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Danvilostomig Biosimilar – Anti-PD1 and CTLA4 mAb – Research Grade

Reference:
Size

100ug, 1MG

Isotype

IgG1-kappa_scFv

Brand

ProteoGenix

Product type

Primary Antibodies

Clonality

Monoclonal Antibody

Expression system

XtenCHO

Applications

Elisa, WB

Product nameDanvilostomig Biosimilar - Anti-PD1 and CTLA4 mAb - Research Grade
SpeciesHomo sapiens
Expression systemXtenCHO
Purity>90% by SDS-PAGE.
Buffer0.01M PBS, pH 7.4.
Delivery conditionBlue ice (+4°C)
Delivery Time3-5 days if in stock; 3-5 weeks if production needed
Storage condition4°C for short term; -20°C for long term
BrandProteoGenix
Aliases /Synonymsanti-PD1, Programmed cell death protein 1, Protein PD-1, hPD-1, PDCD1, CD279, CTLA4, CTLA-4
ReferencePX-TA2076
NoteFor research use only. Not suitable for clinical or therapeutic use.
IsotypeIgG1-kappa_scFv
ClonalityMonoclonal Antibody

Description of Danvilostomig Biosimilar - Anti-PD1 and CTLA4 mAb - Research Grade

Danvilostomig Biosimilar – Anti-PD1 and CTLA4 mAb – Research Grade

Danvilostomig Biosimilar is a novel therapeutic antibody that targets two important immune checkpoint proteins, PD1 and CTLA4. This biosimilar is designed to mimic the structure and function of the original antibody, making it a highly effective and safe treatment for various types of cancer.

Structure of Danvilostomig Biosimilar

Danvilostomig Biosimilar is a monoclonal antibody (mAb) that is composed of two heavy chains and two light chains. The heavy chains are made up of four constant regions (Fc) and one variable region (VH), while the light chains consist of two constant regions (CL) and one variable region (VL). The variable regions of the antibody are responsible for binding to the target proteins, PD1 and CTLA4.

The structure of Danvilostomig Biosimilar is similar to that of the original antibody, with a few minor modifications to improve its potency and specificity. The constant regions of the antibody are derived from human sequences, making it less likely to cause an immune response in patients. The variable regions, on the other hand, are derived from mouse sequences, which have been carefully selected and engineered to bind to PD1 and CTLA4 with high affinity.

Activity of Danvilostomig Biosimilar

Danvilostomig Biosimilar exerts its therapeutic effect by blocking the activity of PD1 and CTLA4, two important immune checkpoint proteins. These proteins are expressed on the surface of immune cells, and their main function is to regulate the activity of T cells, which play a crucial role in the body’s immune response against cancer cells.

PD1 and CTLA4 act as brakes on T cells, preventing them from attacking healthy cells in the body. However, cancer cells can exploit these proteins to evade detection and destruction by the immune system. Danvilostomig Biosimilar works by binding to PD1 and CTLA4, effectively disabling their inhibitory function and allowing T cells to attack and destroy cancer cells.

Application of Danvilostomig Biosimilar

Danvilostomig Biosimilar has shown promising results in preclinical studies, demonstrating its potential as a highly effective and safe treatment for various types of cancer. It has been specifically designed for use in research settings, where it can be used to study the role of PD1 and CTLA4 in cancer and to develop new therapeutic strategies.

Moreover, Danvilostomig Biosimilar can also be used in clinical trials to evaluate its efficacy and safety in cancer patients. As a biosimilar, it has the advantage of being more affordable than the original antibody, making it more accessible to patients who may not be able to afford expensive treatments.

Conclusion

Danvilostomig Biosimilar is a novel therapeutic antibody that targets PD1 and CTLA4, two important immune checkpoint proteins involved in cancer progression. Its unique structure and mechanism of action make it a highly effective and safe treatment option for various types of cancer. With its potential to improve cancer treatment and outcomes, Danvilostomig Biosimilar holds great promise for the future of cancer therapy.

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