2. PI3K/Akt/mTOR Metabolic Enzyme/Protease JAK/STAT Signaling Epigenetics Stem Cell/Wnt Protein Tyrosine Kinase/RTK NF-κB Apoptosis Immunology/Inflammation
  3. PI3K Akt Pyruvate Kinase JAK STAT NF-κB Apoptosis Reactive Oxygen Species (ROS)
  4. Iridin

Iridin is an orally active natural isoflavone. Iridin inhibits the PI3K/AKT and PKM2 signaling pathways, and downregulates the JAK/STAT and NF-κB pathways. Iridin induces Fas-mediated extrinsic apoptosis, G2/M cell cycle arrest, and inhibits cell proliferation. Iridin reduces inflammation, inhibits ROS production, suppresses glycolysis, and also exhibits antioxidant and antidiabetic activities. Iridin can be used in research related to gastric cancer and acute lung injury.

For research use only. We do not sell to patients.

Iridin

Iridin Chemical Structure

CAS No. : 491-74-7

Size Price Stock Quantity
Solid + Solvent (Highly Recommended)
10 mM * 1 mL in DMSO
ready for reconstitution
 In-stock
Solution
10 mM * 1 mL in DMSO In-stock
Solid
5 mg In-stock
10 mg In-stock
50 mg   Get quote  
100 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Customer Review

Based on 1 publication(s) in Google Scholar

Other Forms of Iridin:

Iridin Related Antibodies

Top Publications Citing Use of Products

View All PI3K Isoform Specific Products:

View All Isoforms
PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

View All Akt Isoform Specific Products:

View All Isoforms
Akt Akt1 Akt2 Akt3

View All JAK Isoform Specific Products:

View All Isoforms
JAK1 JAK2 JAK3 Tyk2 JAK

View All STAT Isoform Specific Products:

View All Isoforms
STAT3 STAT5 STAT6 STAT1

View All NF-κB Isoform Specific Products:

View All Isoforms
NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Iridin is an orally active natural isoflavone. Iridin inhibits the PI3K/AKT and PKM2 signaling pathways, and downregulates the JAK/STAT and NF-κB pathways. Iridin induces Fas-mediated extrinsic apoptosis, G2/M cell cycle arrest, and inhibits cell proliferation. Iridin reduces inflammation, inhibits ROS production, suppresses glycolysis, and also exhibits antioxidant and antidiabetic activities. Iridin can be used in research related to gastric cancer and acute lung injury[1][2][3].

In Vitro

Iridin (12.5-200 μM) induces apoptosis via the extrinsic pathway and regulates the PI3K/AKT signaling pathway in AGS gastric cancer cells, HaCaT cells, and TRAIL-resistant gastric cancer cells[1].
Iridin (12.5-50 μM; 18 h) inhibits the production of proinflammatory mediators in LPS (HY-D1056)-stimulated RAW 264.7 cells in a dose-dependent manner[1].
Iridin (10 nM-100 μM) exerts no anticancer effects on MCF-7 and T-47D breast cancer cells[1].
Iridin (12.5-200 μM; 48 h) inhibits the proliferation and induces the death of human gastric cancer AGS cells, with an IC50 of 161.3 μM; whereas it exerts no significant effect on the cell viability of human keratinocyte HaCaT cells after 48 h of treatment[2].
Iridin (50-200 μM; 48 h) induces G2/M cell cycle arrest in human gastric cancer AGS cells after 48 h of treatment by downregulating the expression of cell cycle regulatory proteins Cdc25C, CDK1, and Cyclin B1[2].
Iridin (50-200 μM; 48 h) induces apoptotic cell death in human gastric cancer AGS cells via the extrinsic apoptotic pathway[2].
Iridin (50-200 μM; 48 h) inhibits the PI3K/AKT signaling pathway in human gastric cancer AGS cells by downregulating the phosphorylated (active) forms of PI3K and AKT, without affecting the expression of total PI3K or AKT[2].
Iridin (6.25-200 μM; 24 h) shows no cytotoxicity against RAW264.7 cells even at concentrations up to 100 μM. Based on its anti-inflammatory efficacy, concentrations of 12.5, 25 and 50 μM are selected for subsequent studies[3].
Iridin (12.5-50 μM; 18 h) reverses LPS-induced Warburg effect in RAW264.7 cells in a dose-dependent manner by enhancing oxidative phosphorylation and reducing glycolytic activity[3].
Iridin (12.5-50 μM; 18 h) dose-dependently inhibits LPS-induced production of NO, TNF-α, IL-1β and MCP-1 in RAW264.7 cells[3].
Iridin (12.5-50 μM; 18 h) dose-dependently abrogates LPS-induced accumulation of ROS and NO in RAW264.7 cells[3].
Iridin (12.5-50 μM; 18 h) dose-dependently inhibits LPS-induced excessive phagocytic activity in RAW264.7 cells[3].
Iridin (12.5-50 μM; 18 h) dose-dependently downregulates the expression of PKM2 and its downstream JAK/STAT and NF-κB pathway proteins in LPS-stimulated RAW264.7 cells, and this effect is reversed by PKM2 activation or ROS scavenging[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Iridin Related Antibodies

