Cat. No.: HY-119487

MMPP

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MMPP is an orally active inhibitor of STAT3 and VEGFR2, as well as an activator of PPARγ. MMPP blocks the VEGFR2/AKT/ERK/NF-κB signaling pathway to inhibit angiogenesis. MMPP inhibits ferroptosis and inflammation, and alleviates sepsis-induced myocardial injury. MMPP induces G1-phase cell cycle arrest and apoptosis, and inhibits the growth of non-small cell lung cancer (NSCLC) and solid tumors. MMPP promotes adipogenesis and glucose uptake. MMPP can be used in research related to NSCLC, type 2 diabetes and myocardial injury.

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

Purity: 98.06%
CAS No.: 1895957-18-2
Formula: C₁₇H₁₈O₃
Molecular Weight:270.32

Storage:

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

MMPP Chemical Structure

CAS No.: 1895957-18-2

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Biological Activity
- Description
- IC₅₀ & Target
- 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]

STAT3

VEGFR2

PPARγ

All STAT Isoforms :

All VEGFR Isoforms :

All PPAR Isoforms :

All Akt Isoforms :

All ERK Isoforms :

All NF-κB Isoforms :

In Vitro

MMPP inhibits the viability of NCI-H460 non-small cell lung cancer cells, with an IC₅₀ value of 12.3 μg/mL^[1].
MMPP (5-20 μg/mL; 24 h) inhibits the viability of various cancer cell lines, including the NCI-H460 non-small cell lung cancer cell line, in a concentration-dependent manner (IC₅₀ = 11.99 μg/mL), but exerts no effect on the viability of non-cancerous LL-24 lung epithelial cells^[1].
MMPP (5-15 μg/mL; 24 h) induces apoptosis and G1-phase cell cycle arrest in NCI-H460 and A549 non-small cell lung cancer cells in a concentration-dependent manner^[1].
MMPP (10 μg/mL; 24 h) significantly inhibits VEGFA-induced migration of human umbilical vein endothelial cells (HUVECs) in scratch wound healing assays^[2].
MMPP (10 μg/mL) significantly inhibits VEGFA-induced invasion of HUVECs in Transwell assays^[2].
MMPP (10 μg/mL; 16 h) significantly inhibits VEGFA-induced angiogenesis in HUVECs^[2].
MMPP (10 μg/mL; 1.5 h) inhibits the VEGFR2/AKT/ERK signaling pathway in HUVECs by reducing the phosphorylation levels of VEGFR2, AKT and ERK^[2].
MMPP (10 μg/mL; 2 h) inhibits VEGFA-induced nuclear translocation of NF-κB p65 in HUVECs^[2].
MMPP (10 μg/mL; 25 h) significantly downregulates the mRNA expression of VEGFA, VEGFR2, MMP2 and MMP9 in HUVECs^[2].
MMPP (15 μg/mL; 24 h) upregulates the transcriptional activity of PPARγ in HEK 293T cells, and synergistically enhances this activity with Rosiglitazone (HY-17386)^[3].
MMPP (7.5-15 μg/mL; 2-8 days) dose-dependently promotes lipid accumulation in differentiated 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) increases glucose uptake in mature 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) enhances the expression of adipogenesis-related genes and reduces Il6 mRNA levels in mature 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) enhances the expression of adipogenesis-related proteins in fully differentiated 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) upregulates the expression of C/ebpb mRNA in early-stage (day 2) 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 2-8 days) upregulates the expression of C/EBPβ protein in early-stage (day 2) 3T3-L1 MBX adipocytes^[3].
MMPP (7.5-15 μg/mL; 1 h) enhances the phosphorylation levels of AKT, GSK3 and AMPKα in 3T3-L1 MBX cells co-treated with MDI for 1 h^[3].
MMPP (5-100 mg/L; 10 min) potently scavenges ABTS•⁺ in a cell-free system, and achieves nearly complete inhibition at a concentration of 100 mg/L^[4].
MMPP (40-200 mg/L) scavenges •OH in a cell-free system, with a scavenging rate of 48.14% at 200 mg/L^[4].
MMPP (100-1000 mg/L) scavenges O₂•^- in a cell-free system, with a scavenging rate of 61.24% at 1000 mg/L^[4].
MMPP (100-500 mg/L; 1 h) chelates Fe²⁺ in a cell-free system, with a chelating efficiency of up to 51.0% at the concentration of 500 mg/L^[4].
MMPP (100 μg/mL; 12.5 h) restores the viability of H9c2 cells treated with LPS (HY-D1056) after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces LDH release in LPS-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the Ptgs2 mRNA expression level in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the PTGS2 protein expression level in LPS-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) inhibits LPS-induced release of cytochrome c (Cyt c) from mitochondria to cytoplasm in neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces the MDA level in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) restores SOD levels in LPS-treated neonatal rat ventricular myocytes after 12 hours of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces intracellular ROS accumulation in lipopolysaccharide-treated neonatal rat ventricular myocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) reduces lipid ROS accumulation in neonatal rat ventricular myocytes treated with LPS after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) maintains the mitochondrial membrane potential of lipopolysaccharide-treated neonatal rat ventricular cardiomyocytes after 12 h of incubation^[4].
MMPP (100 μg/mL; 12.5 h) maintains mitochondrial function in LPS-treated neonatal rat ventricular cardiomyocytes after 12 h of incubation^[4].

