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.
Biological Activity
Description
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DGAT1 |
In Vivo
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.
Protocols
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Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
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Multiplex immunofluorescence IHC
Multiplex immunofluorescence IHC detects multiple protein biomarkers in one tissue section by sequential antibody staining, HRP-mediated tyramide fluorophore deposition, heat-mediated antibody stripping, nuclear counterstaining, multispectral imaging, spectral unmixing, and digital cell phenotyping; TSA deposits fluorophore near the antigen so the fluorescence signal remains after primary and secondary antibodies are removed, enabling repeated staining cycles, including with antibodies from the same host species. Classic FFPE tumor immune-profiling applications use panels such as CD3, CD8, CD68/CD163, FOXP3, PD-1, PD-L1, pancytokeratin, Ki67, and DAPI to identify tumor cells, immune-cell subsets, checkpoint-marker expression, co-expression phenotypes, cell density, and spatial relationships in the tumor microenvironment.
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Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Chemotaxis Gradient Chamber Assay 1
The chemotaxis gradient chamber assay is based on the principle of observing directional cell migration in response to a stable, linear or quasi-linear concentration gradient of a chemoattractant formed between two fluid reservoirs separated by a narrow observation chamber. Cells placed within the chamber respond to the gradient by polarized movement toward higher chemoattractant concentrations, allowing quantification of chemotactic behavior in real time under microscopy. The classic Zigmond chamber design enables simultaneous visualization of gradient formation and individual cell trajectories, making it suitable for studying leukocyte chemotaxis and other motile cell types in vitro.
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Under-Agarose Cell Migration Assay
The under-agarose cell migration assay is a classical in vitro chemotaxis method designed to evaluate directed cell movement through a semi-solid agarose matrix toward soluble chemoattractant gradients, enabling visualization and quantification of leukocyte or motile cell migration in a confined 2D-like environment. In this system, cells and chemoattractants are placed in separate wells cut into an agarose gel, allowing diffusion-driven gradient formation that guides directional migration, which is typically assessed by measuring migration distance, cell morphology changes, and accumulation toward the chemoattractant source. This assay has been widely used to study neutrophil and leukocyte chemotaxis as a simple alternative to filter-based migration systems and allows direct microscopic observation of migrating cells under near-physiological confinement conditions.
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Transwell/Boyden Chamber Migration Assay
The Transwell/Boyden chamber migration assay measures cell movement through a porous membrane separating an upper and lower chamber, usually after a chemoattractant gradient is established by placing cells in the upper chamber and chemoattractant-containing medium in the lower chamber. The readout is generated by quantifying cells that traverse the membrane and appear on the lower membrane surface or in the lower chamber, depending on whether the cell type is adherent or non-adherent. This assay reflects chemotactic or haptotactic migration rather than matrix invasion unless an extracellular-matrix barrier is added to the membrane.
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Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
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Multiplex immunohistochemistry
Multiplex immunohistochemistry (mIHC), also known as tyramide dignal amplification (TSA), is an enzymatic detection method that uses horseradish peroxidase (HRP) to perform high-density in-situ labeling of target proteins or nucleic acids.
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Chemotaxis Gradient Chamber Assay 2
Chemotaxis gradient chamber assays measure directional cell migration in response to a soluble chemical gradient by imaging cells as they move across a defined observation region; the readout is generated from time-lapse cell trajectories, displacement toward the gradient, forward migration index, trajectory plots, rose/polar plots, and statistical tests of non-random directionality. The Dunn chamber is a direct-viewing glass chamber in which cells migrate across a bridge between control and chemoattractant wells, allowing observation of cells in a linear concentration gradient; related direct-viewing formats include the Insall chamber, which supports defined unidirectional gradients and high numerical-aperture microscopy, and the μ-Slide Chemotaxis chamber, which supports long-term live-cell imaging and gradient characterization with fluorescent dye.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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)