cx40/pannexin-1

β-Amyloid (1-40) TFA, a principal protein in plaques observed in the brains of Alzheimer's disease patients [1], is pivotal in research focused on this neurodegenerative disorder.

β-Amyloid (1-40), FAM-labeled, is a β-Amyloid (1-40) peptide tagged with a FAM fluorescent label, exhibiting an excitation wavelength (λ ex) of 492 nm and an emission wavelength (λ em) of 518 nm.

β-Amyloid (1-40), FAM-labeled TFA, is a FAM fluorescently-labeled β-Amyloid (1-40) peptide (λ ex = 492 nm and λ em = 518 nm) [1].

Biotin-β-Amyloid (1-40) is an amyloid-β-(1-40) peptide with an N-terminal biotinylation.

Amyloid beta-protein(1-40) Arctic variant (Ab40ARC (E22G)), featuring a glycine at position 22 (Gly22), is a peptide utilized in Alzheimer's disease research [1].

Amyloid β1-40 is one of the fragments generated after cleavage of the amyloid peptide precursor protein by β and γ secretases.

pTH-Related Protein (1-40) (human, mouse, rat) enhances calcium absorption in rat intestinal cells by activating the PTHR1 receptor and the PKCα β signaling pathways. This compound also increases the expression of the parathyroid hormone 1 receptor (PTHR1) and four key proteins involved in transcellular calcium transport: potential vanillin member 6 (TRPV6), calcium-binding protein-D9K (CaBP-D9k), sodium-calcium exchanger 1 (NCX1), and plasma membrane calcium ATPase 1 (PMCA1) [1].

Peptide fragment corresponding to residues 1 - 40 of Nogo-66, the domain of the myelin protein Nogo that inhibits axonal outgrowth. Acts as a competitive antagonist at the Nogo-66 receptor (NgR); blocks Nogo-66- and CNS myelin-induced inhibition of axonal

Rat form of the beta-Amyloid (1-40) peptide

NEP(1-40) TFA is a peptide antagonist of the Nogo-66 receptor (NgR), which attenuates myelin-derived inhibition and mitigates injury-induced shifts in microglial morphology distributions [1].

β-Amyloid (1-40), England mutation, is a biologically active peptide with a histidine (His) to arginine (Arg) substitution at position 6, known to enhance oligomerization kinetics that serve as fibril seeds and increase neurotoxicity in cultured neurons. This alteration is one of several mutations in the beta-amyloid precursor gene implicated in autosomal dominant Alzheimer's Disease across multiple kindreds.

(Gln22,Asn23)-Amyloid β-Protein (1-40) is a peptide used to study Cerebral Amyloid Angiopathy Mutations [1].

[Asn23] β-Amyloid (1-40), Iowa mutation, is a biologically active peptide linked to autosomal dominant Alzheimer's Disease in multiple families. This involves the substitution of Asp 23 with Asn, causing severe cerebral amyloid beta-protein angiopathy (CAA). Individuals with this mutation exhibit a missense alteration in the APP gene at position 694, resulting in the mutated β-amyloid peptide aggregating more quickly and forming toxic fibrils.

Gap19 is a peptide that corresponds to a sequence on the cytoplasmic loop (CL) of Cx43.

Gap19 TFA is a selective and potent blocker of connexin 43 (Cx43) hemichannels, originating from nine amino acids within the Cx43 cytoplasmic loop (CL). It operates by hindering intramolecular interactions between the C-terminus (CT) and the CL, effectively inhibiting hemichannel activity without affecting GJ channels or Cx40/pannexin-1 hemichannels. This peptide offers protective benefits for the myocardium.