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

Cell Viability Assay^[1]

Cell Line:

multiple cancer cell lines (colon: HCT116, SW480; prostate: PC3, LNCaP; ovary: PA-1, SK-OV-3; liver: Hep-G2, Huh-7; breast: MCF-7; skin: SK-MEL-28; lung: A549, NCI-H460) and non-cancerous LL-24 lung epithelial cells
Concentration:

5, 10, 15 and 20 μg/mL
Incubation Time:

24 h
Result:

Significantly reduced viability of all tested cancer cell lines at 10 μg/mL.
Reduced viability of NCI-H460 cells in a concentration-dependent manner with an IC₅₀ of 11.99 μg/mL.
Showed no toxicity to non-cancerous LL-24 lung epithelial cells at tested concentrations.

Apoptosis Analysis^[1]

Cell Line:

NCI-H460 and A549 NSCLC cells
Concentration:

5, 10 and 15 μg/mL
Incubation Time:

24 h
Result:

Induced apoptosis in NCI-H460 and A549 cells in a concentration-dependent manner, with the apoptotic index increasing from near 0% in vehicle controls to ~60% at 15 μg/mL MMPP in NCI-H460 cells.

Western Blot Analysis^[1]

Cell Line:

NCI-H460 and A549 NSCLC cells
Concentration:

5, 10 and 15 μg/mL
Incubation Time:

24 h
Result:

Increased expression of pro-apoptotic proteins Bax, cleaved caspase-3, and cleaved caspase-8, and decreased expression of anti-apoptotic protein Bcl-2 in a concentration-dependent manner.
Increased expression of cell cycle inhibitor p21, and decreased expression of CDK6 and cyclin D1 in a concentration-dependent manner.

Cell Cycle Analysis^[1]

Cell Line:

NCI-H460 and A549 NSCLC cells transfected with wild-type or T456A mutant STAT3
Concentration:

10 μg/mL
Incubation Time:

24 h
Result:

Inhibited viability and induced G1-phase cell cycle arrest in cells transfected with wild-type STAT3, but these inhibitory effects were attenuated in cells transfected with STAT3-T456A mutant.

Cell Migration Assay ^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

10 μg/mL
Incubation Time:

24 h
Result:

Resulted in a wider scratched area compared to VEGFA-stimulated controls.
Significantly inhibited VEGFA-induced HUVEC migration.

Western Blot Analysis^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

10 μg/mL
Incubation Time:

1 h pre-incubation, followed by 30 min VEGFA stimulation
Result:

Reduced the phosphorylation levels of VEGFR2, AKT, and ERK.
Left total protein levels unchanged.

RT-PCR^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

10 μg/mL
Incubation Time:

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

Significantly suppressed the mRNA expressions of VEGFA, VEGFR2, MMP2, and MMP9.

Western Blot Analysis^[3]

Cell Line:

fully differentiated 3T3-L1 MBX adipocytes
Concentration:

7.5 and 15 μg/mL
Incubation Time:

added on day 2, day 4, and day 6 of differentiation, with incubation through day 8
Result:

Increased the protein expression levels of adipogenic transcription factors (PPARγ, C/EBPα) and markers (GLUT4, FAS, ACC) in a dose-dependent manner, compared to the MDI-only control group.

Real Time qPCR^[3]

Cell Line:

early-stage (day 2) 3T3-L1 MBX adipocytes
Concentration:

7.5 and 15 μg/mL
Incubation Time:

48 h (from day 0 to day 2 of differentiation)
Result:

Increased the mRNA expression level of C/ebpb in a dose-dependent manner, with significantly higher levels at 15 μg/mL compared to the MDI-only control group.

Western Blot Analysis^[3]

Cell Line:

early-stage (day 2) 3T3-L1 MBX adipocytes
Concentration:

7.5 and 15 μg/mL
Incubation Time:

48 h (from day 0 to day 2 of differentiation)
Result:

Increased the protein expression level of C/EBPβ in a dose-dependent manner, with significantly higher levels at both tested concentrations compared to the MDI-only control group.

