Cartoon representation of the antibody golimumab's variable fragment. The heavy and light chain fragments are coloured blue and yellow, respectively. From PDB entry 5yoy
Golimumab binds to both soluble and transmembrane forms of TNFα. The antibody was isolated from a hybridoma clone produced by transgenic mice immunized with human TNFα. The golimumab-secreting clone was selected after being assayed for human light and heavy chains and TNFα-binding. The commercial product is produced in a recombinant cell line cultured by continuous perfusion.[18]
Golimumab was developed by Janssen Biotech, Inc. (formerly Centocor Biotech, Inc.) which also markets the product in the United States. Janssen markets golimumab in Canada, Central and South America, the Middle East, Africa and Asia Pacific. In the European Union, Russia, and Turkey, golimumab distribution rights are held by MSD (Ireland), a subsidiary of Merck & Co., Inc. In Japan, Indonesia, and Taiwan, distribution rights are held by Mitsubishi Tanabe Pharma Corporation.[19]
Large, double-blind randomized controlled trials in patients with rheumatoid arthritis have shown that golimumab in combination with methotrexate was more effective than methotrexate alone.[20] When clinically indicated, golimumab is estimated as a moderate cost-effective treatment option. National Institutes for Health and Care Excellence (NICE) stated that treatment with golimumab is recommended for RA patients who have failed prior TNFi treatment.[21] Unlike other TNFi treatments such as adalimumab and certolizumab pegol, there have been no reported cases of drug-induced lupus-like syndrome (DILS).[22]
^World Health Organization (2023). The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023). Geneva: World Health Organization. hdl:10665/371090. WHO/MHP/HPS/EML/2023.02.
^Tosh J, Archer R, Davis S, Stevenson M, Stevens JW (August 2013). "Golimumab for the treatment of rheumatoid arthritis after the failure of previous disease-modifying antirheumatic drugs: a NICE single technology appraisal". PharmacoEconomics. 31 (8): 653–61. doi:10.1007/s40273-013-0052-7. PMID23576019. S2CID23085023.
^Williams VL, Cohen PR (May 2011). "TNF alpha antagonist-induced lupus-like syndrome: report and review of the literature with implications for treatment with alternative TNF alpha antagonists". International Journal of Dermatology. 50 (5): 619–25. doi:10.1111/j.1365-4632.2011.04871.x. PMID21506984. S2CID21538173.
^Rifkin LM, Birnbaum AD, Goldstein DA (August 2013). "TNF inhibition for ophthalmic indications: current status and outlook". BioDrugs. 27 (4): 347–57. doi:10.1007/s40259-013-0022-9. PMID23568177. S2CID391892.
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