Metabolic Enzyme/Protease NF-κB Immunology/Inflammation Epigenetics Stem Cell/Wnt Protein Tyrosine Kinase/RTK JAK/STAT Signaling Apoptosis Anti-infection
Dipeptidyl Peptidase NF-κB MyD88 JAK Toll-like Receptor (TLR) STAT Interleukin Related COX Reactive Oxygen Species (ROS) Glutathione S-transferase SOD Bcl-2 Family Caspase Apoptosis Dengue Virus
Azaleatin

Cat. No.: HY-N7653

Azaleatin

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Based on 1 Customer Validation

Azaleatin is an orally active inhibitor of hQC, NS2B-NS3 protease and E. coli β-glucuronidase, with IC₅₀ values of 1.1 μM, 38.00 μg/mL and 0.57 μM, respectively. Azaleatin inhibits the activities of NF-κB, MyD88, JAK1, TLR4, STAT3, IL-1β, IL-6, COX-2, TNF-α and β-glucuronidase, blocks pro-inflammatory signaling pathways, reduces the levels of ROS, MDA and uric acid, elevates the levels of GPx, GSR, GST, SOD, CAT, HO-1 and GSH, scavenges free radicals and exerts reducing capacity. Azaleatin inhibits the expression of pro-apoptotic proteins Bax, Caspase-9 and Caspase-3, and upregulates the expression of anti-apoptotic protein Bcl-2. Azaleatin reduces the levels of cardiac injury markers, restores cardiac histological structure, inhibits Aβ aggregation, dengue protease activity, hepatic stellate cell proliferation and cancer cell growth, and also exhibits antibacterial activity. Azaleatin can be used in studies related to subchronic cardiotoxicity, Alzheimer's disease, dengue fever, hyperuricemia, liver fibrosis, gastric cancer and bacterial infections.

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

Purity: 98.86%
CAS No.: 529-51-1
Formula: C₁₆H₁₂O₇
Molecular Weight:316.26

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

Azaleatin Chemical Structure

CAS No.: 529-51-1

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]

DPP-4

JAK1

TLR4

STAT3

IL-6

IL-1β

COX-2

hQC

1.1 μM (IC₅₀)

hQC

0.4 nM (Kd)

GSR

GST

Caspase-9

Caspase-3

All Dipeptidyl Peptidase Isoforms :

All NF-κB Isoforms :

All JAK Isoforms :

All Toll-like Receptor (TLR) Isoforms :

All STAT Isoforms :

All Interleukin Related Isoforms :

All COX Isoforms :

All Bcl-2 Family Isoforms :

All Caspase Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HEK293	IC₅₀	0.74 μM Compound: 7b	Inhibition of NOX4 expressed in HEK293 FS cells assessed as H2O2 production by H2O2/Tyr/LPO assay Inhibition of NOX4 expressed in HEK293 FS cells assessed as H2O2 production by H2O2/Tyr/LPO assay	[PMID: 20731357]

