Idalaptican pegol
Ldalaptican pegol (AON-D21; NOX-D21) is a PEGylated mixed RNA/DNA L-aptamer that specifically binds to complement C5a. Ldalaptican pegol binds to C5a and the C5a moiety on uncleaved C5, thereby blocking C5a signaling. This inhibition suppresses downstream inflammatory responses, immune cell infiltration and chemotaxis, the release of pro-fibrotic factors, and abnormalities in lipid metabolism signaling pathways. Ldalaptican pegol can also alleviate allograft rejection. Ldalaptican pegol can be used in research on inflammatory muscle diseases, Duchenne muscular dystrophy (DMD), diabetes, renal fibrosis, and allograft organ transplant rejection.
For research use only. We do not sell to patients.
- CAS No.: 2364414-05-9
- Formula: C398H498N160O310P40(C2H4O)2n (n≈450)
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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DGAT1 |
Ldalaptican pegol (NOX-D21) (20 mg/kg; s.c.; three times weekly; 4 weeks) modulates muscle inflammation and protects muscle fibers in male mdx mice (C57BL/6, a model of Duchenne muscular dystrophy/DMD)[2].
Ldalaptican pegol (NOX-D21) (10 mg/kg; i.p.; every other day; 12 weeks) improves renal function, attenuates fibrosis, and modulates lipid metabolism in db/db mice (C57BLKS/J-LepRdb/db, a model of diabetic nephropathy)[3].
Ldalaptican pegol (AON-D21) (10 mg/kg; i.p.; administered on the day of transplantation (d0) and every other day thereafter; up to 28 days post-transplantation) induces regulatory T-cell expansion, promotes microvascular reperfusion, improves tissue oxygenation, maintains healthy epithelium, and prevents subepithelial collagen deposition in an orthotopic tracheal allograft model using C57BL/6 mice[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mdx mice (C57BL/6 background, male, 4-week-old) were used to establish the Duchenne muscular dystrophy (DMD) model, assigned to non-exercised or low-intensity swimming training groups[2]
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Dosage:20 mg/kg
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Administration:s.c.; three times per week; for 4 weeks
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Result:Rescued the phenotype of non-exercised mdx mice, improving their grip strength and force-to-weight ratio.
Reduced the number of necrotic muscle fibers and switched the muscle fibers toward the glycolytic fast type in non-exercised mice.
Increased the expression level of IL-1 receptor antagonist (IL-1RA).
Increased the number of CD68+ cells and shifted the macrophage balance in favor of the pro-inflammatory M1 type.
Increased muscle damage and switched fibers to the oxidative slow type when combined with low-intensity training.
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Animal Model:db/db mice (C57BLKS/J-LepRdb/db, male, 10-week-old) were used and underwent uninephrectomy to hasten the progression of diabetic nephropathy (DN)[3]
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Dosage:10 mg/kg
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Administration:i.p.; every other day; for 12 weeks
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Result:Prevented the elevations of serum creatinine and blood urea nitrogen (BUN) levels.
Attenuated glomerular mesangial matrix expansion and tubulointerstitial damage.
Significantly reduced the expression of fibrotic markers, including TGF-β1, fibronectin, and collagen type I.
Decreased serum triglyceride levels and reduced renal lipid deposition by downregulating DGAT1, SREBP-1, and ADRP expressions.
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Animal Model:Tracheal segments from BALB/c mice were used as allografts and orthotopically sutured into the tracheas of recipient C57BL/6 mice[4]
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Dosage:10 mg/kg
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Administration:i.p.; administered on day 0 and every second day thereafter; treatment duration lasted up to 28 days post-transplantation
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Result:Significantly increased the number of CD4+CD25+FOXP3+ regulatory T cells in peripheral blood and the local allograft.
Restored the functional microvasculature between donor and recipient.
Improved tissue oxygenation (tpO2) and microvascular blood perfusion of the allografts.
Shortened the hypoxic and ischemic periods.
Maintained the health of airway epithelial cells.
Prevented subepithelial collagen deposition at day 28 post-transplantation.
Upregulated the gene expression of IL-5, TGF-β, IL-10, VEGF, and ANGPT1.
Downregulated the pro-inflammatory gene IL-6.
Elevated serum levels of TGF-β, IL-5, and IL-10.
Decreased the levels of IFN-γ, IL-6, and IL-15.
Chemical Information
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CAS No. 2364414-05-9
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Formula C398H498N160O310P40(C2H4O)2n (n≈450)
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SMILES
[Idalaptican pegol]
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Synonyms
NOX-D21; AON-D21
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Bujko K, et al. Signaling of the Complement Cleavage Product Anaphylatoxin C5a Through C5aR (CD88) Contributes to Pharmacological Hematopoietic Stem Cell Mobilization. Stem Cell Rev Rep. 2017 Dec;13(6):793-800. [Content Brief]
[2]. Hyzewicz J, et al. Low-Intensity Training and the C5a Complement Antagonist NOX-D21 Rescue the mdx Phenotype through Modulation of Inflammation. Am J Pathol. 2017 May;187(5):1147-1161. [Content Brief]
[3]. Yiu WH, et al. Complement C5a inhibition moderates lipid metabolism and reduces tubulointerstitial fibrosis in diabetic nephropathy. Nephrol Dial Transplant. 2018 Aug 1;33(8):1323-1332. [Content Brief]
[4]. Khan MA, et.al. C5a Blockade Increases Regulatory T Cell Numbers and Protects Against Microvascular Loss and Epithelial Damage in Mouse Airway Allografts. Front Immunol. 2018 May 24;9:1010. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Idalaptican pegol Related Classifications
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