Cat. No.: HY-N2392

Kukoamine A

1 Cited Publications

Customer Review

Based on 1 publication(s) in Google Scholar

Kukoamine A, a spermine alkaloid, is an orally active and brain-penetrant component found in the root barks of Lycium chinense (L. chinense) Miller. Kukoamine A inhibits purified Crithidia fasciculata trypanothione reductase and soybean lipoxygenase, activates μ-opioid receptor. Kukoamine A can inhibt cancer cell proliferation, migration and invasion, cause G0/G1 phase cell cycle arrest and induce apoptosis. Kukoamine A exerts neuroprotective effect and can induce autophagy . Kukoamine A inhibits LPS (HY-D1056)-induced NO, ROS, PGE₂, TNF-α, IL-1β, IL-6 production and COX-2 activity. Kukoamine A reverses palmitic acid-induced insulin resistance, lipid accumulation, and oxidative stress via downregulation of Srebp-1c. Kukoamine A can be used for the research of cancer, infection, inflammation, metabolic and neurological disease, such as glioblastoma and Parkinson's disease.

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

Purity: 99.88%
CAS No.: 75288-96-9
Formula: C₂₈H₄₂N₄O₆
Molecular Weight:530.66

Storage:

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

Kukoamine A Chemical Structure

CAS No.: 75288-96-9

Size

Price

Stock

Quantity

Amount: USD 0.00

* Please select Quantity before adding items.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (1)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]

μ Opioid Receptor/MOR

IL-1β

IL-6

COX-2

All Parasite Isoforms :

All Lipoxygenase Isoforms :

All Opioid Receptor Isoforms :

All Interleukin Related Isoforms :

All TNF Receptor Isoforms :

All COX Isoforms :

In Vitro

Kukoamine A (1-10 μM; ~0.5-2.0 times its estimated K_i) potently inhibits purified Crithidia fasciculata trypanothione reductase as a mixed inhibitor with a K_i of 1.8 μM and K_ii of 13 μM for enzyme-substrate complex, while displaying no significant inhibition of human glutathione reductase^[1].
Kukoamine A (0.1 mM; 20-60 min) shows high DPPH free radical scavenging activity, with 96% reducing activity at 0.1 mM after 20 min and 60 min incubation in a cell-free system^[2].
Kukoamine A potently inhibits cell-free soybean lipoxygenase, with an IC₅₀ of 9.5 μM^[2].
Kukoamine A (0.1 mM) inhibits AAPH-induced linoleic acid lipid peroxidation by 72% at 0.1 mM^[2].
Kukoamine A reverses palmitic acid-induced insulin resistance, lipid accumulation, and oxidative stress in AML-12 cells via downregulation of Srebp-1c, as these protective effects are abrogated by Srebp-1c overexpression^[3].
Kukoamine A (10-80 μg/mL; 1-5 days) selectively inhibits the viability of human glioblastoma U251 and WJ1 cells in a time- and dose-dependent manner, with IC₅₀ values of 73.4 μg/mL and 22.1 μg/mL respectively at day 5, and has minimal effect on human normal liver LO2 cells and rat glioma C6 cells^[4].
Kukoamine A (5-20 μg/mL; 12 days) inhibits the clonogenicity of human glioblastoma U251 and WJ1 cells in a dose-dependent manner^[4].
Kukoamine A (10-80 μg/mL; 48 h) induces apoptosis in human glioblastoma U251 and WJ1 cells in a dose-dependent manner, downregulating 5-LOX and antiapoptotic Bcl-2 protein expression, and upregulating proapoptotic Bax and active caspase-3 protein expression^[4].
Kukoamine A (5-20 μg/ml; 48 h) induces G0/G1 phase cell cycle arrest in human glioblastoma U251 and WJ1 cells in a dose-dependent manner^[4].
Kukoamine A (10-80 μg/mL；24 h) inhibits the migration and invasion of human glioblastoma U251 and WJ1 cells in a dose-dependent manner^[4].
Kukoamine A (10-40 μM; 4 h pre-incubation, followed by 24 h co-incubation with MPP⁺) dose-dependently protects SH-SY5Y cells from MPP⁺-induced injury, inhibits apoptosis and preserves mitochondrial membrane potential^[5].
Kukoamine A (10-40 μM; 4 h pre-incubation, followed by 24 h co-incubation with MPP⁺) dose-dependently reduces Bax/Bcl-2 ratio, p-JNK and p-p38 levles and increases p-AKT, p-ERK levels in SH-SY5Y cells^[5].
Kukoamine A (10-40 μM; 4 h) dose-dependently induces autophagy in SH-SY5Y cells, inducing visible autophagosomes at the highest concentration, increasing the LC3-II/LC3-I ratio, Beclin-1 and decreasing p62 ^[5].
Kukoamine A binds to human μ-opioid receptors expressed in HEK293T cell membranes with high affinity, with a K_i value of 1.3 ± 0.18 μM and an EC₅₀ value of 5.6 ± 0.65 μM^[6].
Kukoamine A (5-40 μM; 24 h) does not reduce the viability of RAW 264.7 macrophage cells^[7].
Kukoamine A (5-40 μM; 24 h) significantly inhibits LPS (HY-D1056)-induced NO, ROS, PGE₂, TNF-α, IL-1β, and IL-6 production in RAW 264.7 macrophage cells in a concentration-dependent manner^[7].
Kukoamine A (5-40 μM) significantly inhibits LPS-induced COX-2 activity in RAW 264.7 macrophage cells^[7].