In Vitro

Azaleatin binds strongly to NF-κB, TLR4, and STAT3 proteins, with the highest affinity for NF-κB (-8.5 kcal/mol), indicating its potential to regulate pro-inflammatory signaling pathways^[1].
Azaleatin (multiple concentrations; 5 min) potently inhibits human glutaminyl cyclase (hQC) in biochemical assays, with an IC₅₀ of 1.1 μM^[2].
Azaleatin (12.5-100 μM) binds to purified human glutaminyl cyclase (hQC) with high affinity, and its K_D is determined to be 0.4 nM by surface plasmon resonance^[2].
Azaleatin binds to the active site of human glutaminyl cyclase (hQC) via coordination with catalytic zinc ions, hydrogen bonding, anion-π interactions, and hydrophobic interactions with key residues, thereby supporting its inhibitory activity^[2].
Azaleatin complies with Lipinski's Rule of Five and possesses favorable pharmacokinetic properties, including good absorbability, non-carcinogenicity, and higher bioavailability compared with quercetin^[3].
Azaleatin binds to the central active site of β-glucuronidase (PDB ID: 3K4D) with a binding affinity of -8.5 kcal/mol, and forms polar and hydrophobic interactions with key enzyme residues^[4].
Azaleatin forms a stable complex with β-glucuronidase (PDB ID: 3K4D) during a 50 ns MD simulation, exhibiting characteristics of strong electrostatic interactions, stable hydrogen bonding, and reduced enzyme flexibility, which is consistent with its potent in vitro inhibitory activity^[4].
Azaleatin (10-30 μM; 2 h) inhibits uric acid production in a concentration-dependent manner in AML12 hepatocytes^[5].
Azaleatin (5-80 μM; 6-24 h) inhibits the proliferation of rat hepatic stellate cells (HSC-T6) at a concentration of 80 μM after 24 h of incubation; it promotes cell proliferation in a dose-dependent manner at 6 h, while exerts no effect at low doses within 12 h^[6].
Azaleatin (20-40 μM; 24 h) reduces αSMA accumulation in a dose-dependent manner, and effectively inhibits TGFβ-induced type I collagen production in rat hepatic stellate cells (HSC-T6) after 24 h of co-treatment at concentrations of 20 μM and 40 μM^[6].
Azaleatin (20 μM; 1-6 h) does not inhibit TGFβ-induced αSMA or Timp1 mRNA expression, but reduces type I collagen mRNA expression in a time-dependent manner in TGFβ-induced rat hepatic stellate cells (HSC-T6) after 6 hours of co-treatment at a concentration of 20 μM^[6].
Azaleatin (5-1,000 μg/mL) exhibits in vitro antioxidant activity by scavenging DPPH, superoxide anion and hydroxyl radicals, as well as through its reducing capacity, but shows no metal chelating activity, with EC₅₀ values of 37 μg/mL (DPPH), 90 μg/mL (superoxide anion), 688 μg/mL (hydroxyl radical) and 27 μg/mL (reducing capacity)^[7].
Azaleatin is present in the ethanol extract of *Rhododendron anthopogonoides*, and its content is determined to be 0.10 mg/g fresh weight via UPLC quantitative analysis^[7].
Azaleatin (5 mg) exists as its 3-O-α-L-rhamnoside derivative (azaleatin-3-O-α-L-rhamnoside) in the ethanolic fruit extract of *Azara dentata*. This compound is identified via UHPLC-ESI-Q-TOF-MS, with a pseudomolecular ion m/z value of 461.1064, corresponding to the product ion m/z value of 287.0555 for azaleatin-3-O-α-L-rhamnoside^[8].
Azaleatin (3.125-200 μg/mL; 20-100 μg/mL) acts as a non-competitive inhibitor against dengue NS2B-NS3 serotype 2 protease, with an IC₅₀ of 38 μg/mL and a K_i of 26.82 μg/mL^[3].
Azaleatin binds to the allosteric pocket of dengue virus NS2B-NS3 protease (PDB ID: 3U1I) with a docking score of -8.2 kcal/mol, and forms hydrogen bonds and hydrophobic interactions with key functional residues^[3].
Azaleatin (100 ns) forms a stable complex with dengue virus NS2B-NS3 protease (PDB ID: 3U1I) during the 100 ns simulation, stabilizes the closed conformation of this enzyme, and supports its non-competitive inhibition mode^[3].
Azaleatin (0.001-1000 μM; 30 min) potently inhibits Escherichia coli β-glucuronidase via a non-competitive mechanism, with an IC₅₀ of 0.57 μM and a K_i of 0.66 μM^[4].
Azaleatin (10-250 μM; 48 h) inhibits the viability of HGC-27 cells. Its significant growth-inhibitory effect emerges starting at 10 μM, and cell viability drops to approximately 40% of that in the control group at the highest tested concentration. Among the three flavonoids tested, it exhibits the weakest cell growth inhibitory activity^[9].
Azaleatin (20-35 μM; 24 h) significantly increases pentoside levels in HGC-27 cells at concentrations of 20 μM and above following 24 h of incubation. It exhibits moderate potency, which is higher than that of kaempferol but lower than that of myricetin^[9].
Azaleatin (15-35 μM; 24 h) induces a dose-dependent increase in 3-deoxyglucosone levels in HGC-27 cells, with a significant elevation starting at 15 μM and reaching 2.5 times the control level at the highest tested concentration. Among the tested flavonoids, it exhibits the weakest effect on this indicator^[9].
Azaleatin (5-35 μM; 24 h) potently elevates methylglyoxal levels in HGC-27 cells, with an initial effective concentration of 5 μM. At the highest tested concentration, the methylglyoxal level reaches approximately 3.3 times that of the control group. In terms of this indicator, its efficacy is far superior to that of other tested flavonoid compounds^[9].

