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Chemical Structure
Chemical Structure
Chemical Structure

CA77.1 [CMA Activator]

Research Use Only
AG-CR1-0165
AdipoGen Life Sciences
CAS Number2412270-22-3
Product group Chemicals
Estimated Purity>98%
Molecular Weight297.7
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Packing Size
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Overview

  • Supplier
    AdipoGen Life Sciences
  • Product Name
    CA77.1
  • Delivery Days Customer
    10
  • CAS Number
    2412270-22-3
  • Certification
    Research Use Only
  • Estimated Purity
    >98%
  • Molecular Formula
    C16H12ClN3O
  • Molecular Weight
    297.7
  • Scientific Description
    CA77.1 is a novel selective chaperone-mediated autophagy (CMA) activator by increasing the expression of the lysosomal receptor for this pathway, LAMP2A, in lysosomes. Chaperone-mediated autophagy (CMA), is a selective autophagy shown to degrade neurodegeneration-related proteins such as alpha-synuclein (alpha-syn) or tau. Loss of neuronal CMA leads to altered neuronal function, selective changes in the neuronal metastable proteome and proteotoxicity. Chemical upregulation of CMA has been shown to ameliorate pathology in AD experimental mouse models, reduce brain pathology and improve disease phenotype. CA77.1 is able to activate CMA in vitro and in vivo (in contrary to its derivative AR7 which was not suitable for in vivo application). CA77.1 is able to activate CMA in vivo, and demonstrates brain penetrance and favorable pharmacokinetics. It has been shown in animal studies that administration of CA77.1 to enhance chaperone-mediated autophagy, may help to degrade toxic pathogenic protein products such as tau proteins and has potential applications in the treatment of Alzheimers disease. - Chemical. CAS: 2412270-22-3. Formula: C16H12ClN3O. MW: 297.7. CA77.1 is a novel selective chaperone-mediated autophagy (CMA) activator by increasing the expression of the lysosomal receptor for this pathway, LAMP2A, in lysosomes. Chaperone-mediated autophagy (CMA), is a selective autophagy shown to degrade neurodegeneration-related proteins such as alpha-synuclein (alpha-syn) or tau. Loss of neuronal CMA leads to altered neuronal function, selective changes in the neuronal metastable proteome and proteotoxicity. Chemical upregulation of CMA has been shown to ameliorate pathology in AD experimental mouse models, reduce brain pathology and improve disease phenotype. CA77.1 is able to activate CMA in vitro and in vivo (in contrary to its derivative AR7 which was not suitable for in vivo application). CA77.1 is able to activate CMA in vivo, and demonstrates brain penetrance and favorable pharmacokinetics. It has been shown in animal studies that administration of CA77.1 to enhance chaperone-mediated autophagy, may help to degrade toxic pathogenic protein products such as tau proteins and has potential applications in the treatment of Alzheimers disease.
  • SMILES
    ClC1=CC=C(N=C(C2=CC=C(NC(C)=O)C=C2)C=N3)C3=C1
  • Storage Instruction
    -20°C,2°C to 8°C
  • UNSPSC
    12352200