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Merck

14365C

EX-CELL® CD CHO Fusion

Animal-component free, without L-glutamine, without hypoxanthine, without thymidine, liquid, sterile-filtered, suitable for cell culture

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About This Item

NACRES:
NA.75
UNSPSC Code:
12352207
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Quality Level

sterility

sterile-filtered

product line

EX-CELL®

form

liquid

technique(s)

cell culture | mammalian: suitable (suspension)

components

L-glutamine: no

shipped in

ambient

storage temp.

2-8°C

General description

EX-CELL® CD CHO Fusion is a chemically defined, animal-component free medium developed for the long-term growth of Chinese Hamster Ovary (CHO) cells. The absence of any large macro molecules allows for isolation and purification of secreted proteins from the cells. This medium is supplied without L-glutamine to aid in media stability, to avoid L-glutamine degradation that causes ammonia build-up and to provide an appropriate medium for the culture of CHO cells using glutamine synthetase selection (example: MilliporeSigma’s CHOZN GS knockout cell line). This medium does not contain hypoxanthine or thymidine to allow for its use with dihydrofolate reductase(DHFR-) gene amplification systems (example: MilliporeSigma’s CHOZN DHFR knockout cell line).

Preparation Note

Formulated to contain 20.9 grams of powder per liter of medium.

Legal Information

EX-CELL is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Donot freeze. Protect from light. Several components of the medium arelight labile and should not be exposed to light for lengthy periods of time.


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Storage Class

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable



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Scientific reports, 10(1), 17612-17612 (2020-10-21)
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Biotechnology and bioengineering, 116(9), 2303-2315 (2019-05-08)
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Biotechnology progress, 37(1), e3061-e3061 (2020-08-05)
Antibody-dependent cellular cytotoxicity (ADCC) is the primary mechanism of actions for several marketed therapeutic antibodies (mAbs) and for many more in clinical trials. The ADCC efficacy is highly dependent on the ability of therapeutic mAbs to recruit effector cells such