Metabolic Enzyme/Protease Immunology/Inflammation Apoptosis Autophagy Membrane Transporter/Ion Channel Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR MAPK/ERK Pathway NF-κB Neuronal Signaling
Glycosidase Phosphatase Interleukin Related TNF Receptor COX Beclin1 GLUT FAK Akt mTOR p38 MAPK Keap1-Nrf2 Apoptosis Amyloid-β Tau Protein Autophagy
Pongamol

Cat. No.: HY-121811

Pongamol

(Synonyms: Lanceolatin C)

Customer Review

Based on 1 Customer Validation

Pongamol (Lanceolatin C) is an orally active flavonoid with an IC₅₀ of 75 μM and a K_i of 58 μM against PTPase-1B, and an IC₅₀ of 103.5 μM against intestinal α-Glycosidase. Pongamol reduces the release of IL‑1β, TNF‑α, COX‑2 and iNOS in cells, reverses the nuclear translocation of NF‑κB, and upregulates the levels of Beclin 1 and LC3 Ⅱ/LC3 Ⅰ. Pongamol promotes glucose uptake by increasing the level of GLUT4 on the surface of skeletal muscle cells. Pongamol inhibits epithelial-mesenchymal transition by suppressing the FAK/Akt-mTOR signaling pathway. Pongamol inhibits neuronal cytotoxicity, suppresses cell apoptosis and extends the lifespan of Caenorhabditis elegans by activating the MAPKs/Nrf2 signaling pathway. Pongamol exerts hypoglycemic effects in diabetic mouse models. Pongamol exhibits antibacterial activity. Pongamol alleviates oxidative stress, neuroinflammation, Aβ deposition and excessive phosphorylation of Tau Protein, and restores autophagy function in Alzheimer's disease mouse models by inhibiting the Akt/mTOR signaling pathway. Pongamol is applicable to research related to Alzheimer's disease, type 2 diabetes, non-small cell lung cancer and postprandial hyperglycemia.

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

Purity: 99.81%
CAS No.: 484-33-3
Formula: C₁₈H₁₄O₄
Molecular Weight:294.30

Storage:

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

Pongamol Chemical Structure

CAS No.: 484-33-3

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Fluorescent Dye

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

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

Biological Activity

Description

All Interleukin Related Isoforms :

All TNF Receptor Isoforms :

All COX Isoforms :

All GLUT Isoforms :

All Akt Isoforms :

All mTOR Isoforms :

All p38 MAPK Isoforms :

In Vitro

Pongamol (25-100 μM, pre-incubated for 1 h followed by LPS stimulation for 24 h) inhibits LPS (HY-D1056)-induced NO release in BV2 mouse microglia. It suppresses LPS-induced activation of the NF-κB pathway in cells by reducing IκB phosphorylation and blocking NF-κB nuclear translocation, and downregulates the expression of pro-inflammatory genes (IL-1β, TNF-α, iNOS, COX-2) in cells^[1].
Pongamol (100 μM, pretreated for 1 h followed by LPS stimulation for 24 h) reduces the levels of proinflammatory proteins (IL-6, IL-1β) and upregulates the expression of autophagy markers (Beclin 1, LC3 II/LC3 I) in LPS-stimulated mouse BV2 microglial cells, and these effects depend on the Akt pathway^[1].
Pongamol (0-10 μM; 0-16 h) increases both basal and insulin-superimposed glucose uptake in L6-GLUT4myc myotubes, elevates both basal and insulin-enhanced GLUT4 translocation to the cell surface by activating PI3-kinase activity, and potentiates Insulin (HY-P0035)-induced AKT (Ser-473) phosphorylation in myotubes^[2].
Pongamol (0-100 μM, 2 h) increases the survival rate of H₂O₂-induced PC12 cells, reduces LDH release, inhibits cell apoptosis, restores mitochondrial membrane potential, decreases the levels of pro-apoptotic proteins and increases the levels of anti-apoptotic proteins, suppresses the activation of the MAPKs signaling pathway (reduces the levels of p-ERK, p-JNK and p-p38), elevates GSH levels and reduces ROS levels, promotes Nrf2 nuclear translocation, upregulates the expression of downstream antioxidant genes and directly binds to Keap1, thereby activating the Nrf2/HO-1 signaling pathway^[3].
Pongamol (0-100 μM; 24-48 h) reduces the viability of H460 non-small cell lung cancer cells in a dose-dependent manner, and inhibits cell proliferation, anchorage-independent growth, migration and invasion^[4].
Pongamol (25-100 μM; 24 h) upregulates the epithelial marker E-cadherin, downregulates the mesenchymal markers N-cadherin, vimentin, Slug and Snail, inhibits the activation of the FAK/Akt-mTOR signaling pathway, and reduces the levels of phosphorylated FAK, Akt and mTOR in H460 non-small cell lung cancer cells^[4].
Pongamol (Compound 1) potently inhibits recombinant protein tyrosine phosphatase-1B (PTPase-1B) in cell-free assays, with an IC₅₀ of 75 μM and a K_i of 58 μM^[5].
Pongamol (Compound 6) potently inhibits rat intestinal α-glucosidase with an IC₅₀ of 103.5 μM^[6].
Pongamol is active against E. coli and S. aureus (MICs = 8 and 6 µg/mL, respectively)^[7].

