TRAMADOL
Tramadol is a centrally acting analgesic that activates opioid receptors and inhibits serotonin/norepinephrine reuptake. Used for moderate pain. Side effects include dizziness, constipation, nausea, seizures, respiratory depression, and dependence risk. Only GMP materials will be supplied, logistics all according to GDP.
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Product Description
Mechanism of Action
TRAMADOL demonstrates a multilayer biochemical interaction architecture integrating highbandwidth signalling interference, catalyticdomain perturbation, mitochondrialnetwork recalibration, ionflux redistribution, cytoskeletal restructuring, membranepotential modulation and transcriptionfactor pathway realignment. Its molecular conformation enables docking to catalytic residues, allosteric nodes, transmembrane helices, nucleotidebinding pockets, redoxbuffer centres and polymeric scaffolding complexes, providing systemwide influence across metabolic, electrophysiological, structural and genomic domains.
At the signalling stratum, TRAMADOL may reshape phosphorylation landscapes, alter the propagation kinetics of ERK, MAPK, JNK and p38 pathways, modulate PI3KAKT survival gating, adjust Gprotein coupling efficiency, redistribute Ca²⁺ microdomains, influence IP/DAG signalling geometry, and redefine cAMPPKA amplitude. Mitochondrial effects include ETCcomplex rebalancing, ATP/ADP cycle remapping, ROSthreshold displacement, membranepotential polarity modulation and crossorganelle stress signalling.
HighPrecision
- Kinomescale cascade interference mapping & catalyticpathway reconstruction
- Highresolution docking, ligandmetastability tracking & conformationalflow modelling
- UPR/ERstress, mitophagy and organelle crosstalk quantification
- Multiomics regulatorynetwork reconstruction (RNAseq, metabolomics, phosphoproteomics, proteomics)
- Cytoskeletal mechanics including actin/tubulin turnover and forcedistribution modelling
- Cellfate simulations across apoptosis, necroptosis, ferroptosis & parthanatos pathways
- AIenhanced SAR/QSAR optimisation engines for predictive compound modelling
Toxicodynamics & Cellular Hazard Spectrum
- Acute ROS surge and antioxidantbuffer saturation
- Mitochondrial fragmentation or ETCaxis collapse
- Severe Na⁺/K⁺/Ca²⁺ ionhomeostasis destabilisation
- Cytoskeletal depolymerisation & structuralintegrity failure
- Membranetension breakdown & lipidbilayer thinning
- Hyperactivation of inflammatory master regulators (NF-κB, STAT, IRF families)
- Activation of multiple programmed-cell-death pathways
- Epigenetic drift including methylation and acetylation instability
For expert not intended for biological or therapeutic exposure.
Only GMP materials will be supplied, logistics all according to GDP.
Datasheet
| Molecular Formula | C16H25NO2 |
|---|---|
| Molecular Weight | 263.37 g/mol |
| CAS Number | 27203-92-5 |
| Storage Condition | Store at 25 °C (77 °F); excursions permitted to 15 – 30 °C (59 -86 °F). |
| Solubility | Soluble |
| Purity | Purity information is available upon request (COA). |
| Synonym | Tramadol; 27203-92-5; Ralivia flashtab; Ralivia ER; Tramadon |
| IUPAC/Chemical Name | cis-(1R,2R)-2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexan-1-ol |
| InChl Key | TVYLLZQTGLZFBW-ZBFHGGJFSA-N |
| InChl Code | InChI=1S/C16H25NO2/c1-17(2)12-14-7-4-5-10-16(14,18)13-8-6-9-15(11-13)19-3/h6,8-9,11,14,18H,4-5,7,10,12H2,1-3H3/t14-,16+/m1/s1 |
| References |
3D Conformer.
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