ddTTP trisodium solution (100 mM)
Based on 1 Customer Validation
ddTTP trisodium solution (100 mM) is a DNA polymerase γ inhibitor, with Ki values of 0.05 μM and 0.4 μM against bovine testicular DNA polymerase γ. ddTTP trisodium solution (100 mM) can be incorporated into DNA to cause termination of the extended DNA strand. ddTTP trisodium solution (100 mM) can be used in the research of HIV infection.
For research use only. We do not sell to patients.
- Purity : 99.91%
- Formula: C10H14N2Na3O13P3
- Molecular Weight:532.11
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Storage:
Solution, -20°C, 2 years
All DNA/RNA Synthesis Isoforms
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Biological Activity
Description
In Vitro
ddTTP trisodium solution (100 mM) (0-100 μM; 30 min) potently inhibits bovine testicular DNA polymerase γ in a competitive manner relative to dTTP, with a Ki value of 0.05 μM when poly (rA)-oligo (dT) serves as the template-primer[1].
trisodium solution (100 mM) ddTTP (0-100 μM; 30 min) potently inhibits bovine testicular DNA polymerase γ in a competitive manner relative to dTTP, with a Ki value of 0.4 μM when activated calf thymus DNA is used as the template-primer[1].
trisodium solution (100 mM) ddTTP (2.5-10 μM; 60 min) can be incorporated into DNA by bovine testicular DNA polymerase γ and induce chain termination, and this effect is independent of 3'-exonuclease proofreading activity (verified by treatment with 1 mM 5'-GMP)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Appearance Liquid
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Molecular Weight 532.11
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Formula C10H14N2Na3O13P3
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Color Colorless to light yellow
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SMILES
O=[P](O[P](O[P](O)(O[Na])=O)(O[Na])=O)(O[Na])OC[C@@H](O1)CC[C@@H]1N(C(NC2=O)=O)C=C2C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Solution, -20°C, 2 years
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
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Data Sheet (271 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)