AZACITIDINE
Azacitidine is a hypomethylating nucleoside analog that incorporates into DNA and RNA, inhibiting DNA methyltransferases and restoring normal gene expression in MDS and AML. Side effects include myelosuppression, infections, injectionsite reactions, and GI disturbances. Only GMP materials will be supplied, logistics all according to GDP.
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Product Description
Mechanism of Action
AZACITIDINE exhibits a broad-spectrum mechanistic footprint involving catalyticdomain modulation, multiaxis signalling interference, mitochondrial energynetwork recalibration, membranepotential stabilization/destabilization, ionflux redistribution, cytoskeletalarchitecture remodelling, redoxequilibrium disruption and transcriptionfactor network reprogramming. Its physicochemical and conformational architecture supports interaction with catalytic microdomains, allosteric regulators, transmembrane helices, hydrophobic receptor pockets, nucleotidebinding centres, redoxbuffer modules and multiprotein scaffoldsproducing wideband influence across metabolic, genomic, structural and electrophysiological systems.
AZACITIDINE may alter phosphorylation topology across ERK/MAPK/JNK/p38 and PI3KAKT signalling chains, shift Gprotein signalling geometry, reconfigure Ca²⁺ microdomain amplitude/propagation, reshape IP/DAG cascade architecture, and recalibrate cAMPPKA signalling thresholds. Mitochondrially, it can rebalance ETCcomplex activation, modulate ATP/ADP turnover kinetics, shift ROSleakage thresholds, alter membranepotential polarity and propagate ERmitochondrial crossstress signals. These features make it highly relevant for deep mechanistic and translational research.
Advanced
- Kinomescale interference modelling and catalyticcascade rebuilding
- Ultraresolution ligand docking and conformationaltransition prediction algorithms
- UPR/ERstress, mitochondrialstress, autophagy and mitophagy axis modelling
- Fullstack multiomics system reconstruction (RNAseq, metabolomics, proteomics, phosphoproteomics)
- Cytoskeletal tensionmapping, actin/tubulin turnover modelling and forcedistribution analytics
- Cellfate modelling across apoptosis, necroptosis, pyroptosis, ferroptosis and parthanatos
- Advanced AIdriven SAR/QSAR predictive molecularperformance mapping
Toxicodynamics & Hazard Spectrum
- Accelerated ROS accumulation and antioxidantbuffer collapse
- Mitochondrial fragmentation, ETC shutdown or hyperleakage states
- Severe Na⁺/K⁺/Ca²⁺ iontransport dysregulation
- Cytoskeletal depolymerisation, microtubule instability and global mechanical failure
- membrane-integrity disruption, bilayer thinning and permeability shifts
- NF-κB / STAT / IRF inflammatoryaxis hyperactivation
- Multiaxis programmed celldeath initiation
- Epigenetic drift across methylation/acetylation landscapes
For expert laboratory research only not intended for biological or therapeutic exposure.
Only GMP materials will be supplied, logistics all according to GDP.
Datasheet
| Molecular Formula | C8H12N4O5 |
|---|---|
| Molecular Weight | 244.20 g/mol |
| CAS Number | 320-67-2 |
| Storage Condition | Intact vials should be stored under refrigeration & are stable for a least 4 yr. Although the drug is stable for 3 yr at room temp, refrigeration is recommended because degradation may result at elevated temperatures. The constituted soln hydrolyzes at room temp & should be used within 30 min. … Azacitidine 0.5 & 2 mg/ml in Ringer's injection, lactated, was stable for up to one month when frozen at -20 °C in polypropylene syringes. |
| Solubility | 5 to 10 mg/mL at 70 °F (NTP, 1992) |
| Purity | Purity information is available upon request (COA). |
| Synonym | 5-azacytidine; Azacitidine; 320-67-2; Azacytidine; Ladakamycin |
| IUPAC/Chemical Name | 4-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2-one |
| InChl Key | NMUSYJAQQFHJEW-KVTDHHQDSA-N |
| InChl Code | InChI=1S/C8H12N4O5/c9-7-10-2-12(8(16)11-7)6-5(15)4(14)3(1-13)17-6/h2-6,13-15H,1H2,(H2,9,11,16)/t3-,4-,5-,6-/m1/s1 |
| References |
3D Conformer.
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