Secukinumab |
رقم الكتالوجGC19532
One-Click Copy Product Info
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سيكيوكينيوماب (AIN457) هو جسم مضاد بشري وحيد النسيلة ذو صلة عالية يستهدف الإنترلوكين (IL) -17A
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 875356-43-7
Sample solution is provided at 25 µL, 10mM.
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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.
| Cell experiment [1]: | |
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Cell lines |
HepG2 cells, SMMC-7721 cells and MHCC97H cells (human hepatoma cell lines) |
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Preparation Method |
HepG2 cells, SMMC-7721 cells and MHCC97H cells were cultured in DMEM supplemented with 10% fetal bovine serum at 37°C, 5% CO₂. The cells were treated with 4μg/mL Secukinumab. After treatment, Transwell assays were performed to assess cell invasion and migration capabilities, quantitative polymerase chain reaction was conducted to measure the mRNA levels of Hes1, Hes5 and Hey1, and Western blot was used to detect the protein expression of N1ICD, Snail and E-cadherin. |
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Reaction Conditions |
4μg/mL; 24h |
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Applications |
Secukinumab inhibited the invasion and migration capabilities of HepG2 cells, SMMC-7721 cells and MHCC97H cells, down-regulated the mRNA expression of Hes1, Hes5 and Hey1, decreased the protein levels of N1ICD and Snail, and increased the protein expression of E-cadherin. |
| Animal experiment [2]: | |
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Animal models |
Sprague Dawley P7 rat pups |
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Preparation Method |
Germinal matrix hemorrhage was induced by stereotactic-guided intraparenchymal injection of 0.3 units of collagenase VII-S. Secukinumab at dosages of 0.3, 0.6 and 0.9mg/kg was administered intranasally 1 hour postictus. Short-term neurobehavioral assessments were evaluated at 24, 48 and 72 hours postictus, and long-term neurobehavioral assessments were performed at 24-28 days postictus. Western blot, histology, and immunohistochemistry were used to assess treatment regimens. |
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Dosage form |
0.3, 0.6 or 0.9mg/kg; intranasal; single injection |
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Applications |
Secukinumab improved short- and long-term neurological function, reduced ventricular volume, preserved cortical thickness, decreased astrocyte proliferation and glial scarring around the site of perihematoma, downregulated C/EBPβ, CyclinD1, PCNA and GFAP expression, and upregulated SIRT1 expression. |
References: [1] 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. [2] 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. | |
| Cas No. | 875356-43-7 | SDF | |
| Formula | C6584H10134N1754O2042S44 | M.Wt | 147941.89 |
| الذوبان | Storage | Store at 4°C, Do not freeze | |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.8 μL | 33.8 μL | 67.6 μL |
| 5 mM | 1.4 μL | 6.8 μL | 13.5 μL |
| 10 mM | 0.7 μL | 3.4 μL | 6.8 μL |
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
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Calculation results:
Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
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- Purity: >99.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 6 reference(s) in Google Scholar.)