1,3-Dibenzyl-5-fluorouracil
1,3-Dibenzyl-5-fluorouracil is a chemical inhibitor of osteoclastogenesis. 1,3-Dibenzyl-5-fluorouracil inhibits the expression of osteoclast markers by downregulating the receptor activator of NF-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) signaling pathways. 1,3-Dibenzyl-5-fluorouracil can be used in the study of metabolic bone diseases.
For research use only. We do not sell to patients.
- CAS No.: 75500-02-6
- Formula: C18H15FN2O2
- Molecular Weight:310.32
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
-
CAS No. 75500-02-6
-
Molecular Weight 310.32
-
Formula C18H15FN2O2
-
SMILES
C1=CC=C(C=C1)CN2C=C(C(=O)N(C2=O)CC3=CC=CC=C3)F
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
-
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
-
Osteoclast differentiation from monocyte/macrophage precursors
Osteoclast differentiation is an in vitro induction assay in which monocyte/macrophage-lineage precursors are exposed to macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL), generating multinucleated osteoclasts that are commonly identified by tartrate-resistant acid phosphatase (TRAP) staining and functionally confirmed by resorption pits on dentin, bone, or mineralized substrates. M-CSF supports survival and expansion of osteoclast precursors, while RANKL binding to RANK drives osteoclast commitment, fusion, maturation, and resorptive function; osteoprotegerin inhibits this pathway by binding RANKL and preventing RANK activation. The main readouts are the number of TRAP-positive multinucleated cells, formation of F-actin rings, and resorbed surface area; TRAP-positive multinucleated cells indicate osteoclast differentiation, whereas pit formation on dentin, bone, or mineralized coating indicates functional bone-resorbing activity.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)