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

Cell Proliferation Assay^[6]

Cell Line:

HSC-T6 (rat hepatic stellate cells)
Concentration:

5, 10, 20, 40 and 80 μM
Incubation Time:

6, 12 and 24 h
Result:

Increased HSC-T6 proliferation in a dose-dependent manner after 6 h treatment.
Decreased proliferation to levels comparable to non-treated controls after 12 h treatment.
Markedly suppressed HSC-T6 proliferation at 80 μM after 24 h incubation; no inhibitory effect was observed at lower doses (5, 10, 20, 40 μM) up to 12 h.

Immunofluorescence^[6]

Cell Line:

HSC-T6 (TGFβ-induced rat hepatic stellate cells)
Concentration:

20 and 40 μM
Incubation Time:

24 h
Result:

Reduced αSMA accumulation compared to TGFβ-induced positive controls, with dose-dependent enhancement from 20 μM to 40 μM; the inhibitory effect was weaker than other methylated quercetin derivatives.
Effectively inhibited collagen I production in TGFβ-induced HSC-T6 cells.

Real Time qPCR^[6]

Cell Line:

HSC-T6 (TGFβ-induced rat hepatic stellate cells)
Concentration:

20 μM
Incubation Time:

1 and 6 h
Result:

Did not inhibit TGFβ-induced augmentation of αSMA mRNA after 1 h co-treatment.
Decreased αSMA mRNA levels after 6 h co-treatment, though levels remained higher than non-treated controls.
Increased collagen I mRNA after 1 h co-treatment but decreased it after 6 h in a time-dependent manner.
Did not inhibit TGFβ-induced increases in Timp1 mRNA expression after 6 h co-treatment.

Cell Viability Assay^[10]

Cell Line:

HGC-27 immortalised human-stomach adenocarcinoma cells
Concentration:

0, 50, 100, 150, 200 and 250 μM
Incubation Time:

48 h
Result:

Significantly inhibited HGC-27 cell growth starting at 10 μM.
Reduced cell viability to approximately 40% of control at the highest tested concentration.
Ranked as the least effective cell growth inhibitor among kaempferol, myricetin, and azaleatin.

Cell Viability Assay^[5]

Cell Line:

AML12 cells
Concentration:

0, 3, 10 and 30 μM
Incubation Time:

2 h
Result:

Significantly and dose-dependently decreased the uric acid production in the hepatocytes.
At dose of 3 μM did not inhibit uric acid production.
At 10 μM significantly suppressed uric acid production.
At 30 μM significantly suppressed uric acid production .
Showed more notable inhibitory effect at 30 μM than that at lower concentrations.

In Vivo

Azaleatin (25 mg/kg; p.o.; daily; 8 weeks) exerts cardioprotective effects against sodium arsenite-induced sub-chronic cardiotoxicity in male Sprague Dawley rats by restoring redox balance, suppressing pro-inflammatory gene expression, reducing cardiac injury markers, modulating apoptotic pathways, and preserving cardiac histology^[1].
Azaleatin (25 mg/kg; p.o.; daily; 8 weeks) is well-tolerated and does not induce adverse cardiac effects in healthy male Sprague Dawley rats^[1].