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

Western Blot Analysis^[1]

Cell Line:

LPS-stimulated BV2 mouse microglia
Concentration:

25, 50, 100 μM
Incubation Time:

1 h pre-incubation, followed by 24 h LPS stimulation
Result:

Dose-dependently decreased the p-IκB/IκB ratio in cytoplasmic fractions and significantly inhibited the nuclear translocation of p-NF-κB/NF-κB relative to the LPS-only model group.

Real Time qPCR^[1]

Cell Line:

LPS-stimulated BV2 mouse microglia
Concentration:

25, 50, 100 μM
Incubation Time:

1 h pre-incubation, followed by 4 h LPS stimulation
Result:

Dose-dependently reduced the mRNA expression levels of IL-1β, TNF-α, iNOS, and COX-2 relative to the LPS-only model group.

Western Blot Analysis^[1]

Cell Line:

LPS-stimulated BV2 mouse microglia
Concentration:

100 μM
Incubation Time:

1 h pre-incubation, followed by 24 h LPS stimulation
Result:

Significantly decreased IL-6 and IL-1β protein expression, and increased Beclin 1 and LC3 II/LC3 I protein levels relative to the LPS-only model group; these effects were reversed by co-treatment with wortmannin.

Western Blot Analysis^[2]

Cell Line:

Differentiated L6-GLUT4myc skeletal muscle myotubes
Concentration:

10 μM
Incubation Time:

16 h
Result:

Significantly potentiated insulin-stimulated AKT (Ser-473) phosphorylation to 7.8-fold of control basal.

Cell Viability Assay^[3]

Cell Line:

Highly differentiated PC12 cells
Concentration:

5-100 μM (5-80 μM for H₂O₂ co-treatment; 5, 10, 20, 40, 60, 80, and
100 μM pongamol)
Incubation Time:

2 h pretreatment, followed by 24 h H₂O₂ co-treatment; duration of assay (for pongamol alone testing)
Result:

Exhibited no significant effect on PC12 cell survival when used alone.
Increased cell survival in a concentration-dependent manner, with survival rates increased by 17.16%, 29.63%, and 44.29% at 20, 40, and 80 μM, respectively, when used to pretreat cells before H₂O₂ exposure.

Cell Cytotoxicity Assay^[3]

Cell Line:

Highly differentiated PC12 cells
Concentration:

20, 40, and 80 μM
Incubation Time:

2 h pretreatment, followed by 24 h H₂O₂ co-treatment
Result:

Significantly reduced LDH release in a dose-dependent manner, with reductions of 33.16%, 50.59%, and 109.84% at 20, 40, and 80 μM, respectively, compared to H₂O₂-only treated cells.

Apoptosis Analysis^[3]

Cell Line:

Highly differentiated PC12 cells
Concentration:

20, 40, and 80 μM
Incubation Time:

2 h pretreatment, followed by 24 h H₂O₂ co-treatment
Result:

Reduced the proportion of early and late apoptotic cells in a concentration-dependent manner; at 80 μM, the total apoptotic rate was reduced to 7.04%, compared to 39.57% in H₂O₂-only treated cells.

Western Blot Analysis^[3]

Cell Line:

Highly differentiated PC12 cells
Concentration:

20, 40, and 80 μM
Incubation Time:

2 h pretreatment, followed by 24 h H₂O₂ co-treatment
Result:

Prevented the H₂O₂-induced increase in pro-apoptotic proteins Bax, Cyto C, Cleaved Caspase-3, and Cleaved PARP1, and prevented the H₂O₂-induced decrease in anti-apoptotic protein Bcl-2, resulting in a reduced Bax/Bcl-2 ratio.

