increases the levels of bax. Neurotoxic.
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Gamma-secretase inhibitor
BMS-708163 is an oral gamma secretase inhibitor designed for selective inhibition of amyloid beta synthesis. -
Neuroprotectant
Dimebon dihydrochloride is a non-selective antihistamine that displays cognitive enhancing abilities. -
Gamma-secretase inhibitor
RO4929097 is an orally bioavailable, small-molecule gamma secretase (GS) inhibitor with an IC50 of 4 nM.- Hirosumi Tamura, .et al. , Oncol Rep, 2018, Aug; 40(2): 635-646 PMID: 29917168
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Amyloid-β production inhibitor
gamma-Secretase Modulators (Amyloid-β production inhibitor) is a Amyloid-β production inhibitor. gamma-Secretase Modulators is useful for Alzheimer's disease. -
amyloid β42 inhibitor
Ro 90-7501 is an inhibitor of amyloid β42 (Aβ42) fibril assembly; reduces Aβ42-induced toxicity (EC50 = 2 μM). - alpha-Amyloid Precursor Protein Modulator is a cell-permeable benzolactam derived PKC activator (Ki = 11.9 nM for PKCα) that efficiently enhances non-amyloidogenic α-processing of amyloid precursor protein (APP) even at 100 nM in human fibroblas.
- Shusen Wang, .et al. , Cell, 2024, Oct 31;187(22):6152-6164 PMID: 39326417
- Amyloid b-peptide (42-1) (human), inactive control for Amyloid b (1-42) peptide.
- Amyloid b-Peptide (10-20) (human), soluble amyloid b-peptide fragment that is a substrate for gelatinase A/type IV collagenase/MMP-2 and APP secretase; cleaved between Lys16 and Leu17.
- Amyloid b-peptide (25-35) (human), fragment of human amyloid beta-peptide, functionally required for the neurotrophic and neurotoxic effects associated with Alzheimer's disease.
- Amyloid b-Peptide (12-28) (human), amyloid b-peptide fragment; minimum section required to bind to brain proteins.
- Amyloid b-Peptide (1-40) (human) is a peptide processed from the amyloid precursor protein (APP).
- Amyloid b-Peptide (1-43) (human), amyloid β peptide fragment. Highly toxic, showing higher neurotoxicity compared to Aβ40 and Aβ42.
- Beta-amyloid (1-11) (Abeta) is a peptide with the sequence H-{Asp}{Ala}{Glu}{Phe}{Arg}{His}{Asp}{Ser}{Gly}{Tyr}{Glu}-OH,which is processed from the Amyloid precursor protein.
- Beta-amyloid protein (A beta), a 39-43 amino acid peptide composed of a portion of the transmembrane domain and the extracellular domain of the amyloid precursor protein (APP), is also the principal component of amyloid.
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RAGE Antagonist
FPS-ZM1 inhibits A??40- and A??42-induced cellular stress in RAGE-expressing cells.- Ahana Banerjee, .et al. , Biomater Adv, 2024, Oct:163:213937 PMID: 38968788
- Ahana Banerjee, .et al. , Int J Biol Macromol, 2024, Jun;270(Pt 2):132384 PMID: 38754682
- Edonerpic, also known as T-817, is a neuroprotectant. Edonerpic is a candidate therapeutic agent for Alzheimer's disease that inhibits oxidative stress and nitric oxide-induced neurotoxicity and acts as a neurotrophic factor.
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β-amyloid (Aβ) inhibitor
ALZ-801 is an oral, small-molecule inhibitor of beta amyloid (Aβ) oligomer formation for Alzheimer's disease (AD). ALZ-801 is a prodrug of tramiprosate with improved pharmacokinetic properties and gastrointestinal tolerability. - Xanthocillin X permethyl ether is a natural compound isolated from fungal extracts, with Aβ-42 lowering activity.
