MAPK/ERK Pathway Stem Cell/Wnt Cell Cycle/DNA Damage PI3K/Akt/mTOR Apoptosis Neuronal Signaling Autophagy NF-κB Metabolic Enzyme/Protease Immunology/Inflammation Anti-infection
ERK JNK p38 MAPK PERK mTOR Akt MDM-2/p53 PINK1/Parkin Apoptosis Reactive Oxygen Species (ROS) Paraptosis Mitophagy Autophagy Bacterial Glycosidase
Chalcomoracin

Cat. No.: HY-N20674

Chalcomoracin

Chalcomoracin is an orally active anticancer agent. Chalcomoracin exhibits anticancer, antibacterial, and α-glucosidase inhibitory activities, with an IC₅₀ of 14.23 µM against yeast α-glucosidase and an IC₅₀ of 5.5 μM against FabI of Staphylococcus aureus. Chalcomoracin reduces the phosphorylation levels of ERK, JNK, and P38; enhances the phosphorylation level of ERK1/2; regulates the MAPK, mTOR, AKT, and p53 signaling pathways; upregulates the expression of Chop, Bip, PINK1, GRP78, and GADD153; and downregulates the expression of Alix. Chalcomoracin induces apoptosis (apoptosis), endoplasmic reticulum stress (endoplasmic reticulum stress), paraptosis (paraptosis), ROS production, mitophagy (mitophagy), and autophagy (autophagy); it inhibits cancer cell viability, colony-forming ability, migration, invasion, proliferation, tumorigenesis, fatty acid synthesis, S. aureus growth, vitreous-stimulated retinal cell activity, and cell cycle progression at the G0/G1 phase. Chalcomoracin can be used in research related to hepatocellular carcinoma, non-small cell lung cancer, triple-negative breast cancer, prostate cancer, proliferative vitreoretinopathy, pancreatic cancer, diabetes, and bacterial infections.

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CAS No.: 76472-89-4
화학식: C₃₉H₃₆O₉
분자량:648.70

보관:

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

Chalcomoracin Chemical Structure

CAS No.: 76472-89-4

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Biological Activity
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Biological Activity

제품 설명

IC₅₀ & Target^[1]^[2]^[3]^[4]^[5]^[6]^[7]

α-Glucosidase

14.23 μM (IC₅₀)

ERK

JNK

p38

ERK1

ERK2

MAPK

mTOR

Akt

p53

Chop

Bip

PINK1

GRP78

GADD153

Alix

α-glucosidase

All ERK Isoforms :

All JNK Isoforms :

All p38 MAPK Isoforms :

All mTOR Isoforms :

All Akt Isoforms :