Western Blot Analysis^[3]

Cell Line:

Highly differentiated PC12 cells
Concentration:

80 μM
Incubation Time:

2 h pretreatment, followed by 1, 2, or 4 h H₂O₂ co-treatment; 2 h pretreatment, after MAPKs inhibitor pretreatment, followed by 24 h H₂O₂ co-treatment
Result:

Reduced the H₂O₂-induced phosphorylation of ERK, JNK, and p38.
Inhibitors of MAPKs pathways attenuated the effect of pongamol on reducing the Bax/Bcl-2 ratio in H₂O₂-treated cells.

Cell Viability Assay^[4]

Cell Line:

H460 non-small cell lung cancer cells
Concentration:

0, 10, 25, 50, 100 μM
Incubation Time:

24 h
Result:

Reduced cell viability in a dose-dependent manner.

Cell Proliferation Assay^[4]

Cell Line:

H460 non-small cell lung cancer cells
Concentration:

25, 50, 100 μM
Incubation Time:

24 h, 48 h
Result:

Significantly suppressed cell proliferation at 48 h compared to control.
Significantly reduced proliferation at 50 and 100 μM compared to control.

Cell Migration Assay ^[4]

Cell Line:

H460 non-small cell lung cancer cells
Concentration:

25, 50, 100 μM
Incubation Time:

24 h (pretreatment); 24 h, 48 h (migration measurement)
Result:

Significantly inhibited cell migration at 48 h post-wounding at 100 μM compared to control.

Cell Invasion Assay^[4]

Cell Line:

H460 non-small cell lung cancer cells
Concentration:

25, 50, 100 μM
Incubation Time:

24 h (pretreatment); 48 h (post-seeding incubation)
Result:

Significantly inhibited cell invasion at 50 and 100 μM compared to control.

Western Blot Analysis^[4]

Cell Line:

H460 non-small cell lung cancer cells
Concentration:

25, 50, 100 μM
Incubation Time:

24 h
Result:

Increased E-cadherin (epithelial marker) protein levels in a dose-dependent manner, with significant increases at 50 and 100 μM compared to control.
Decreased mesenchymal marker protein levels in a dose-dependent manner: significant decreases in N-cadherin, vimentin, Slug, and Snail were observed at 100 μM compared to control; significant decreases in Slug were also observed at 50 μM compared to control.\nReduced the levels of phosphorylated (activated) FAK, Akt, and mTOR, with no significant effect on total FAK, Akt, or mTOR levels.
Showed significant decreases in p-FAK/FAK, p-Akt/Akt, and p-mTOR/mTOR ratios at 100 μM compared to control; significant decreases in p-Akt/Akt and p-mTOR/mTOR ratios were also observed at 50 μM compared to control.

In Vivo

Pongamol (10-20 mg/kg; i.g.; daily; 4 weeks) improves spatial learning and memory abilities in mice with Alzheimer's disease induced by D-gal/NaNO₂/AlCl₃ via inhibiting the Akt/mTOR signaling pathway, alleviates oxidative stress, neuroinflammation, Aβ deposition and excessive phosphorylation of Tau protein, and restores autophagic function^[1].
Pongamol (15-60 μM; in NGM medium; administered from the L1 stage to the adult/L4 stage for 1-5 days) increases the head thrashing activity of the BR5270 Caenorhabditis elegans Alzheimer's disease model expressing human Tau protein, suggesting improved neuronal function. It enhances autophagic activity in the DA2123 Caenorhabditis elegans autophagy reporter model, and reduces lipofuscin deposition levels and Aβ mRNA expression in Caenorhabditis elegans Alzheimer's disease models expressing human Aβ/Tau^[1].
Pongamol (50-100 mg/kg; i.g.; single administration) exerts significant dose-dependent hypoglycemic effects in streptozotocin (HY-13753)-induced diabetic rats^[5].
Pongamol (100 mg/kg; i.g.; daily; for 10 consecutive days) exerts a significant and sustained hypoglycemic effect in type 2 diabetic db/db mice^[5].

