2. Apoptosis Protein Tyrosine Kinase/RTK Stem Cell/Wnt MAPK/ERK Pathway PI3K/Akt/mTOR
  3. Apoptosis VEGFR ERK Akt Caspase Bcl-2 Family
  4. AC-P19M

AC-P19M is an anticancer peptide. AC-P19M induces apoptosis by disrupting the cell membrane of cancer cells. AC-P19M reverses epithelial-mesenchymal transition (EMT). AC-P19M shows anti-angiogenic activity through the inhibition of VEGF-VEGFR2/ERK/Akt signaling. AC-P19M can be used for lung cancer research.

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

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AC-P19M

AC-P19M Chemical Structure

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AC-P19M Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3

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Description

AC-P19M is an anticancer peptide. AC-P19M induces apoptosis by disrupting the cell membrane of cancer cells. AC-P19M reverses epithelial-mesenchymal transition (EMT). AC-P19M shows anti-angiogenic activity through the inhibition of VEGF-VEGFR2/ERK/Akt signaling. AC-P19M can be used for lung cancer research[1].

In Vitro

AC-P19M (0.1-100 μM, 24 h) shows potent anticancer activity against lung cancer cells (A549 and H460), while showing low toxicity towards normal (BEAS-2B) and red blood cells[1].
AC-P19M (0.1-100 μM, 6 h) induces lactate dehydrogenase (LDH) release in A549 and H460 cells, indicating that it disrupts cell membranes, leading to cell death[1].
AC-P19M (2-10 μM, 24 h) induces cell apoptosis in A549 and H460 cells through the Bcl-2/Bax/caspase 3 cascade[1].
AC-P19M (0.2-0.5 μM, 24 h) inhibits the migration and invasion of A549 and H460 cells by reversing mesenchymal properties and the expression of EMT markers, ultimately inhibiting EMT process[1].
AC-P19M (10 μM, 12 h) exhibits an anti-angiogenic effect by contributing to the reduction of tubular morphology in human umbilical vein endothelial cells (HUVECs), while inhibiting VEGF-VEGFR2/ERK/Akt signaling[1].

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

AC-P19M Related Antibodies

Western Blot Analysis[1]

Cell Line: A549 and H460 cells
Concentration: 0.2, 0.5, 2, 5, and 10 μM
Incubation Time: 24 h
Result: Significantly decreased Bcl-2 levels, showing almost no expression at 10 μM.
Upregulated Bax protein levels to 2.5-fold in a concentration-dependent manner.
Resulted in a more than 2-fold increase of caspase 3.
Increased the expression levels of E-cadherin, while decreased the expression levels of N-cadherin and vimentin.

Cell Migration Assay [1]

Cell Line: A549 and H460 cells
Concentration: 0.2 and 0.5 μM
Incubation Time: 24 h
Result: Inhibited cell migration by more than 20% in both A549 and H460 cells.

Cell Invasion Assay[1]

Cell Line: A549 and H460 cells
Concentration: 0.2 and 0.5 μM
Incubation Time: 24 h
Result: Inhibited cell invasion by more than 20% in both A549 and H460 cells.
Molecular Weight

2096.73

Formula

C102H186N26O20
Sequence

Phe-Ala-Lys-Lys-Leu-Ala-Lys-Leu-Lys-Lys-Lys-Leu-Ala-Lys-Leu-Ala-Leu-Ala-Leu
Sequence Shortening

FAKKLAKLKKKLAKLALA
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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AC-P19M Related Classifications

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The molarity calculator equation

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

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The dilution calculator equation

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This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    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.

Keywords:

AC-P19MApoptosisVEGFRERKAktCaspaseBcl-2 FamilyVascular endothelial growth factor receptorExtracellular signal regulated kinasesPKBProtein kinase Banticancer peptideepithelial-mesenchymalanti-angiogenicVEGFR2lung cancerA549H460BEAS-2BHUVECsVEGF-VEGFR2/ERK/AktInhibitorinhibitorinhibit

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