| Description | β-Amyloid (1-42), human, Ala(13C3,15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be β-Amyloid (1-42), human, Ala(13C3,15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death[1][1][2][3][4][5][6][7]... Read More | Endomorphin 2 TFA, a high affinity, highly selective agonist of the µ-opioid receptor, displays reasonable affinities for kappa3 binding sites, with Ki value between 20 and 30 nM[1] | Exoenzyme C3, clostridium botulinum, is a mono-ADP-ribosylating enzyme. Exoenzyme C3, clostridium botulinum specifically modifies RhoA, B, and C by transferring ADP-ribose to them, thereby inactivating these GTPases. Exoenzyme C3, clostridium botulinum can induce neuronal axonal and dendritic growthExoenzyme C3, clostridium botulinum, is a mono-ADP-ribosylating enzyme. Exoenzyme C3, clostridium botulinum specifically modifies RhoA, B, and C by transferring ADP-ribose to them, thereby inactivating these GTPases. Exoenzyme C3, clostridium botulinum can induce neuronal axonal and dendritic growth, inhibit macrophage migration, and regulate cytoskeletal dynamics. Exoenzyme C3, clostridium botulinum can be used in the research of spinal cord injury and diabetic painful neuropathy[1][2][3][4][5]... Read More | Gap 26 TFA is a connexin mimetic peptide, composed of residue numbers 63-75 of the first extracellular loop of connexin 43 (gap junction blocker), containing the SHVR amino acid motif[1] | IIQLPEIVVV TFA is a specific inhibitor of Drp1-Mff interaction. IIQLPEIVVV TFA can distinguish physiological from pathological fission and block physiological fission, thus leading to mitochondrial dysfunction. IIQLPEIVVV TFA can be used in the study of Huntington's disease[1] |