Cell Viability Assay[2]

Cell Line: human gastric cancer AGS cells, human keratinocyte HaCaT cells
Concentration: 12.5, 25, 50, 100 and 200 μM
Incubation Time: 48 h
Result: Caused a concentration-dependent reduction in AGS cell viability, with an IC50 of 161.3 μM.
Did not significantly affect HaCaT cell viability at any tested concentration.
Induced morphological changes in AGS cells including floating dead cells, cell shrinkage, and reduced cell numbers.

Cell Cycle Analysis[2]

Cell Line: human gastric cancer AGS cells
Concentration: 50, 100 and 200 μM
Incubation Time: 48 h
Result: Caused a concentration-dependent increase in the percentage of AGS cells arrested in the G2/M phase, accompanied by reduced percentages of cells in the G0/G1 phase.
Downregulated Cdc25C, CDK1, and Cyclin B1 protein expression in a concentration-dependent manner compared to untreated controls.

Apoptosis Analysis[2]

Cell Line: human gastric cancer AGS cells
Concentration: 50, 100 and 200 μM
Incubation Time: 48 h
Result: Caused a concentration-dependent increase in the apoptotic cell fraction (early apoptosis) in AGS cells, with apoptotic cell percentages rising significantly at 50, 100, and 200 μM.
Upregulated cleaved Caspase-3 and cleaved PARP protein expression in a concentration-dependent manner, along with downregulation of full-length Caspase-3 and PARP.

Western Blot Analysis[2]

Cell Line: human gastric cancer AGS cells
Concentration: 50, 100 and 200 μM
Incubation Time: 48 h
Result: Upregulated Fas and FasL protein expression in a concentration-dependent manner.
Downregulated full-length Caspase-8 and upregulated cleaved Caspase-8 in a concentration-dependent manner.
Caused no significant changes in the expression levels of Bcl-xL, Bax, Caspase-9, or cleaved Caspase-9 compared to untreated controls.\nDownregulated p-PI3K and p-AKT protein expression in a concentration-dependent manner.
Caused no changes in the expression levels of total PI3K and total AKT compared to untreated controls.

Cell Cytotoxicity Assay[3]

Cell Line: murine macrophage RAW264.7 cells
Concentration: 6.25, 12.5, 25, 50, 100, 150, 200 μM
Incubation Time: 24 h
Result: Did not affect RAW264.7 cell proliferation at concentrations ≤100 μM, with no significant difference in cell viability between control, Iridin-only, and LPS+Iridin groups (P>0.05).
Selected concentrations of 12.5, 25, and 50 μM for subsequent experiments based on an IC50 of 24.8 μM for LPS-induced NO release.