Western Blot Analysis^[3]

Cell Line:

3T3-L1 MBX cells
Concentration:

7.5 and 15 μg/mL
Incubation Time:

1 h (co-treatment with MDI)
Result:

Enhanced the phosphorylation levels of AKT, GSK3, and AMPKα in a dose-dependent manner, with significantly higher phosphorylation levels at both tested concentrations compared to the MDI-only control group.

Cell Viability Assay^[4]

Cell Line:

H9c2 cells
Concentration:

100 μg/mL
Incubation Time:

12 h (after 30 min LPS pre-treatment)
Result:

Restored H9c2 cell viability from ~60% (LPS-treated group) to ~90% relative to the control group.

RT-PCR^[4]

Cell Line:

neonatal rat ventricular cardiomyocytes
Concentration:

100 μg/mL
Incubation Time:

12 h (after 30 min LPS pre-treatment)
Result:

Reduced Ptgs2 mRNA levels from ~3.5-fold change (LPS-treated group) to ~2-fold change relative to the control group.

Western Blot Analysis^[4]

Cell Line:

neonatal rat ventricular cardiomyocytes
Concentration:

100 μg/mL
Incubation Time:

12 h (after 30 min LPS pre-treatment)
Result:

Reduced PTGS2 protein levels from ~1.8-fold change (LPS-treated group) to ~1-fold change relative to the control group.
Restored cytoplasmic Cyt c levels from ~0.7 relative units (vs. mitochondrial VDAC1) to ~1 relative unit, and reduced levels from ~1 relative unit (vs. cytoplasmic GAPDH) to ~0.3 relative units.

In Vivo

MMPP (2.5-5 mg/kg; i.p., p.o.; 2-3 times per week; for 3 consecutive weeks) dose-dependently inhibits the growth of NCI-H460 xenograft tumors in BALB/c nude mice^[1].
MMPP (5 mg/kg; p.o.; three times per week; for 1 month) significantly inhibits tumor growth in patient-derived NSCLC xenograft models in immunodeficient mice by suppressing STAT3 activity, with no observed toxicity^[1].
MMPP (5 mg/kg; i.p.; twice weekly; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing A549 non-small cell lung cancer xenografts^[1].
MMPP (5 mg/kg; i.p.; twice weekly; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing HCT116 colon cancer xenografts^[1].
MMPP (5 mg/kg; i.p.; twice a week; for 3 consecutive weeks) inhibits tumor growth and STAT3 activity in BALB/c nude mice bearing PA-1 ovarian cancer xenografts^[1].
MMPP (1 mg; intravenous injection; single dose) inhibits ferroptosis via iron chelation, alleviates oxidative stress, reduces the production of pro-inflammatory cytokines, attenuates sepsis-induced myocardial injury, improves the 14-day survival rate of C57BL/6J mice, and restores key cardiac function parameters including ejection fraction and fractional shortening^[4].

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

Animal Model:

BALB/c nude mice^[1]
Dosage:

2.5 mg/kg; 5 mg/kg
Administration:

i.p.; twice a week; 3 weeks; p.o.; three times a week; 3 weeks
Result:

Significantly reduced tumor volume and weight compared to vehicle controls at 2.5 mg/kg i.p..
Produced a greater, dose-dependent reduction in tumor volume and weight at 5 mg/kg i.p..
Significantly inhibited tumor growth at 5 mg/kg p.o..
Reduced expression of p-STAT3, PCNA, and cyclin D1, and increased active caspase-3 in treated tumors via immunohistochemical staining.
Decreased levels of Cdk4, Cdk6, cyclin D1, and Bcl-2, and increased levels of Bax, cleaved caspase-3, and cleaved caspase-8 in tumor tissues via western blot analysis.
Inhibited STAT3 DNA-binding activity and nuclear translocation of p-STAT3 in tumor tissues.

Animal Model:

Immunodeficient mice^[1]
Dosage:

5 mg/kg
Administration:

p.o.; three times a week; 1 month
Result:

Significantly reduced final tumor volume and weight compared to vehicle controls.
Suppressed p-STAT3 expression in tumor tissues via immunohistochemical analysis.
Inhibited STAT3 DNA-binding activity and reduced nuclear translocation of p-STAT3 via EMSA and western blot analysis.
Showed no signs of body weight loss or liver toxicity in treated animals.

Animal Model:

BALB/c nude mice^[1]
Dosage:

5 mg/kg
Administration:

i.p.; twice a week; 3 weeks
Result:

Effectively suppressed tumor growth and STAT3 activity in A549 xenograft tumors.

Animal Model:

BALB/c nude mice^[1]
Dosage:

5 mg/kg
Administration:

i.p.; twice a week; 3 weeks
Result:

Effectively suppressed tumor growth and STAT3 activity in HCT116 xenograft tumors.

