Reltecimod TFA
Based on 1 Customer Validation
Reltecimod (AB-103) TFA is a T-cell-specific surface glycoprotein CD28 (TP44) antagonist. Reltecimod TFA has beneficial effects against different bacterial infections, their exotoxins and endotoxins, and ionizing radiation. Reltecimod TFA modulates the inflammatory response by targeting and attenuating the critical CD28/B7-2 co-stimulatory pathway, without inhibiting it. Reltecimod TFA can be used to research necrotizing soft-tissue infections (NSTIs).
For research use only. We do not sell to patients.
- Purity : 99.78%
- Formula: C46H72N10O15S.xC2HF3O2
- Molecular Weight:1037.19 (free base)
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Storage:
Sealed storage, away from moisture and light.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Biological Activity
Description
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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Appearance Solid
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Molecular Weight 1037.19 (free base)
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Formula C46H72N10O15S.xC2HF3O2
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Color White to off-white
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Synonyms
AB-103 TFA
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Sequence
{d-Ala}-Ser-Pro-Met-Leu-Val-Ala-Tyr-Asp-{d-Ala}
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Sequence Shortening
{d-Ala}-SPMLVAYD-{d-Ala}
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture and light
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : < 0.1 mg/mL (insoluble)
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (272 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)