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

Animal Model:

Male Sprague-Dawley rats (13-14 weeks old, 225 g) were orally administered sodium arsenite (10 mg/kg) for 8 weeks to induce myocardial injury. Meanwhile, the compound was orally administered to evaluate its cardioprotective effects.
^[1]
Dosage:

25 mg/kg
Administration:

p.o.; daily; 8 weeks
Result:

Significantly downregulated mRNA expressions of pro-inflammatory genes (NF-κB, MyD88, JAK1, TLR4, STAT3, IL-6, IL-1β, TNF-α) to levels not significantly different from the control group.
Restored cardiac antioxidant enzyme activities: catalase (CAT) increased from 2.27 U/mg protein to 8.50 U/mg protein; superoxide dismutase (SOD) increased from 2.02 U/mg protein to 5.47 U/mg protein; glutathione reductase (GSR) increased from 2.48 nM NADPH oxidized/min/mg tissue to 5.24 nM NADPH oxidized/min/mg tissue; glutathione peroxidase (GPx) increased from 3.49 U/mg protein to 11.81 U/mg protein; glutathione (GSH) increased from 3.06 μmol/g tissue to 9.37 μmol/g tissue; glutathione S-transferase (GST) increased from 4.28 U/mg protein to 14.92 U/mg protein; heme-oxygenase-1 (HO-1) increased from 68.58 pmoles bilirubin/mg protein/h to 231.18 pmoles bilirubin/mg protein/h.
Reduced oxidative stress markers: malondialdehyde (MDA) decreased from 13.61 nmol/g to 5.09 nmol/g; reactive oxygen species (ROS) decreased from 13.28 nmol/g to 4.47 nmol/g.
Reduced cardiac injury marker levels: CK-MB decreased from 83.05 ng/mL to 47.02 ng/mL; CPK decreased from 491.67 mcg/L to 273.89 mcg/L; troponin-I decreased from 5.89 pg/mL to 2.33 pg/mL; troponin-T decreased from 3.67 ng/mL to 1.59 ng/mL; LDH decreased from 42.10 mg/mL to 20.63 mg/mL; BNP decreased from 78.75 pg/mL to 40.89 pg/mL; NT-proBNP decreased from 316.73 pg/mL to 178.14 pg/mL; CRP decreased from 19.38 mg/L to 10.91 mg/L.
Modulated apoptotic markers: Bax decreased from 15.15 pg/mL to 4.97 pg/mL; caspase-9 decreased from 14.19 pg/mL to 6.46 pg/mL; caspase-3 decreased from 12.81 pg/mL to 3.43 pg/mL; Bcl-2 increased from 3.84 ng/mL to 8.34 ng/mL.
Prevented sodium arsenite-induced cardiac damage (myofiber degeneration, hypertrophy, vascular congestion, edema, hemorrhage, inflammation, dysregulated intercalated discs), preserving near-normal cardiac architecture.
Showed values for all measured parameters comparable to the control group in the azaleatin-only group, indicating a safe profile at the tested dose.

Animal Model:

Sprague Dawley (male, 13-14 weeks old, 225 g)^[1]
Dosage:

25 mg/kg
Administration:

p.o.; 8 weeks
Result:

Resulted in mRNA expressions of pro-inflammatory genes (NF-κB, MyD88, JAK1, TLR4, STAT3, IL-6, IL-1β, TNF-α), antioxidant enzyme activities, oxidative stress marker levels, cardiac injury marker levels, apoptotic marker levels, and cardiac histology that were all comparable to the control group, with no significant differences detected.

Chemical Information

CAS No. 529-51-1
Appearance Solid
Molecular Weight 316.26
Formula C₁₆H₁₂O₇
Color Off-white to light yellow
SMILES

O=C1C(O)=C(C2=CC=C(O)C(O)=C2)OC3=CC(O)=CC(OC)=C13
Structure Classification
- Flavonoids
- Flavonols
- Phenols
- Polyphenols
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : 50 mg/mL (158.10 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.1620 mL

15.8098 mL

31.6196 mL

5 mM

0.6324 mL

3.1620 mL

6.3239 mL

10 mM

0.3162 mL

1.5810 mL

3.1620 mL

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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

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Dilution Calculator

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In Vivo:

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

Stock Solution Working Solution

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: ≥ 1.25 mg/mL (3.95 mM); Clear solution

This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (12.5 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.

Protocol 2

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

Solubility: ≥ 1.25 mg/mL (3.95 mM); Clear solution

This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (12.5 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

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).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (299 KB)
SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Hassan HM, et al. Cardioprotective potential of azaleatin against sodium arsenite instigated sub-chronic cardiotoxicity via targeting TLR4/MyD88, JAK1/STAT3, and NF-κB in Sprague Dawley rats. J Trace Elem Med Biol. 2025;92:127763.

