1. Epigenetics PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway Metabolic Enzyme/Protease NF-κB Immunology/Inflammation GPCR/G Protein
  2. AMPK mTOR ERK Oxidative Phosphorylation Reactive Oxygen Species (ROS) Ras
  3. NMac1

NMac1 is an orally active Nm23/NDPK activator. NMac1 directly binds to Nm23-H1 and activates the NDPK activity of recombinant Nm23-H1 with an EC50 of 10.7 uM. NMac1 induces AMPK activation and inhibits mTOR and ERK, leading to mitochondrial OXPHOS dysregulation and suppressing mitochondrial ROS production, which in turn induces mitochondrial dysfunction in MDA-MB-231 cells. NMac1 inhibits Complex I activity and suppresses changes in morphology and actin cytoskeleton organization following Rac1 activation in MDA-MB-231 cells. NMac1 inhibits tumor invasion, migration and metastasis. NMac1 is useful for studying metastatic tumors, such as breast cancer. NMac1 can be isolated from the ginger cassumunar Roxb[1][2].

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

NMac1

NMac1 Chemical Structure

CAS No. : 1332290-68-2

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Description

NMac1 is an orally active Nm23/NDPK activator. NMac1 directly binds to Nm23-H1 and activates the NDPK activity of recombinant Nm23-H1 with an EC50 of 10.7 uM. NMac1 induces AMPK activation and inhibits mTOR and ERK, leading to mitochondrial OXPHOS dysregulation and suppressing mitochondrial ROS production, which in turn induces mitochondrial dysfunction in MDA-MB-231 cells. NMac1 inhibits Complex I activity and suppresses changes in morphology and actin cytoskeleton organization following Rac1 activation in MDA-MB-231 cells. NMac1 inhibits tumor invasion, migration and metastasis. NMac1 is useful for studying metastatic tumors, such as breast cancer. NMac1 can be isolated from the ginger cassumunar Roxb[1][2].

In Vitro

NMac1 inhibits the proliferation of cancer cells under glucose starvation (IC50s of 7.197 and 2.849 μM) in MDA-MB-231 and MCF7 cells[1].
NMac1 (0-20 μM, 0-20 h) induces AMPK activation and inhibits mTOR and ERK in the absence of glucose in MDA-MB-231 cells[1].
NMac1 (0-20 μM, 0-20 h) induces mitochondrial dysfunction by inhibiting ATP production and reducing the mitochondrial membrane potential in MDA-MB-231 cells[1].
NMac1 (0-10 μM, 0-100 min) induces ATP depletion by reducing oxygen consumption rate, producing mitochondrial ROS and inducing dysregulation of mitochondrial ATP production system OXPHOS in the absence of glucose in MDA-MB-231 cells[1].
NMac1 (250-500 μM, 0-100 min) inhibits complex I activity in MDA-MB-231 cells[1].
NMac1 (0-30 μM, 2-14 days) inhibits the proliferation of MDA-MB-231 spheroid cells in a dose-dependent manner[1].
NMac1 (0-25 μM, 16-24 h) inhibits Rac1 activation through NDPK activation of Nm23-H1, reduces the invasion and migration in MDA-MB-231 cells[2].

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

Western Blot Analysis[1]

Cell Line: MDA-MB-231 cells
Concentration: 0, 5, 10, 12.5, 20 μM
Incubation Time: 0, 2, 4, 8, 12, 16, 20 h
Result: Induced AMPK activation and inhibited mTOR, ERK, and pS6K, rapidly induces AMPK activation within 2 hours under glucose depletion.

Immunofluorescence[1]

Cell Line: MDA-MB-231 cells
Concentration: 12.5 μM
Incubation Time: 6 h
Result: Deteriorated the mitochondrial integrity of cells in the absence of glucose, reduced TOM20 levels.

Western Blot Analysis[2]

Cell Line: MDA-MB-231 cells
Concentration: 0, 5, 10, 25 μM
Incubation Time: 16 h
Result: Reduced Rac1 activation.

Cell Migration Assay [2]

Cell Line: MDA-MB-231 cells
Concentration: 0, 5, 10, 25 μM
Incubation Time: 24 h
Result: Reduced the invasion and migration in a dose dependent manner, without affecting their proliferation.
In Vivo

NMac1 (10 mg/kg, p.o., once a day, 21 days) inhibits breast cancer metastasis without affecting primary tumor size in breast cancer metastasis mouse model[2].

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

Animal Model: Breast cancer (MDA-MB-231-Luc-D3H2LN cells, 1 × 106) metastasis NOD/SCID mice model[2]
Dosage: 10 mg/kg
Administration: p.o., once a day, 21 days
Result: Significantly inhibited breast cancer metastasis without affecting primary tumor size.
Molecular Weight

380.48

Formula

C24H28O4

CAS No.
SMILES

COC1=CC(/C=C/C2C(C3=CC=C(OC)C(OC)=C3)C=CCC2)=CC=C1OC

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Please store the product under the recommended conditions in the Certificate of Analysis.

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

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