| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
Preparation Method | Using double-antigen enzyme-linked immunosorbent TNF-|A Adalimumab -coated plates and their detection by peroxidase-conjugated IgG. |
Reaction Conditions | These patients received 40 mg adalimumab subcutaneously every other week combined with methotrexate and follow-up was done for 1 year. |
Applications | Thirty patients treated for RA were analysed. The following pharmacokinetic and PK-PD parameters were estimated (interidividual coefficient of variation): apparent volume of distribution (Vd /F) = 10.8 l (92%); apparent clearance (CL/F) = 0.32 l day(-1) (17%); first-order absorption rate (ka ) = 0.28 day(-1) ; CRP input (kin ) = 22.0 mg l(-1) day(-1) (65%); adalimumab concentration leading to a 50% decrease in kin (C50 ) = 3.6 mg l(-1) (88%); baseline DAS28 (DAS0 ) = 5.5 mg l(-1) (11%); and adalimumab concentration leading to 50% decrease of DAS0 (IC50 ) = 11.0 mg l(-1) (71%). Simulations showed that a 160 mg loading dose should reduce the time to reach efficacy in terms of both CRP and DAS28 after the first injection. |
Cell lines | THP-1 monocytes |
Preparation Method | CellTracker green-labelled THP-1 monocytes on a HUVECs monolayer after incubation with conditioned media from oxLDL-stimulated THP-1 macrophages (oxLDL CM) with or without adalimumab (ada) for 4 hours followed by the addition of CellTracker green-labelled THP-1 monocytes. |
Reaction Conditions | 1 |/mL Adalimumab (Anti-Human TNF-alpha, Human Antibody) for 4 hours |
Applications | The TNF-|A inhibitor adalimumab suppresses adhesion of THP-1 monocytes to endothelial cells. |
Animal models | Rd10 mice |
Preparation Method | To evaluate the effect of Adalimumab (Anti-Human TNF-alpha, Human Antibody), each rd10 mouse received one intraperitoneal injection of Adalimumab (Anti-Human TNF-alpha, Human Antibody) aline solution at 3 mg/kg every three days starting at P9 and until P17. |
Dosage form | 3 mg/kg Adalimumab (Anti-Human TNF-alpha, Human Antibody)every three days |
Applications | intraperitoneal administration of Adalimumab (Anti-Human TNF-alpha, Human Antibody) significantly decreased the number of TUNEL-positive cells in the ONL at P18 (2.7?!A?0.4 TUNEL-positive cells) compared to vehicle-treated rd10 retinas (12.5?!A?2.4 TUNEL-positive cells) |
| 文献引用 | |
| 产品描述 | Adalimumab (Anti-Human TNF-alpha, Human Antibody) is one of the leading therapies for the treatment of rheumatoid arthritis. It is a humanized monoclonal antibody that binds to TNF-α and blocks its interaction with the TNF receptor[1]. It neutralizes both soluble as well as transmembrane TNF-α[2]. Adalimumab (Anti-Human TNF-alpha, Human Antibody) prevents major inflammatory effects of TNF-α on endothelial activation, endothelial monocyte adhesion, endothelial leakage[3]. Adalimumab (Anti-Human TNF-alpha, Human Antibody) prevented TNFα upregulation, reduced photoreceptor cell death, slowed microglial and MÜller cell activation, improved antioxidant response and ameliorated the energetic and metabolic dysfunction at P18[4]. VaD rats treated with Adalimumab (Anti-Human TNF-alpha, Human Antibody) exhibited significant improvements in memory. In addition, Adalimumab (Anti-Human TNF-alpha, Human Antibody) treatment significantly alleviated neuronal loss in the hippocampi of VaD rats[5]. The important role of TNF-α for atherosclerotic plaque development in experimental models is well documented, different TNF-α-deficient mice models consistently showed reduced plaque burden[6,7]. Adalimumab (Anti-Human TNF-alpha, Human Antibody) has demonstrated a good prognosis and improvement of physical function in rheumatoid arthritis [8]. References: |
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