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

Animal Model:

C57BL/6 (male)^[1]
Dosage:

10 mg/kg; 20 mg/kg
Administration:

i.g.; daily; 4 weeks
Result:

Significantly reduced escape latency.
Increased platform crossing frequency.
Increased time/distance spent in the target quadrant in the Morris water maze test.
Decreased hippocampal acetylcholinesterase (AChE) and malondialdehyde (MDA) levels.
Increased serum superoxide dismutase (SOD) and catalase (CAT) levels.
Alleviated neuronal disorganization and loss in the hippocampus and cortex.
Reduced Nissl body loss.
Increased tyrosine hydroxylase (TH)-positive cell counts in the hypothalamus.
Reduced neuronal nuclei (NeuN) expression in the cortex and hippocampus.
Reduced glial fibrillary acidic protein (GFAP) and β-amyloid (Aβ) positive cell counts in the cortex and hippocampus.
Inhibited Tau hyperphosphorylation in hippocampal tissue.
Downregulated mRNA expression of IL-1β, TNF-α, iNOS, and COX-2 in the hippocampus.
Increased hippocampal Beclin 1 expression.
Increased the LC3 II/LC3 I ratio.
Reduced p62 mRNA expression.
Increased Atg13 mRNA expression.
Decreased phosphorylated Akt (p-Akt) and phosphorylated mTOR (p-mTOR) protein levels in the hippocampus.

Animal Model:

BR5270 (human Tau-expressing AD model); DA2123 (GFP-labeled LGG-1/LC3 autophagy reporter); UM0001 (human Aβ1-42/Tau-expressing)^[1]
Dosage:

15 μM; 30 μM; 60 μM
Administration:

in NGM medium; from L1 stage through adulthood; 1-5 day treatment at L4 stage
Result:

Significantly increased the number of head wiggles in BR5270 C.
elegans in a dose-dependent manner.
Significantly increased the number of LGG-1:GFP puncta in DA2123 C.
elegans in a dose-dependent manner, indicating enhanced autophagic activity.
Reduced lipofuscin deposition in UM0001 worms in a concentration-dependent manner, with the 60 μM dose producing the greatest reduction in fluorescence intensity per unit area relative to untreated worms.
Reduced Aβ mRNA expression in UM0001 worms in a concentration-dependent manner, with the 60 μM dose producing the lowest Aβ transcript levels.

Animal Model:

UM0001 (human Aβ_1-42/Tau-expressing)^[3]
Dosage:

15 μM; 30 μM
Administration:

NGM plate supplementation
Result:

Increased mRNA expression of Skn-1 and its downstream antioxidant genes Sod-1, Gcs-1, and Gst-4 in UM0001 worms in a concentration-dependent manner.

Animal Model:

Sprague Dawley (male, 7-8 weeks old, 160 g, streptozotocin-induced diabetic)^[5]
Dosage:

50 mg/kg; 100 mg/kg
Administration:

i.g.; single dose
Result:

Reduced blood glucose by 12.8% at 6 hours post-administration.
Reduced blood glucose by 22.0% at 6 hours post-administration.

Animal Model:

db/db (12-18 weeks old, 40 g, genetically diabetic)^[5]
Dosage:

100 mg/kg
Administration:

i.g.; daily; 10 consecutive days
Result:

Reduced blood glucose by 35.7% overall, with significant reductions observed on days 13-15 and days 17-19 .
Improved glucose tolerance by 18.61% compared to controls, with significantly lowered postprandial blood glucose levels at 30, 60, 90, and 120 minutes post-load.

Chemical Information

CAS No. 484-33-3
Appearance Solid
Molecular Weight 294.30
Formula C₁₈H₁₄O₄
Color Off-white to light yellow
SMILES

O=C(CC(C1=CC=CC=C1)=O)C2=CC=C3OC=CC3=C2OC
Synonyms

Lanceolatin C
Structure Classification
- Ketones, Aldehydes, Acids
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 (169.89 mM; ultrasonic and warming and heat to 60°C; 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

3.3979 mL

16.9895 mL

33.9789 mL

5 mM

0.6796 mL

3.3979 mL

6.7958 mL

10 mM

0.3398 mL

1.6989 mL

3.3979 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)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

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

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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 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (8.49 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.

