Enfortumab ELISA Kit

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ARP-BS-261
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Product Name Enfortumab ELISA Kit
Synonyms AGS-22CE, AGS-22M, AGS-22M6E, unconjugated : AGS-22C3 or AGSM6, CAS: 1346452-25-2
Method Quantitative
Detection Range 93.75 - 1,500 ng/mL
Sensitivity 47.39 ng/mL
Sample Types Plasma, Serum
Reconstitution Detection method: Colorimetric. Recovery: 80-120%. Specifications: Enfortumab
Storage When the kit was stored at the recommended temperature for 6 months, the signal intensity decreased by less than 20%. For unopened kits, if you want to prolong the storage time, please store the Standard, Detection A, Detection B and Microplate at - 20°C, the rest reagents should be store at 4°C.
Notes Detection method: Colorimetric. Recovery: 80-120%
Background Enfortumab vedotin is an antibody-drug conjugate (ADC) designed for the treatment of cancer expressing Nectin-4. It was developed through two main lines, hybridoma (ASG-22ME) and Chinese hamster ovary (ASG-22CE). Enfortumab refers to the fully humanized (from mouse) monoclonal antibody (mAb) created by scientists at Agensys (part of Astellas) using Amgen’s transgenic system (XenoMouse), it is the first agent to target Nectin-4 that expressed on many solid tumors especially on bladder cancers. Vedotin refers to the payload drug microtubule-disrupting agent monomethyl auristatin E (MMAE) and the linker. The linker technology holding the antibody and the toxin together was provided by and licensed from Seattle Genetics. Preclinical studies showed that enfortumab vedotin effectively binds to target cells, internalizes and induces cell-killing activity. Mouse and patient xenograft models were used to test enfortumab vedotin’s antitumor activity in human breast, bladder, pancreatic and lung cancers. In March 2018, Seattle Genetics and Astellas received the U.S. Food and Drug Administration (FDA) Breakthrough Therapy Designation for enfortumab vedotin based on interim results from the phase 1 study examining enfortumab vedotin as monotherapy treatment for patients with metastatic urothelial cancer who were previously treated with checkpoint inhibitors.
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