Secukinumab is a fully human IgG1κ monoclonal antibody. Secukinumab selectively binds and neutralizes the pro-inflammatory cytokine interleukin-17A (IL-17A). Secukinumab inhibits the interaction between IL-17A and the IL-17 receptor, thereby suppressing the release of pro-inflammatory cytokines and chemokines. Secukinumab can be used in research related to immune-inflammatory diseases such as moderate-to-severe plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis[1-4].
In vitro, PC12 cells were pre-incubated with Secukinumab (5-10μM) for 2h and then stimulated with MPP+ (50μM) for 22h. Secukinumab did not alleviate the pathological changes in PC12 cells[5]. HepG2, SMMC-7721, and MHCC97H cells were incubated with Secukinumab (4μg/mL) for 24h. Secukinumab inhibited cell invasion and migration capabilities and blocked the Notch signaling pathway[6]. HepG2 cells were incubated with Secukinumab (50μg/mL) for 24h. Secukinumab promoted autophagy and inhibited cell survival, proliferation, invasion, and migration[7].
In vivo, mice with ovalbumin sensitization and lipopolysaccharide-induced acute lung injury received intraperitoneal injections of Secukinumab (10mg/kg) for 4 days. Secukinumab enhanced the production of anti-inflammatory cytokines, reduced peribronchial neutrophils, decreased alveolar wall thickness, diminished inflammatory cell infiltration and alveolar collapse in lung tissue, and improved pulmonary pathological changes[8]. Sprague-Dawley rats with cerebral ischemia-reperfusion received intraperitoneal injections of Secukinumab (3mg/kg; once weekly; for two consecutive weeks). Secukinumab alleviated oxidative damage and histopathological changes caused by cerebral ischemia-reperfusion, lowered malondialdehyde levels, increased activities of glutathione, catalase, glutathione peroxidase, and superoxide dismutase, and reduced the density of Caspase-3-positive cells[9]. Sprague Dawley rat pups with germinal matrix hemorrhage received a single intranasal administration of Secukinumab (0.3-0.9mg/kg). Secukinumab improved short- and long-term neurobehavioral functions, reduced ventricular dilation, preserved ipsilateral cortical thickness, and decreased astrocyte proliferation and glial scar formation[10].
References:
[1] Shirley M, Scott LJ. Secukinumab: A Review in Psoriatic Arthritis. Drugs. 2016 Jul;76(11):1135-45.
[2] Snyder CL, Gibson RS, Porter ML, et al. Secukinumab in the treatment of hidradenitis suppurativa. Immunotherapy. 2023 Dec;15(17):1449-1457.
[3] Chong W, Mattapallil M, Raychaudhuri K, et al. The Cytokine IL-17A Limits Th17 Pathogenicity via a Negative Feedback Loop Driven by Autocrine Induction of IL-24. Immunity. 2020 Aug 18;53(2):384-397.
[4] AL-rasheedi ZF, Nour OA, El-Kashef DH, et al. Secukinumab mitigates diethyl nitrosamine-induced acute liver injury in mice via modulating p-ERK/p-eIF2a/CHOP and NLRP3/Caspase-1/IL-1β pathways. Naunyn-Schmiedeberg's Archives of Pharmacology. 2026;399:13513-13526.
[5] Li Q, Han X, Dong M, et al. FDA-Approved Secukinumab Alleviates Glial Activation and Immune Cell Infiltration in MPTP-Induced Mouse Model of Parkinson's Disease. Inflammation. 2025;48:3314-3325.
[6] Li H, Zhang Y, Liu Y, et al. Effect of IL-17 monoclonal antibody Secukinumab combined with IL-35 blockade of Notch signaling pathway on the invasive capability of hepatoma cells. Genet Mol Res. 2016 Jul 15;15(2):gmr.15028174.
[7] Tang R, Zheng L, Zheng J, et al. Secukinumab plays a synergistic role with starvation therapy in promoting autophagic cell death of hepatocellular carcinoma via inhibiting IL-17A-increased BCL2 level. In Vitro Cell Dev Biol Anim. 2023;59(5):381-393.
[8] Vicovan AG, Petrescu DC, Constantinescu D, et al. Experimental Insights on the Use of Secukinumab and Magnolol in Acute Respiratory Diseases in Mice. Biomedicines. 2024;12(7):1538.
[9] Oztanir MN, Dogan MF, Turkmen NB, et al. Secukinumab ameliorates oxidative damage induced by cerebral ischemia-reperfusion in rats. Turk Neurosurg. 2022;32(1):1-8.
[10] Liu S, Huang L, Flores J, et al. Secukinumab attenuates reactive astrogliosis via IL-17RA/(C/EBPβ)/SIRT1 pathway in a rat model of germinal matrix hemorrhage. CNS Neurosci Ther. 2019;25:1151-1161.