TRILACICLIB
Trilaciclib is a CDK4/6 inhibitor used to reduce chemotherapy-induced myelosuppression by protecting hematopoietic stem cells. Side effects include fatigue, hypocalcemia, headache, neutropenia, and infusion reactions. Only GMP materials will be supplied, logistics all according to GDP.
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Product Description
Mechanism of Action
TRILACICLIB demonstrates multilayer biochemical influence across signalling hierarchies, catalyticdomain regulation, mitochondrialnetwork energetics, iongradient stability, membrane electrochemistry, redox equilibrium and transcriptionfactor axis alignment. Its molecular topology enables interaction with catalytic residues, allosteric nodes, hydrophobic receptor microdomains, transmembrane helices, redoxbuffer matrices and cytoskeletal scaffolds, resulting in widespectrum modulation across metabolic, structural, electrophysiological and genomic systems.
Mechanistically, TRILACICLIB may remodel phosphorylation flux across MAPK/ERK/JNK/p38 pathways, reshape PI3KAKT survival topology, modify Gprotein coupling dynamics, reorganise Ca²⁺ signalling microdomains, influence IP/DAG cascade geometry and adjust cAMPPKA amplitude distributions. Mitochondrial impacts include ETCcomplex rebalancing, ATP/ADP turnover pattern shifts, ROSthreshold displacement, membranepotential polarity modulation and ERmitochondrial stresscrosstalk regulation.
Advanced
- Kinomescale interference mapping and catalyticcascade simulation
- Highresolution docking and conformationaltransition modelling
- UPR/ERstress, autophagymitophagy and organellenetwork integration research
- Multiomics regulatory reconstruction (RNAseq, phosphoproteomics, metabolomics, proteomics)
- Cytoskeletal tensionmapping and polymerturnover analysis
- Cellfate simulations (apoptosis, necroptosis, ferroptosis, parthanatos)
- Machinelearning SAR/QSAR predictive optimisation
Toxicodynamics & Hazard Profile
- Accelerated ROS accumulation & antioxidantbuffer saturation
- Mitochondrial fragmentation or ETCaxis destabilisation
- Severe Na⁺/K⁺/Ca²⁺ ionic-flux dysregulation
- Cytoskeletal collapse & membrane-integrity failure
- Inflammatoryaxis hyperactivation (NF-κB, STAT, IRF pathways)
- Activation of multiaxis programmed-cell-death pathways
- Epigenetic methylation/acetylation drift
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 | C24H30N8O |
|---|---|
| Molecular Weight | 446.5 g/mol |
| CAS Number | 1374743-00-6 |
| Storage Condition | Store in a cool, dry place. Keep container tightly closed. Protect from moisture and light. |
| Solubility | Solubility depends on solvent and conditions (e.g., pH). Please contact us for solvent-specific guidance. |
| Purity | Purity information is available upon request (COA). |
| Synonym | Trilaciclib; 1374743-00-6; G1T28; 2'-((5-(4-methylpiperazin-1-yl)pyridin-2-yl)amino)-7',8'-dihydro-6'H-spiro[cyclohexane-1,9'-pyrazino[1',2':1,5]pyrrolo[2,3-d]pyrimidin]-6'-one; U6072DO9XG |
| IUPAC/Chemical Name | 4-[[5-(4-methylpiperazin-1-yl)-2-pyridinyl]amino]spiro[1,3,5,11-tetrazatricyclo[7.4.0.02,7]trideca-2,4,6,8-tetraene-13,1'-cyclohexane]-10-one |
| InChl Key | PDGKHKMBHVFCMG-UHFFFAOYSA-N |
| InChl Code | InChI=1S/C24H30N8O/c1-30-9-11-31(12-10-30)18-5-6-20(25-15-18)28-23-26-14-17-13-19-22(33)27-16-24(7-3-2-4-8-24)32(19)21(17)29-23/h5-6,13-15H,2-4,7-12,16H2,1H3,(H,27,33)(H,25,26,28,29) |
| References |
3D Conformer.
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