Amyloid β Peptides
Amyloid β (Aβ) peptides are the major component of amyloid plaques found in the brains of Alzheimer's patients. Aβ is formed from the progressive cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Two Aβ peptides are formed from APP degradation.
Modulators |
|
|---|---|
| Cat No | Product Name / Activity |
| 5343 | TPPB |
| APP modulator; also high affinity PKC activator | |
Inhibitors |
|
| Cat No | Product Name / Activity |
| 6363 | AvagacestatNew |
| Highly potent γ-secretase inhibitor; orally bioavailable | |
| 4283 | Begacestat |
| γ-secretase inhibitor; lowers Aβ40 and Aβ42 levels | |
| 2870 | BMS 299897 |
| γ-secretase inhibitor; reduces Aβ levels | |
| 4924 | CEP 1347 |
| Neuroprotective; blocks Aβ-induced cortical neuron apoptosis. Also inhibitor of JNK signaling | |
| 3360 | CGP 52411 |
| Inhibits Aβ42 fibril formation. Also EGFR inhibitor | |
| 2442 | CGP 53353 |
| Inhibitor of de novo Aβ42 assembly | |
| 2654 | Compound W |
| γ-secretase inhibitor; reduces Aβ42 levels | |
| 2634 | DAPT |
| γ-secretase inhibitor; reduces Aβ42 levels | |
| 4524 | EGCG |
| Inhibits formation of amyloid fibrils | |
| 4495 | Flurizan |
| γ-secretase inhibitor; lowers Aβ42 levels in vitro | |
| 2677 | JLK 6 |
| Inhibitor of γ-secretase-mediated βAPP processing | |
| 2627 | L-685,458 |
| Potent and selective γ-secretase inhibitor; inhibits Aβ40 and Aβ42 | |
| 4000 | MRK 560 |
| γ-secretase inhibitor; attenuates amyloid plaque deposition | |
| 5398 | NQTrp |
| Potent inhibitor of Aβ oligomer and fibril formation | |
| 5751 | PF 3084014 hydrobromide |
| Potent γ-secretase inhibitor | |
| 2408 | Ro 90-7501 |
| Inhibitor of Aβ42 fibril formation | |
| 4699 | SEN 1269 |
| Amyloid-β aggregation inhibitor | |
| 4426 | Tanshinone IIA |
| Inhibits Aβ aggregation; inhibits NF-κB and AP-1 DNA binding | |
Other |
|
| Cat No | Product Name / Activity |
| 5053 | AC 186 |
| Decreases Aβ levels in combination with ACP-105; ERβ agonist | |
| 6550 | AC 253 |
| Prevents Aβ-induced neuronal death; amylin receptor antagonist | |
| 3391 | Amyloid β-peptide (42-1) (human) |
| Inactive control peptide for amyloid β-peptide (1-42) (Cat. No. 1428) | |
| 1191 | Amyloid β-Peptide (1-40) (human) |
| Amyloid β-protein fragment | |
| 2424 | Amyloid β-peptide (1-40) (rat) |
| Amyloid β-protein fragment | |
| 1428 | Amyloid β-Peptide (1-42) (human) |
| Predominant amyloid β-protein fragment | |
| 2425 | Amyloid β-peptide (1-42) (rat) |
| Predominant amyloid β-protein fragment | |
| 1938 | Amyloid β-Peptide (1-43) (human) |
| Amyloid β-protein fragment | |
| 1894 | Amyloid β-Peptide (12-28) (human) |
| Amyloid β-peptide; minimum required for binding to brain proteins | |
| 1429 | Amyloid β-peptide (25-35) (human) |
| Human amyloid β-protein fragment functionally required for neurotoxicity | |
| 5908 | Bis-ANS |
| Fluorescent probe for nonpolar cavities in proteins; used to detect Aβ fibres | |
| 6549 | cAC 253 |
| Inhibits Aβ-induced neuronal death; amylin receptor antagonist | |
| 3945 | Colivelin |
| Neuroprotective peptide; protects against β-amyloid neurotoxicity | |
| 4803 | CRANAD 2 |
| Near-infrared probe that detects Aβ40 aggregates | |
| 3713 | Cryptotanshinone |
| Reduces Aβ generation. Also displays multiple other activities | |
| 3201 | Dimebon dihydrochloride |
| Neuroprotectant; protects against β-amyloid neurotoxicity | |
| 5081 | J 147 |
| Neuroprotective and neurotrophic compound; reduces Aβ40 and Aβ42 levels | |
| 3144 | K 114 |
| Amyloid fibril-specific fluorescent dye | |
| 4084 | LPYFD-NH2 |
| Binds Aβ; protects from aggregation induced toxicity | |
| 4920 | Methoxy-X04 |
| Fluorescent amyloid β detector; brain penetrant | |
| 3619 | Tramiprosate |
| Targets soluble Aβ to decrease amyloid plaque deposition. Also GABA analog | |
| 1098 | Tranilast |
| Antiallergic; binds to Aβ40 monomers | |
| 1634 | Y-29794 oxalate |
| Inhibitor of prolyl endopeptidase; prevents amyloid β-peptide-like deposition in vivo | |
Amyloid β (Aβ) peptides are the major component of amyloid plaques found in the brains of Alzheimer's patients. Aβ is formed from the progressive cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Two Aβ peptides are formed from APP degradation; Aβ40 and Aβ42. Aβ40 is the most abundant form, but Aβ42 is more fibrillogenic, thus is associated with disease states.
Mutations in APP have been linked to early onset Alzheimer's disease, as proteolytic cleavage of the altered protein increases the levels of Aβ42 relative to Aβ40. Furthermore, Aβ proteins have been associated with other diseases including Lewy body dementia, inclusion body myositis and cerebral amyloid angiopathy.
Literature for Amyloid β Peptides
Tocris offers the following scientific literature for Amyloid β Peptides to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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