1. Metabolic Enzyme/Protease Immunology/Inflammation
  2. MMP IFNAR
  3. MEDI-3622

MEDI-3622 is a human monoclonal antibody against ADAM17. MEDI-3622 blocks the ADAM17-mediated shedding of CD16A and CD62L on NK cells, and binds with high specificity to a surface loop unique to the metalloprotease catalytic domain of ADAM17. MEDI-3622 enhances IFNγ production by NK cells when they bind to antibody-coated tumor cells. MEDI-3622 can be used in the research of ovarian cancer, Burkitt lymphoma, head and neck cancer, and colorectal cancer.

For research use only. We do not sell to patients.

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Description

MEDI-3622 is a human monoclonal antibody against ADAM17. MEDI-3622 blocks the ADAM17-mediated shedding of CD16A and CD62L on NK cells, and binds with high specificity to a surface loop unique to the metalloprotease catalytic domain of ADAM17. MEDI-3622 enhances IFNγ production by NK cells when they bind to antibody-coated tumor cells. MEDI-3622 can be used in the research of ovarian cancer, Burkitt lymphoma, head and neck cancer, and colorectal cancer[1].

Species Reactivity

Human

IC50 & Target[1]

ADAM17

 

In Vitro

MEDI-3622 specifically recognizes ADAM17 on human peripheral blood leukocytes, including both CD56bright CD3 and CD56dim CD3 human NK cell subsets[1].
MEDI-3622 (1 µg/mL; 2 h) blocks ADAM17-mediated shedding of CD16A and CD62L by enriched human peripheral blood NK cells activated by trastuzumab-bound SKOV-3 ovarian cancer cells, without inhibiting NK cell activation (CD107a upregulation)[1].
MEDI-3622 (1 µg/mL; 4 h) significantly enhances IFNγ secretion by enriched human peripheral blood NK cells stimulated by trastuzumab-bound SKOV-3 or MA-148 ovarian cancer cells, and rituximab-bound Raji Burkitt's lymphoma cells, across all tested effector:target ratios (10:1 to 1:10), but does not affect granzyme A or granzyme B secretion[1].
MEDI-3622 (1 µg/mL; 4 h) enhancement of IFNγ secretion by enriched human peripheral blood NK cells stimulated with trastuzumab-bound SKOV-3 ovarian cancer cells is dependent on CD16A activity[1].
MEDI-3622 (1 µg/mL; 4 h) enhances IFNγ secretion by NK92 human NK cells expressing wildtype CD16A (but not non-cleavable CD16A) stimulated by trastuzumab-bound SKOV-3 ovarian cancer cells, indicating the effect is mediated by blocking CD16A shedding[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ELISA Assay[1]

Cell Line: recombinant CD16A-expressing NK92 human NK cell line (wildtype CD16A and non-cleavable CD16A variants)
Concentration: 1 µg/mL
Incubation Time: 4 h
Result: Significantly enhanced IFNγ secretion by NK92 cells expressing wildtype CD16A exposed to trastuzumab-bound SKOV-3 cells.
Had no effect on IFNγ secretion by NK92 cells expressing non-cleavable CD16A (ncCD16A) exposed to trastuzumab-bound SKOV-3 cells.
NK92 cells expressing ncCD16A secreted significantly higher levels of IFNγ than NK92 cells expressing wildtype CD16A when exposed to trastuzumab-bound SKOV-3 cells, even without MEDI-3622 treatment.
Gene ID

6868  [NCBI]

Accession
Target

ADAM17/TACE

Application

ELISA, FACS, Functional assay

Conjugated

Unconjugated

Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.

Formulation

Please refer to the lot-specific COA for specific buffer information.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Product Name:
MEDI-3622
Cat. No.:
HY-P992406
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