CNTO 148
Modify Date: 2024-01-09 08:31:35
CNTO 148 structure
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Common Name | CNTO 148 | ||
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| CAS Number | 476181-74-5 | Molecular Weight | N/A | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | N/A | Melting Point | N/A | |
| MSDS | N/A | Flash Point | N/A | |
Use of CNTO 148Golimumab (CNTO-148) is a potent human IgG1 TNFα antagonist monoclonal antibody. Golimumab has anti-inflammation activitity and inhibits IL-6 and IL-1β production. Golimumab acts via targeting and neutralizing TNF to prevent inflammation and destruction of cartilage and bone. Golimumab has the anticancer activity and induces cell apoptosis. Golimumab can be used for rheumatoid arthritis, Crohn's disease and cancer research[1][2][3]. |
| Name | CNTO 148 |
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| Description | Golimumab (CNTO-148) is a potent human IgG1 TNFα antagonist monoclonal antibody. Golimumab has anti-inflammation activitity and inhibits IL-6 and IL-1β production. Golimumab acts via targeting and neutralizing TNF to prevent inflammation and destruction of cartilage and bone. Golimumab has the anticancer activity and induces cell apoptosis. Golimumab can be used for rheumatoid arthritis, Crohn's disease and cancer research[1][2][3]. |
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| Related Catalog | |
| Target |
TNFα |
| In Vitro | Golimumab (CNTO-148) (0.1-10 μg /mL; 24-72 hours; transmembrane TNFα–transfected Jurkat cells) induces reductions in the viability of transmembrane TNFα–expressing cells[1]. Golimumab (CNTO-148) (10 μg /mL; 48 hours; transmembrane TNFα–transfected Jurkat cells) induces apoptosis, increase the levels of active caspase-3 and induces apoptotic DNA fragmentation[1]. Cell Viability Assay[1] Cell Line: Transmembrane TNFα–transfected Jurkat cells Concentration: 0.1, 1 and 10 μg/mL Incubation Time: 24, 48 and 72 hours Result: Reduced cell viability in a dose- and time-dependent manner. Apoptosis Analysis[1] Cell Line: Transmembrane TNFα–transfected Jurkat cells Concentration: 10 μg /mL Incubation Time: 48 hours Result: Had the percentage of apoptotic cells for 30.29%. Western Blot Analysis[1] Cell Line: Transmembrane TNFα–transfected Jurkat cells Concentration: 10 μg /mL Incubation Time: 48 hours Result: Increased the levels of active caspase-3 and induces apoptotic DNA fragmentation. |
| In Vivo | Golimumab (CNTO-148) (24 mg/kg; i.h.; daily, for 7 days; swiss-albino healthy male mice) inhibits oxidative stress, apoptotic cell death inflammatory response, thus improving renal function. Golimumab reduces all markers of kidney injury and attenuates cell death[2]. Golimumab (CNTO-148) (1-10 mg/kg; i.p.;daily; for 4 weeks; Tg197 transgenic mouse model) relieves TNFα-induced arthritis in a mouse model of human[3]. Animal Model: Swiss-albino healthy male mice[2] Dosage: 24 mg/kg Administration: Subcutaneous injection; daily, for 7 days Result: Reduced serum parameters like BUN, NGAL creatinine, cystatin C, and urinary parameters like KIM-1, NAG, albumin clusterin. Animal Model: Swiss-albino healthy male mice[2] Dosage: 24 mg/kg Administration: Subcutaneous injection; daily, for 7 days Result: Inhibited oxidative stress, reduces MDA concentrations and increases the GSH and catalase levels. Animal Model: Swiss-albino healthy male mice[2] Dosage: 24 mg/kg Administration: Subcutaneous injection; daily, for 7 days Result: Inhibitd cisplatin-induced inflammation, decreased TNF-α, including IL-6, IL-1β, MCP-1, ICAM-1, and TGF-β1 levels and increases IL-10 concentrations, reduced caspase 3 in cisplatin injected mice kidneys. Animal Model: Tg197 transgenic mouse model[3] Dosage: 1 and 10 mg/kg Administration: Intraperitoneal injection;for 4 weeks Result: Reduced the arthritic index. |
| References |
| No Any Chemical & Physical Properties |