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β-amyloid PET tracer
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. -
amyloid imaging agent
4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine is a potent amyloid imaging agent which binds to Amyloid-β (1-40) with a KD of 1.7 nM. -
glutaminyl cyclase inhibitor
Glutaminyl Cyclase Inhibitor 2 is a glutaminyl cyclase inhibitor with an IC50 of 1.23 μM. -
glutaminyl cyclase inhibitor
Glutaminyl Cyclase Inhibitor 1 is a glutaminyl cyclase inhibitor with an IC50 of 0.5 μM. -
Oligomeric aggregation inhibitor
Anle138b is an oligomeric aggregation inhibitor. Anle138b is an oligomer modulator for neurodegenerative diseases such Parkinson's disease. -
GC inhibitor
Glutaminyl Cyclase Inhibitor 3 (compound 212 ), a designed anti-Alzheimer??s compound, is a potent human Glutaminyl Cyclase (GC) inhibitor, with an IC50 of 4.5 nM. -
RAGE inhibitor
Azeliragon (TTP488) is an orally bioavailable inhibitor of the receptor for advanced glycation end products (RAGE) in development as a potential treatment to slow disease progression in patients with mild Alzheimer??s disease (AD). Azeliragon also can cross the blood-brain barrier (BBB). - amyloid P-IN-1 is used in the research of diseases or disorders wherein depletion of serum amyloid P component (SAP), including amyloidosis, Alzheimer's disease, type 2 diabetes mellitus and osteoarthritis.
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Aβ-ABAD inhibitor
Frentizole, an FDA-approved immunosuppressive drug, is a novel inhibitor of the Aβ-ABAD interaction.
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antiinflammation agent
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. -
Colivelin TFA is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro. Colivelin TFA exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease. Colivelin TFA has the potential for the treatment of alzheimer's disease and ischemic brain injury.
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Colivelin is a brain penetrant neuroprotective peptide and a potent activator of STAT3, suppresses neuronal death by activating STAT3 in vitro. Colivelin exhibits long-term beneficial effects against neurotoxicity, Aβ deposition, neuronal apoptosis, and synaptic plasticity deficits in neurodegenerative disease. Colivelin has the potential for the treatment of alzheimer's disease and ischemic brain injury
- β-Amyloid (35-42) is a peptide consisting of amino acid of 35 to 42 of beta amyloid protein.
- 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).
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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.
- Pyridoxal 5′-phosphate monohydrate is the active coenzyme form of vitamin B6 and is essential for the function of numerous enzymes. It serves as a key cofactor for aromatic L-amino acid decarboxylase, which catalyzes the final step in the biosynthesis of the neurotransmitters dopamine and serotonin. Pyridoxal 5′-phosphate is the primary intracellular phosphorylated form of vitamin B6 and is interconvertible with other forms, including pyridoxine 5′-phosphate (PNP) and pyridoxamine 5′-phosphate (PMP).
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Vitamin B6 Derivative
Pyridoxal 5′-phosphate hydrate (PLP) is the biologically active form of vitamin B6 and serves as an essential cofactor for over 100 enzymatic reactions, particularly those involved in amino acid metabolism. It plays a critical role in the function of aromatic L-amino acid decarboxylase, the enzyme responsible for catalyzing the final step in the synthesis of key neurotransmitters such as dopamine and serotonin. PLP is the principal coenzyme form generated through intracellular phosphorylation of vitamin B6 precursors and is interconvertible with other phosphorylated forms, including pyridoxine 5′-phosphate (PNP) and pyridoxamine 5′-phosphate (PMP). - The Italian mutation of β-amyloid 1-40 (E22K) exhibits faster aggregation kinetics and greater neurotoxicity compared to the wild-type peptide. Solid-state NMR studies (Masuda et al.) suggest this enhanced toxicity may be linked to the formation of a salt bridge between Lys²² and Asp²³ in a minor conformer. Similar to the Arctic, Flemish, and Dutch Aβ variants, the Italian mutant also shows significantly reduced degradation by the Aβ-cleaving enzyme neprilysin, contributing to its pathological accumulation.