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

Apoptosis Analysis^[4]

Cell Line:

human glioblastoma U251 cells, human glioblastoma WJ1 cells
Concentration:

40, 60, 80 μg/ml (U251 cells); 10, 20, 30 μg/ml (WJ1 cells)
Incubation Time:

48 h
Result:

Induced a significant, dose-dependent increase in both early and late apoptotic cells, as well as total apoptotic cells, in both U251 and WJ1 cells compared to untreated controls.

Cell Cycle Analysis^[4]

Cell Line:

human glioblastoma U251 cells, human glioblastoma WJ1 cells
Concentration:

5, 10, 20 μg/ml
Incubation Time:

48 h
Result:

Caused a significant, dose-dependent increase in the cell population in the G0/G1 phase in both U251 and WJ1 cells compared to untreated controls.
Caused a corresponding significant, dose-dependent decrease in the cell population in the S phase in both U251 and WJ1 cells compared to untreated controls.

Western Blot Analysis^[4]

Cell Line:

human glioblastoma U251 cells, human glioblastoma WJ1 cells
Concentration:

40, 60, 80 μg/ml (U251 cells); 10, 20, 30 μg/ml (WJ1 cells)
Incubation Time:

48 h
Result:

Caused a dose-dependent decrease in 5-LOX and Bcl-2 protein expression in U251 and WJ1 cells.
Caused a dose-dependent increase in Bax and active caspase-3 protein expression in U251 and WJ1 cells.
Caused a dose-dependent decrease in C/EBPβ, N-cadherin, vimentin, twist, and snail+slug protein expression in U251 and WJ1 cells.
Caused a dose-dependent increase in E-cadherin protein expression in U251 and WJ1 cells.

Western Blot Analysis^[5]

Cell Line:

MPP⁺-treated SH-SY5Y human neuroblastoma cells
Concentration:

10 μM, 20 μM, 40 μM
Incubation Time:

4 h pre-incubation, followed by 24 h co-incubation with MPP⁺
Result:

Decreased the Bax/Bcl-2 ratio to 3.77 ± 0.36, 2.22 ± 0.17, and 0.68 ± 0.31 at 10, 20, and 40 μM, respectively.
Increased p-AKT levels to 2.05 ± 0.07.
Increased p-ERK levels to 3.31 ± 0.14.
Decreased p-JNK levels to 0.57 ± 0.02.
Decreased p-p38 levels to 0.21 ± 0.06 compared to MPP⁺-treated cells.

ELISA Assay^[7]

Cell Line:

LPS-stimulated RAW 264.7 macrophage cells
Concentration:

5, 10, 20, 40 μM
Incubation Time:

12 h (pretreatment); 12 h (LPS stimulation)
Result:

Significantly attenuated LPS-induced increases in TNF-α, IL-1β, and IL-6 levels in a concentration-dependent manner, with all tested concentrations showing statistically significant inhibition relative to LPS-only treated cells.
Significantly reduced LPS-induced PGE2 levels, with all tested concentrations showing statistically significant inhibition relative to LPS-only treated cells.
Markedly inhibited LPS-induced COX-2 activity.