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
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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 + +
%
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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 (302 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]. Hu K, et al. Pongamol Alleviates Neuroinflammation and Promotes Autophagy in Alzheimer's Disease by Regulating the Akt/mTOR Signaling Pathway. J Agric Food Chem. Published online June 6, 2024. [Content Brief]

[2]. Tamrakar AK, et al. Pongamol from Pongamia pinnata stimulates glucose uptake by increasing surface GLUT4 level in skeletal muscle cells. Mol Cell Endocrinol. 2011;339(1-2):98-104. [Content Brief]

[3]. Wu S, et al. Pongamol Prevents Neurotoxicity via the Activation of MAPKs/Nrf2 Signaling Pathway in H₂O₂-Induced Neuronal PC12 Cells and Prolongs the Lifespan of Caenorhabditis elegans. Mol Neurobiol. 2024;61(10):8219-8233. [Content Brief]

[4]. Putri HE, et al. Pongamol Inhibits Epithelial to Mesenchymal Transition Through Suppression of FAK/Akt-mTOR Signaling. Anticancer Res. 2021;41(12):6147-6154. [Content Brief]

[5]. Tamrakar AK, et al. Identification of pongamol and karanjin as lead compounds with antihyperglycemic activity from Pongamia pinnata fruits. J Ethnopharmacol. 2008;118(3):435-439. [Content Brief]

[6]. Ranga Rao R, et al. New furanoflavanoids, intestinal alpha-glucosidase inhibitory and free-radical (DPPH) scavenging, activity from antihyperglycemic root extract of Derris indica (Lam.). Bioorg Med Chem. 2009;17(14):5170-5175. [Content Brief]

[7]. Jahan S, et al. Health promoting benefits of pongamol: An overview. Biomed Pharmacother. 2021 Oct;142:112109. [Content Brief]

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	3.3979 mL	16.9895 mL	33.9789 mL	84.9473 mL
	5 mM	0.6796 mL	3.3979 mL	6.7958 mL	16.9895 mL
	10 mM	0.3398 mL	1.6989 mL	3.3979 mL	8.4947 mL
	15 mM	0.2265 mL	1.1326 mL	2.2653 mL	5.6632 mL
	20 mM	0.1699 mL	0.8495 mL	1.6989 mL	4.2474 mL
	25 mM	0.1359 mL	0.6796 mL	1.3592 mL	3.3979 mL
	30 mM	0.1133 mL	0.5663 mL	1.1326 mL	2.8316 mL
	40 mM	0.0849 mL	0.4247 mL	0.8495 mL	2.1237 mL
	50 mM	0.0680 mL	0.3398 mL	0.6796 mL	1.6989 mL
	60 mM	0.0566 mL	0.2832 mL	0.5663 mL	1.4158 mL
	80 mM	0.0425 mL	0.2124 mL	0.4247 mL	1.0618 mL
	100 mM	0.0340 mL	0.1699 mL	0.3398 mL	0.8495 mL

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Pongamol

Apoptosis Compound Library

Immunology/Inflammation Compound Library

Kinase Inhibitor Library

MAPK Compound Library

Membrane Transporter/Ion Channel Compound Library

Metabolism/Protease Compound Library

Neuronal Signaling Compound Library

NF-κB Signaling Compound Library

PI3K/Akt/mTOR Compound Library

Protein Tyrosine Kinase Compound Library

Stem Cell Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Antioxidant Compound Library

Differentiation Inducing Compound Library

Reprogramming Compound Library

Anti-diabetic Compound Library

Lipid Compound Library

Oxygen Sensing Compound Library

Antibacterial Compound Library

Ferroptosis Compound Library

Glycolysis Compound Library

Pyroptosis Compound Library

Cytoskeleton Compound Library

Orally Active Compound Library

Glutamine Metabolism Compound Library

Anti-Alzheimer's Disease Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Phosphatase Inhibitor Library

Anti-Cancer Metabolism Compound Library

Anti-Parkinson's Disease Compound Library

Neurodegenerative Disease-related Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Transcription Factor-Targeted Library

Glucose Metabolism Compound Library

Anti-Liver Cancer Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Cancer Natural Product Library

Antidepressant Compound Library

Plant-Sourced Natural Product Library

Human Metabolite Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Osteogenesis 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

Serine/Threonine Kinase Inhibitor Library

Extracellular Vesicles (EVs) Compound Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Radioprotector Library

Mitophagy Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Natural Product Library Plus

Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

Anti-Gastric Cancer Compound Library

Anti-Fibrosis Compound Library

Anti-Brain Cancer Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

RO5 Drug-like Natural Product Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library