Animal Model:

BALB/c nude mice^[1]
Dosage:

5 mg/kg
Administration:

i.p.; twice a week; 3 weeks
Result:

Effectively suppressed tumor growth and STAT3 activity in PA-1 xenograft tumors.
Demonstrated superior antitumor activity to cisplatin (5 mg/kg) and similar antitumor activity to docetaxel (5 mg/kg).

Animal Model:

C57BL/6J (adult male, 7-8 weeks old, 18 g-20 g, intravenous injection of 10 mg/kg LPS to induce sepsis)^[4]
Dosage:

1 mg
Administration:

i.v.; single dose
Result:

Increased 14-day survival rate significantly compared to the LPS-only group.
Reduced serum CK-MB from ~10000 pg/mL to ~5000 pg/mL.
Reduced serum LDH from ~45 U/mL to ~25 U/mL.
Restored left ventricular ejection fraction (EF%) from ~40% to ~60%.
Restored left ventricular fractional shortening (FS%) from ~20% to ~30%.
Reduced cardiac Ptgs2 mRNA fold change from ~7 to ~2.
Reduced cardiac PTGS2 protein fold change from ~2 to ~1.
Reduced cardiac MDA levels from ~650 nmol/g protein to ~400 nmol/g protein.
Increased cardiac SOD levels from ~25 U/g protein to ~35 U/g protein.
Reduced cardiac iron levels from ~8 μmol/g protein to ~6 μmol/g protein.
Reduced serum IL-1β from ~30 pg/mL to ~10 pg/mL.
Reduced serum TNF-α from ~80 pg/mL to ~30 pg/mL.
Reduced serum IL-6 from ~35000 pg/mL to ~20000 pg/mL.
Alleviated sepsis-induced cardiac inflammation, hemorrhage, and structural disorders.

Chemical Information

CAS No. 1895957-18-2
Appearance Solid
Molecular Weight 270.32
Formula C₁₇H₁₈O₃
Color Off-white to light brown
SMILES

OC1=CC=C(C=C1OC)/C=C/CC2=CC=C(C=C2)OC
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 : 100 mg/mL (369.93 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

3.6993 mL

18.4966 mL

36.9932 mL

5 mM

0.7399 mL

3.6993 mL

7.3986 mL

10 mM

0.3699 mL

1.8497 mL

3.6993 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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Volume _(start) Volume _(start)

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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: ≥ 2.5 mg/mL (9.25 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 (9.25 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 (9.25 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
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 (305 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 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]. Son DJ, et al. MMPP Attenuates Non-Small Cell Lung Cancer Growth by Inhibiting the STAT3 DNA-Binding Activity Direct Binding to the STAT3 DNA-Binding Domain. Theranostics. 2017;7(18):4632-4642. [Content Brief]

[2]. Kim NY, et al. MMPP is a novel VEGFR2 inhibitor that suppresses angiogenesis via VEGFR2/AKT/ERK/NF-κB pathway. BMB reports. 2024 May;57(5):244-249. [Content Brief]

[3]. Kim NY, et al. MMPP promotes adipogenesis and glucose uptake via binding to the PPARγ ligand binding domain in 3T3-L1 MBX cells. Front Pharmacol. 2022 Oct 21;13:994584.
[Content Brief]

[4]. Liu C, et al. Melanin nanoparticles alleviate sepsis-induced myocardial injury by suppressing ferroptosis and inflammation. Bioactive materials. 2023 Jun;24:313-321. [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	3.6993 mL	18.4966 mL	36.9932 mL	92.4830 mL
	5 mM	0.7399 mL	3.6993 mL	7.3986 mL	18.4966 mL
	10 mM	0.3699 mL	1.8497 mL	3.6993 mL	9.2483 mL
	15 mM	0.2466 mL	1.2331 mL	2.4662 mL	6.1655 mL
	20 mM	0.1850 mL	0.9248 mL	1.8497 mL	4.6241 mL
	25 mM	0.1480 mL	0.7399 mL	1.4797 mL	3.6993 mL
	30 mM	0.1233 mL	0.6166 mL	1.2331 mL	3.0828 mL
	40 mM	0.0925 mL	0.4624 mL	0.9248 mL	2.3121 mL
	50 mM	0.0740 mL	0.3699 mL	0.7399 mL	1.8497 mL
	60 mM	0.0617 mL	0.3083 mL	0.6166 mL	1.5414 mL
	80 mM	0.0462 mL	0.2312 mL	0.4624 mL	1.1560 mL
	100 mM	0.0370 mL	0.1850 mL	0.3699 mL	0.9248 mL

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MMPP

MCE Bioactive Compound Library

All STAT Isoforms

All VEGFR Isoforms

All PPAR Isoforms

All Akt Isoforms

All ERK Isoforms

All NF-κB Isoforms

Biological Activity

Chemical Information

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

MMPP Related Classifications

HY-119487 Related Classifications