In Vivo

Kukoamine A (0.01 mmol/kg; i.p.; single dose) inhibits Carrageenan (HY-125474)-induced rat paw edema by 43%^[2].
Kukoamine A (5-20 mg/kg; i.p.; daily; 4 weeks) dose-dependently attenuates high fat diet-induced insulin resistance, fatty liver, inflammation, and oxidative stress in mice by inhibiting Srebp-1c and its downstream target gene expression^[3].
Kukoamine A (10-40 mg/kg; i.p.; 5 times weekly; 4 weeks) inhibits in vivo glioblastoma growth in a dose-dependent manner, achieving up to 55.3% tumor inhibition at 40 mg/kg, while maintaining mouse body weight, via apoptosis induction and epithelial-mesenchymal transition attenuation mediated by downregulating 5-LOX and C/EBPβ expression^[4].
Kukoamine A (5-20 mg/kg; i.g.; daily; 12 days) exerts dose-dependent neuroprotective effects in MPTP (HY-W114750)-induced Parkinson's disease mice by improving motor function, reducing neuronal apoptosis, lowering α-synuclein levels, preserving dopaminergic neurons, and enhancing autophagy, without affecting MAO-B activity^[5].
Kukoamine A (5-20 mg/kg; i.g.; daily; 12 days) enhances autophagy in the SN and Str of healthy mice by regulating autophagy-related proteins, without inducing apoptosis or altering MAO-B activity^[5].
Kukoamine A (25-50 mg/kg; p.o.; daily; 5 days) exerts Concentration-dependent anti-inflammatory and antioxidant effects in rats with carrageenan-induced acute inflammation, reducing paw edema, proinflammatory cytokine levels, and oxidative stress markers while enhancing liver antioxidant enzyme activity^[7].

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

Animal Model:

Carrageenan-induced edema Fischer-344 rats (male and female, 150-200 g, non-pregnant females; 6-15 animals per group)^[2]
Dosage:

0.01 mmol/kg
Administration:

I.p.; single dose
Result:

Inhibited carrageenan-induced rat paw edema by 43%.

Animal Model:

C57 (6-8 weeks old; high fat diet-induced model)^[3]
Dosage:

5 mg/kg; 10 mg/kg; 20 mg/kg
Administration:

I.p.; daily; 4 weeks
Result:

Dose-dependently inhibited HFD-induced increases in fasting blood glucose and insulin levels, and dose-dependently reduced glucose levels in response to glucose and insulin loads during IPGTT and IPITT.
Dose-dependently decreased HFD-induced liver histological injury, hepatic triglyceride levels, and serum AST and ALT activities.
Dose-dependently inhibited HFD-induced increases in serum TNFα, IL-1β, IL-6, and C reactive protein levels.
Dose-dependently reversed HFD-induced reductions in hepatic MnSOD and CuZnSOD activities, and dose-dependently inhibited HFD-induced increases in hepatic MDA and H2O2 levels.
Dose-dependently inhibited HFD-induced upregulation of hepatic Srebp-1c protein and mRNA expression, as well as hepatic mRNA expression of the Srebp-1c target genes FAS and ACC1.

Animal Model:

BALB/C-nu/nu nude mice (5-week-old, male, intraperitoneal inoculation of human GBM WJ1 cells)^[4]
Dosage:

10 mg/kg; 20 mg/kg; 40 mg/kg
Administration:

I.p.; 5 times weekly; 4 weeks
Result:

Reduced mean tumor weight.
Achieved tumor inhibitory rates of 35.2%, 48.8%, and 55.3% at 10, 20, and 40 mg/kg doses, respectively.
Showed no difference in body weight increase compared to control mice.
Significantly decreased 5-LOX, Bcl-2, C/EBPβ, N-cadherin, vimentin, twist, and snail+slug protein expression in tumor tissues in a dose-dependent manner.
Significantly increased Bax, active caspase-3, and E-cadherin protein expression in tumor tissues in a dose-dependent manner.

