Molecular Formula | C19H12N2O |
Molar Mass | 284.31 |
Density | 1.463±0.06 g/cm3(Predicted) |
Boling Point | 630.3±35.0 °C(Predicted) |
Solubility | Soluble in DMSO (up to 10 mg/ml). |
Appearance | powder |
Color | yellow to orange |
pKa | 15.66±0.30(Predicted) |
Storage Condition | -20°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 1 month. |
Physical and Chemical Properties | Bioactive FICZ (6-Formylindolo[3,2-b]carbazole) is a potent agonist of aryl hydrocarbon receptor (AhR) that is efficiently metabolized by the AHR-regulated cytochrome P4501 enzyme. |
In vitro study | FICZ (0.01 nM-1 µM) alone or in combination with 50 nM MNF induces sustained CYP1A1 activity and leads to oxidative stress and activation of apoptosis via a mitochondrial-dependent pathway. In HepG2 cells, FICZ stimulates cell growth at low concentrations but inhibits cell growth at high concentrations. FICZ (10,000-30,000 nM) significantly decreases CEH viability with an estimated LC 50 (95% confidence intervals) of 14,000 nM. FICZ shows concentration-dependent effects on EROD activity in CEH cultures, with the mean EC 50 values at 3, 8, and 24 h of 0.016 nM, 0.80 nM, and 11 nM, respectively. FICZ treatment increases transcript expression of CYP1A1 in a dose-dependent manner in both the parental iPSC line and the CYP1A1 targeted clone. CYP1 inhibition in the presence of FICZ results in enhanced AHR activation, suggesting that FICZ accumulates in the cell when its metabolism is blocked. CYP1 enzymes plays a role in regulating biological effects of FICZ. Nuclear export and degradation of the AHR protein are two additional steps in the AHR-mediated signal transduction pathway. Exposure to AhR agonists causes AhR-expressing cells to downregulate the receptor through the ubiquitin/proteasome degradation pathway. |
WGK Germany | 1 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.542 ml | 17.712 ml | 35.424 ml |
5 mM | 0.708 ml | 3.542 ml | 7.085 ml |
10 mM | 0.354 ml | 1.771 ml | 3.542 ml |
5 mM | 0.071 ml | 0.354 ml | 0.708 ml |
Target
Target Value
AhR
in vitro studies
FICZ (0.01 nM-1 µM) alone or in combination with 50 nM MNF induces sustained CYP1A1 activity and leads to oxidative stress and activation of apoptosis via a mitochondrial-dependent pathway. In HepG2 cells, FICZ stimulates cell growth at low concentrations but inhibits cell growth at high concentrations. FICZ (10,000-30,000 nM) significantly decreases CEH viability with an estimated LC 50 (95% confidence intervals) of 14,000 nM. FICZ shows concentration-dependent effects on EROD activity in CEH cultures, with the mean EC 50 values at 3, 8, and 24 h of 0.016 nM, 0.80 nM, and 11 nM, respectively. FICZ treatment increases transcript expression of CYP1A1 in a dose-dependent manner in both the parental iPSC line and the CYP1A1 targeted clone. CYP1 inhibition in the presence of FICZ results in enhanced AHR activation, suggesting that FICZ accumulates in the cell when its metabolism is blocked. CYP1 enzymes plays a role in regulating biological effects of FICZ.
Nuclear export and degradation of the AHR protein are two additional steps in the AHR-mediated signal transduction pathway.
Exposure to AhR agonists causes AhR-expressing cells to downregulate the receptor through the ubiquitin/proteasome degradation pathway.
Biological activity | FICZ (6-Formydolo [3,2-b]carbazole) is an effective agonist of aryl hydrocarbon receptor (AhR), which can be effectively metabolized by AHR-regulated cytochrome P4501 enzyme. |
target | TargetValue AhR () |
Target | Value |
in vitro study | FICZ (0.01 nM-1 m) alone or in combination with 50 nM MNF induces sustained CYP1A1 activity and led to oxidative stress and activation of apoptosis via a mitochondrial-dependent pathway. In HepG2 cells, FICZ stimulates cell growth at low concentrations but inhibits cell growth at high concentrations. FICZ (10,000-30,000 nM) significantly decreases CEH viability with an estimated LC 50 (95% confidence intervals) of 14,000 nM. FICZ shows concentration-dependent effects on EROD activity in CEH cultures, with the mean EC 50 values at 3, 8, and 24 h of 0.016 nM, 0.80 nM, and 11 nM, respectively. FICZ treatment increases transcript expression of CYP1A1 in a dose-dependent banner in both the parental iPSC line and the CYP1A1 targeted clone. CYP1 inhibition in the presence of FICZ results in enhanced AHR activation, suggesting that FICZ accumulates in the cell when its metabolism is blocked. CYP1 enzymes plays a role in regulating biological effects of FICZ. Nuclear export and degradation of the AHR protein are two additional steps in the AHR-mediated signal transduction pathway. Exposure to AhR agonists AhR-expressing cells to downregulate the receptor through the ubiquitin/proteasome degradation pathway. |