[2]. Tsai KC, et al. Pharmacophore-driven identification of human glutaminyl cyclase inhibitors from foods, plants and herbs unveils the bioactive property and potential of Azaleatin in the treatment of Alzheimer's disease. Food Funct. 2022;13(24):12632-12647. Published 2022 Dec 13.

[3]. Mustafa NF, Cheng KK, Nadri MH, Razali SA, Zakaria II, Salin NH, Amran SI. Discovery of azaleatin as a potential allosteric inhibitor for dengue NS2B-NS3 protease using in vitro and in silico studies. Journal of Biomolecular Structure and Dynamics. 2025 Sep 22;43(14):7759-70.

[4]. Kamel EM, et al. Deciphering molecular mechanisms underlying the inhibition of β-glucuronidase by xanthones from Centaurium spicatum. Bioorg Chem. 2024;150:107609.

[5]. Adachi SI, et al. Anti-hyperuricemic effect of isorhamnetin in cultured hepatocytes and model mice: structure-activity relationships of methylquercetins as inhibitors of uric acid production. Cytotechnology. 2019;71(1):181-192.

[6]. Ganbold M, et al. Antifibrotic effect of methylated quercetin derivatives on TGFβ-induced hepatic stellate cells. Biochem Biophys Rep. 2019;20:100678. Published 2019 Aug 16.

[7]. Dai L, He J, Miao X, Guo X, Shang X, Wang W, Li B, Wang Y, Pan H, Zhang J. Multiple biological activities of Rhododendron przewalskii Maxim. extracts and UPLC-ESI-Q-TOF/MS characterization of their phytochemical composition. Frontiers in Pharmacology. 2021 Feb 10;12:599778.

[8]. Ramos LC, Palacios J, Barrientos RE, Gómez J, Castagnini JM, Barba FJ, Tapia A, Paredes A, Cifuentes F, Simirgiotis MJ. UHPLC-MS phenolic fingerprinting, aorta endothelium relaxation effect, antioxidant, and enzyme inhibition activities of azara dentata ruiz & pav berries. Foods. 2023 Feb 2;12(3):643.

[9]. Boojar FM, Golmohamad S, Tafreshi G. Comparative study on the status of glycation precursors, advanced glycation end products, and cell viability under effects of kaempferol, myricetin, and azaleatin in HGC-27 cell line. Journal of Young Investigators. 2019 Jan 1;36(1).

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. 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	3.1620 mL	15.8098 mL	31.6196 mL	79.0489 mL
	5 mM	0.6324 mL	3.1620 mL	6.3239 mL	15.8098 mL
	10 mM	0.3162 mL	1.5810 mL	3.1620 mL	7.9049 mL
	15 mM	0.2108 mL	1.0540 mL	2.1080 mL	5.2699 mL
	20 mM	0.1581 mL	0.7905 mL	1.5810 mL	3.9524 mL
	25 mM	0.1265 mL	0.6324 mL	1.2648 mL	3.1620 mL
	30 mM	0.1054 mL	0.5270 mL	1.0540 mL	2.6350 mL
	40 mM	0.0790 mL	0.3952 mL	0.7905 mL	1.9762 mL
	50 mM	0.0632 mL	0.3162 mL	0.6324 mL	1.5810 mL
	60 mM	0.0527 mL	0.2635 mL	0.5270 mL	1.3175 mL
	80 mM	0.0395 mL	0.1976 mL	0.3952 mL	0.9881 mL
	100 mM	0.0316 mL	0.1581 mL	0.3162 mL	0.7905 mL

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Azaleatin

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All Dipeptidyl Peptidase Isoforms

All NF-κB Isoforms

All JAK Isoforms

All Toll-like Receptor (TLR) Isoforms

All STAT Isoforms

All Interleukin Related Isoforms

All COX Isoforms

All Bcl-2 Family Isoforms

All Caspase Isoforms

Biological Activity

Chemical Information

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

Azaleatin Related Classifications

HY-N7653 Related Classifications