Animal Model:

C57BL/6 (male, 7~8 weeks old, 20~22 g, MPTP-induced modeling)^[5]
Dosage:

5 mg/kg; 20 mg/kg
Administration:

I.g.; daily; 12 days
Result:

Increased the time mice stayed on the rota-rod, reduced the time to climb down the pole, and increased traction test scores at all tested time points compared to MPTP-only mice.
Increased the level of Nissl substance in the substantia nigra (SN), reversed the MPTP-induced increase in Bax and cytochrome c expression, reversed the decrease in Bcl-2 expression, and reduced caspase-3 activity in both SN and striatum (Str) in a dose-dependent manner.
Decreased MPTP-induced α-synuclein elevation in SN and Str, attenuated MPTP-induced loss of tyrosine hydroxylase (TH)-positive cells in SN and Str, and attenuated MPTP-induced reduction in TH protein levels in SN and Str.
Upregulated the LC3-II/LC3-I ratio and Beclin-1 expression, and downregulated p62 expression in both SN and Str.\nDid not alter MAO-B activity in the brain.

Animal Model:

Carrageenan-induced Wistar rats (male, 180-220 g)^[7]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

P.o.; daily; 5 days
Result:

Significantly reduced carrageenan-induced paw edema volume in a concentration-dependent manner over the 4-hour observation period.
Significantly reduced serum levels of proinflammatory cytokines TNF-α, IL-1β, and IL-6.
Significantly increased liver activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px).
Significantly reduced liver malondialdehyde (MDA) levels.\nAll results were statistically significant.

Chemical Information

CAS No. 75288-96-9
Appearance Solid
Molecular Weight 530.66
Formula C₂₈H₄₂N₄O₆
Color White to off-white
SMILES

O=C(NCCCNCCCCNCCCNC(CCC1=CC=C(O)C(O)=C1)=O)CCC2=CC=C(O)C(O)=C2
Structure Classification
- Alkaloids
- Other Alkaloids
- Phenols
- Polyphenols
Initial Source
- Plants
- other families
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Publications (1)

All

Sort by:

Journal Impact Factor

Biomed Res Int

Kukoamine A Improves Mycoplasma pneumoniae Pneumonia by Regulating miR-222-3p/Superoxide Dismutase 2. [Abstract]

2022 Jun 21:2022:2064013. PMID: 35774277

Solvent & Solubility

In Vitro:

H₂O : 125 mg/mL (235.56 mM; Need ultrasonic)

DMSO : 100 mg/mL (188.44 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

1.8844 mL

9.4222 mL

18.8445 mL

5 mM

0.3769 mL

1.8844 mL

3.7689 mL

10 mM

0.1884 mL

0.9422 mL

1.8844 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.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

Molarity Calculator

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

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

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: ≥ 2.5 mg/mL (4.71 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.

Protocol 2

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

Solubility: ≥ 2.5 mg/mL (4.71 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.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (4.71 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

Working Solution

For the following dissolution methods, please prepare the working solution directly:

It is recommended to prepare fresh solutions and use them promptly within a short period of time.

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: PBS

Solubility: 100 mg/mL (188.44 mM); Clear solution; Need ultrasonic

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.

Working solution concentration: 0.22 mg/mL

This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.

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) .

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (291 KB)
SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 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]. Ponasik JA, et al. Kukoamine A and other hydrophobic acylpolyamines: potent and selective inhibitors of Crithidia fasciculata trypanothione reductase. Biochem J. 1995 Oct 15;311 ( Pt 2)(Pt 2):371-5. [Content Brief]

[2]. Hadjipavlou-Litina D, et al. Kukoamine A analogs with lipoxygenase inhibitory activity. J Enzyme Inhib Med Chem. 2009;24(5):1188-1193. [Content Brief]

[3]. Li G, et al. Kukoamine A attenuates insulin resistance and fatty liver through downregulation of Srebp-1c. Biomed Pharmacother. 2017;89:536-543. [Content Brief]

[4]. Wang Q, et al. Kukoamine A inhibits human glioblastoma cell growth and migration through apoptosis induction and epithelial-mesenchymal transition attenuation. Sci Rep. 2016;6:36543. Published 2016 Nov 8. [Content Brief]

[5]. Hu X, et al. Neuroprotective effects of Kukoamine A on neurotoxin-induced Parkinson's model through apoptosis inhibition and autophagy enhancement. Neuropharmacology. 2017;117:352-363. [Content Brief]

[6]. Saller J, et al. Identification and quantification of kukoamine A and kukoamine B as novel μ-opioid receptor agonists in potato and other solanaceous plants. Food Chem. 2023;427:136637. [Content Brief]

[7]. Wang L, et al. Anti-inflammatory activities of kukoamine A from the root bark of Lycium chinense miller[J]. Natural Product Communications, 2020, 15(3): 1934578X20912088.

