1. Autophagy Apoptosis
  2. p62 Autophagy Apoptosis
  3. EAD1

EAD1 is a Chloroquine (HY-17589A) analog with anticancer activity. EAD1 blocks autophagy, leading to the intracellular accumulation of autophagosome-related proteins LC3-II and p62. EAD1 induces cancer cell apoptosis and inhibits cancer cell proliferation. EAD1 can be used in the research of lung cancer and pancreatic cancer.

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EAD1

EAD1 Chemical Structure

CAS No. : 1644388-26-0

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Description

EAD1 is a Chloroquine (HY-17589A) analog with anticancer activity. EAD1 blocks autophagy, leading to the intracellular accumulation of autophagosome-related proteins LC3-II and p62. EAD1 induces cancer cell apoptosis and inhibits cancer cell proliferation. EAD1 can be used in the research of lung cancer and pancreatic cancer[1].

Cellular Effect
Cell Line Type Value Description References
BXPC-3 IC50
5.8 μM
Compound: 3h, EAD1
Antiproliferative activity against human BxPC3 cells after 72 hrs by SRB method
Antiproliferative activity against human BxPC3 cells after 72 hrs by SRB method
[PMID: 25699157]
HCC827 IC50
7.6 μM
Compound: 3h, EAD1
Antiproliferative activity against human HCC827 cells after 72 hrs by SRB method
Antiproliferative activity against human HCC827 cells after 72 hrs by SRB method
[PMID: 25699157]
NCI-H460 IC50
11 μM
Compound: 3h, EAD1
Antiproliferative activity against human H460 cells after 72 hrs by SRB method
Antiproliferative activity against human H460 cells after 72 hrs by SRB method
[PMID: 25699157]
In Vitro

EAD1 (compound 3h) potently inhibits the proliferation of H460, HCC827 and BxPC3 cancer cells at 72 h, with IC50 values of 11 μM, 7.6 μM and 5.8 μM, respectively[1].
EAD1 (6.5-100 μM; 24 h) potently inhibits colony formation of H460 non-small cell lung cancer cells[1].
EAD1 (5-75 μM; 24 h) induces concentration-dependent apoptosis in H460 non-small cell lung cancer (NSCLC) cells[1].
EAD1 (25-50 μM; 6 h) enhances the expression of punctate LC3 in H3122 non-small cell lung cancer cells[1].
EAD1 (1-25 μM, 10 μM; 2-72 h, 24 h) induces concentration- and time-dependent accumulation of autophagy-related proteins LC3-II and p62 in H460 non-small cell lung cancer (NSCLC) cells[1].

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

Cell Proliferation Assay[1]

Cell Line: H460 human NSCLC cells
Concentration: 6.5, 13, 25, 50, 100 μM
Incubation Time: 24 h
Result: Inhibited colony formation of H460 non-small cell lung cancer cells.

Apoptosis Analysis[1]

Cell Line: H460 human NSCLC cells
Concentration: 5, 25, 50, 75 μM
Incubation Time: 24 h
Result: Induced apoptosis in H460 cells in a concentration-dependent manner.

Western Blot Analysis[1]

Cell Line: H460 human NSCLC cells
Concentration: 1, 2.5, 5, 10, 25 μM (24 h incubation); 10 μM (time-course incubation)
Incubation Time: 2, 4, 6, 24, 48, 72 h (10 μM concentration); 24 h (1-25 μM concentration)
Result: Caused concentration- and time-dependent increases in autophagosome-bound LC3-II levels.
Showed larger increase in LC3-II levels at each tested concentration compared to HCQ.
Made the effect of 25 μM HCQ on LC3-II approximately equal to that of 5 μM EAD1.
Caused concentration-dependent accumulation of p62 (an autophagy substrate), with more potent activity than HCQ.
Molecular Weight

484.42

Formula

C24H27Cl2N7

CAS No.
SMILES

CN(CCNCC1=CN(CC2=CC=C(Cl)C=C2)N=N1)CCNC3=CC=NC4=CC(Cl)=CC=C34

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

Purity & Documentation
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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.

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EAD1
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HY-123056
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