ED11
ED11 is a potent and selective caspase-6 inhibitor with an IC50 of 12.12 nM. ED11 competes with Htt for the caspase-6 active site, and thus reduce Htt cleavage. ED11 can cross the blood-brain barrier (BBB). ED11 has the potential for the study of Huntington's disease (HD).
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- CAS No.: 1593480-56-8
- Formule: C116H205N47O37
- Masse moléculaire:2850.16
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
Chemical Information
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CAS No. 1593480-56-8
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Masse moléculaire 2850.16
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Formule C116H205N47O37
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Sequence
Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Pro-Pro-Gln-Ser-Ser-Glu-Ile-Val-Leu-Asp-Gly-Thr-Asp-Asn
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Sequence Shortening
GRKKRRQRRRPPQSSEIVLDGTDN
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)