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 / H₂O	1 mM	1.8844 mL	9.4222 mL	18.8445 mL	47.1111 mL
	5 mM	0.3769 mL	1.8844 mL	3.7689 mL	9.4222 mL
	10 mM	0.1884 mL	0.9422 mL	1.8844 mL	4.7111 mL
	15 mM	0.1256 mL	0.6281 mL	1.2563 mL	3.1407 mL
	20 mM	0.0942 mL	0.4711 mL	0.9422 mL	2.3556 mL
	25 mM	0.0754 mL	0.3769 mL	0.7538 mL	1.8844 mL
	30 mM	0.0628 mL	0.3141 mL	0.6281 mL	1.5704 mL
	40 mM	0.0471 mL	0.2356 mL	0.4711 mL	1.1778 mL
	50 mM	0.0377 mL	0.1884 mL	0.3769 mL	0.9422 mL
	60 mM	0.0314 mL	0.1570 mL	0.3141 mL	0.7852 mL
	80 mM	0.0236 mL	0.1178 mL	0.2356 mL	0.5889 mL
	100 mM	0.0188 mL	0.0942 mL	0.1884 mL	0.4711 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent:

Product Name:
CAS No.:
Species:
Purity:
Quantity:

Kukoamine A

Anti-Infection Compound Library

Apoptosis Compound Library

GPCR/G Protein Compound Library

Immunology/Inflammation Compound Library

Metabolism/Protease Compound Library

Neuronal Signaling Compound Library

NF-κB Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

CNS-Penetrant Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Differentiation Inducing Compound Library

Oxygen Sensing Compound Library

Ferroptosis Compound Library

Medicine Food Homology Compound Library

Phenols Library

Pyroptosis Compound Library

Orally Active Compound Library

Neurotransmitter Receptor Compound Library

Traditional Chinese Medicine Active Compound Library

Neuroprotective Compound Library

Alkaloids Library

Anti-Pancreatic Cancer Compound Library

Antiparasitic Compound library

Anti-Cancer Metabolism Compound Library

Anti-Parkinson's Disease Compound Library

Neurodegenerative Disease-related Compound Library

Angiogenesis-Related Compound Library

Lipid Metabolism Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Cancer Natural Product Library

Antidepressant Compound Library

Anti-inflammatory Traditional Chinese Medicine Active Compound Library

Plant-Sourced Natural Product Library

Human Metabolite Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Cancer Stem Cells Compound Library

Pain-Related Compound Library

Mitochondrial Protection Compound Library

Metabolic Enzyme Compound Library

Membrane Protein-targeted Compound Library

Membrane Receptor-targeted Compound Library

Autoimmune Disease Compound Library

Cytokine Inhibitors Library

Cell Death Library

Anti-Drug-Resistant Compound Library

Multi-Target Compound Library

Radioprotector Library

Bioactive Compound Library Max

Natural Product Library Plus

Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

Anti-Fibrosis Compound Library

Miao Ethnicity Medicine Compound Library

Tibetan Medicine Compound Library

Heat-Clearing and Detoxification Traditional Chinese Medicine Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

High-Throughput Bioactive Compound Library

High-Throughput Natural Product Library

Ancient Chinese Classical Formulas Traditional Chinese Medicine Active Compound Library

Anti-Rheumatic Arthritis Compound Library

Mass Spectrometry Human Metabolite Library

Diarrhea-Related Traditional Chinese Medicine Active Compound Library

Mongolian Medicine Compound Library

Natural Product Diversity Scaffold Library

Tonifying Traditional Chinese Medicine Monomer Compound Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

Publications Citing Use of MedChemExpress (MCE) Kukoamine A

All Parasite Isoforms

All Lipoxygenase Isoforms

All Opioid Receptor Isoforms

All Interleukin Related Isoforms

All TNF Receptor Isoforms

All COX Isoforms

Biological Activity

Chemical Information