Western Blot Analysis[3]

Cell Line: LPS-stimulated murine macrophage RAW264.7 cells
Concentration: 12.5, 25, 50 μM
Incubation Time: 2 h pre-incubation, followed by 16 h LPS stimulation
Result: Dose-dependently reduced the expression of PKM2, p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2 proteins.
Inhibitory effects were fully reversed by PKM2 agonist DASA-58 or antioxidant NAC, and partially reversed by NF-κB activator CUT129 or JAK1 activator RO8191.
In Vivo

Iridin (20-80 mg/kg; p.o.; once daily; 5 days) dose-dependently ameliorates LPS-induced acute lung injury in male ICR mice by reducing inflammatory cell infiltration, modulating macrophage polarization to an anti-inflammatory M2 phenotype, and inhibiting the PKM2-mediated JAK/STAT and NF-κB signaling pathways[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: ICR (male, 24 g body weight, LPS-induced acute lung injury model)[3]
Dosage: 20 mg/kg; 40 mg/kg; 80 mg/kg
Administration: p.o.; once daily; 5 days
Result: Dose-dependently reduced lung pathologic scores, lung index, total cell count, and neutrophil count in bronchoalveolar lavage fluid compared to the LPS-challenged model group.
Dose-dependently decreased serum levels of iNOS and TNF-α, and increased serum levels of IL-10 compared to the LPS-challenged model group.
Dose-dependently reduced mRNA expressions of M1 macrophage markers iNOS and TNF-α, and increased mRNA expressions of M2 macrophage markers IL-10 and Arg-1 in lung tissue macrophages compared to the LPS-challenged model group.
Dose-dependently downregulated protein expressions of PKM2, p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2 in lung tissues compared to the LPS-challenged model group.
Molecular Weight

522.46

Formula

C24H26O13
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C1C2=C(O)C(OC)=C(O[C@@H]3O[C@@H]([C@@H](O)[C@H](O)[C@H]3O)CO)C=C2OC=C1C4=CC(OC)=C(OC)C(O)=C4
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, sealed storage, away from moisture and light

*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 (191.40 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.9140 mL 9.5701 mL 19.1402 mL
5 mM 0.3828 mL 1.9140 mL 3.8280 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

  • Molarity Calculator

  • Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass
=
Concentration
×
Volume
×
Molecular Weight *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start)

C1

×
Volume (start)

V1

=
Concentration (final)

C2

×
Volume (final)

V2

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.5 mg/mL (4.79 mM); Clear solution

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 2.5 mg/mL (4.79 mM); Clear solution

    This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

Dosage

mg/kg

Animal weight
(per animal)

g

Dosing volume
(per animal)

μL

Number of animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO +
% 
+
%
Tween-80 +
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation

Purity: 99.72%

SDS (252 KB)

COA (251 KB) HNMR (315 KB) CNMR (320 KB) LCMS (98 KB)

Handling Instructions (2659 KB)
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.9140 mL 9.5701 mL 19.1402 mL 47.8506 mL
5 mM 0.3828 mL 1.9140 mL 3.8280 mL 9.5701 mL
10 mM 0.1914 mL 0.9570 mL 1.9140 mL 4.7851 mL
15 mM 0.1276 mL 0.6380 mL 1.2760 mL 3.1900 mL
20 mM 0.0957 mL 0.4785 mL 0.9570 mL 2.3925 mL
25 mM 0.0766 mL 0.3828 mL 0.7656 mL 1.9140 mL
30 mM 0.0638 mL 0.3190 mL 0.6380 mL 1.5950 mL
40 mM 0.0479 mL 0.2393 mL 0.4785 mL 1.1963 mL
50 mM 0.0383 mL 0.1914 mL 0.3828 mL 0.9570 mL
60 mM 0.0319 mL 0.1595 mL 0.3190 mL 0.7975 mL
80 mM 0.0239 mL 0.1196 mL 0.2393 mL 0.5981 mL
100 mM 0.0191 mL 0.0957 mL 0.1914 mL 0.4785 mL
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Iridin Related Classifications

Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Iridin491-74-7PI3KAktPyruvate KinaseJAKSTATNF-κBApoptosisReactive Oxygen Species (ROS)Phosphoinositide 3-kinasePKBProtein kinase BJanus kinaseNuclear factor-κBNuclear factor-kappaBgastric cancerNF-κB signaling pathwayAGS gastric cancer cellsHaCaT cellsFas-mediated extrinsic apoptosisJAK/STAT signaling pathwayPKM2acute lung injuryRAW 264.7 cellsPI3K/AKT signaling pathwayInhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
Iridin
Cat. No.:
HY-N3011
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

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)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.