In Vitro

Chalcomoracin (1.5-6 µM; 24-72 h) significantly reduces the viability of human Hep3B and SNU-387 HCC cells in a time- and concentration-dependent manner, with the most potent effect at 6 µM over 72 h^[1].
Chalcomoracin (1.5-6 µM; 24 h) inhibits clonogenic proliferation of human Hep3B and SNU-387 HCC cells in a concentration-dependent manner, with the strongest effect at 6 µM^[1].
Chalcomoracin (1.5-6 µM; 48 h) suppresses activation of the MAPK pathway in human Hep3B and SNU-387 HCC cells by reducing p-ERK, p-P38, and p-JNK protein levels after 48 h of treatment^[1].
Chalcomoracin (2-32 μM; 24-72 h) dose-dependently inhibits the viability of human non-small cell lung cancer H460, A549, and PC-9 cells, with IC₅₀ values ranging from 4.8 μM to 12.3 μM across 24, 48, and 72 h incubations^[2].
Chalcomoracin (2-6 μM; 48 h) induces dose-dependent cytoplasmic vacuolation in human non-small cell lung cancer H460, A549, and PC-9 cells, with 6 μM CMR causing 24.5% to 36.6% vacuolated cells after 48 h incubation^[2].
Chalcomoracin (2-6 μM; 2 h) pretreatment enhances the radiosensitivity of human non-small cell lung cancer H460 and A549 cells, with a maximum sensitizer enhancement ratio of 1.35 (H460) and 1.28 (A549) at 6 μM CMR^[2].
Combination treatment with chalcomoracin and ionizing radiation exerts a synergistic cytotoxic effect on human non-small cell lung cancer H460 and A549 cells^[2].
Chalcomoracin (2.5-10 μM; 24-72 h) potently inhibits viability and induces death in MDA-MB-231, PC-3, and LNCaP cancer cells with IC₅₀ values of 6 μM (MDA-MB-231, PC-3) and 8 μM (LNCaP) at 48 h, while showing much lower cytotoxicity toward normal mammary epithelial MCF-10A and normal prostate RWPE-2 cells^[3].
Chalcomoracin (6 μM; 24-48 h) induces paraptotic, non-apoptotic cell death characterized by ER-derived cytoplasmic vacuolation in MDA-MB-231 and PC-3 cells, but not in LNCaP cells^[3].
Chalcomoracin (2.5-40 μM; 24-72 h) exhibits dose- and time-dependent cytotoxicity to ARPE-19 retinal pigment epithelial cells, with an IC₅₀ of 35.5 μM at 72 hours, and 5 μM Chalcomoracin is non-toxic to these cells^[4].
Chalcomoracin (5 μM; 8 h) prevents vitreous-induced activation of AKT and reduction of p53 expression in ARPE-19 retinal pigment epithelial cells^[4].
Chalcomoracin (5 μM; 48 h) completely blocks vitreous-induced proliferation of ARPE-19 retinal pigment epithelial cells^[4].
Chalcomoracin (2.5-10 μM; 24 h) dose-dependently blocks vitreous-induced migration of ARPE-19 retinal pigment epithelial cells^[4].
Chalcomoracin (5 μM; 48 h) completely blocks vitreous-induced collagen gel contraction by ARPE-19 retinal pigment epithelial cells^[4].
Chalcomoracin (2.5-10 μM; 24-72 h) inhibits PANC-1 cells viability in a concentration- and time-dependent manner^[5].
Chalcomoracin (6-8 μM; 48 h) persistently suppresses clonogenic capacity and long-term proliferation of pancreatic cancer cells^[5].
Chalcomoracin (1.5-6 µM; 24 h) promotes apoptosis of human Hep3B and SNU-387 HCC cells in a concentration-dependent manner, with significant effects starting at 3 µM and the strongest effect at 6 µM after 24 h^[1].
Chalcomoracin (1.5-6 µM; 24 h) modulates apoptosis-related protein expression in human Hep3B and SNU-387 HCC cells, reducing Bcl2 levels and increasing Bax, cleaved caspase-3, and cleaved PARP levels in a concentration-dependent manner^[1].
Chalcomoracin (1.5-6 µM; 24 h) induces endoplasmic reticulum stress in human Hep3B and SNU-387 HCC cells, increasing ATF4, GRP78, and CHOP protein levels in a concentration-dependent manner^[1].
Chalcomoracin (1.5-6 µM; 24 h) reduces MMP2 and MMP9 protein levels in human Hep3B and SNU-387 HCC cells in a concentration-dependent manner, supporting its anti-invasive activity^[1].
Chalcomoracin (1.5-6 µM; 24 h pretreatment) suppresses migration and invasion of human Hep3B and SNU-387 HCC cells in a concentration-dependent manner, with the strongest effect at 6 µM after 24 h of pretreatment^[1].
Chalcomoracin (2-6 μM; 48 h) induces endoplasmic reticulum dilation-derived cytoplasmic vacuolation in a dose-dependent manner in human non-small cell lung cancer H460 and A549 cells after 48 h incubation^[2].
Chalcomoracin (6 μM; 48 h) induces endoplasmic reticulum swelling and cytoplasmic vacuolation without apoptotic nuclear changes in human non-small cell lung cancer H460 and A549 cells^[2].
Chalcomoracin (6 μM; 2 h preincubation, 48 h post-treatment) enhances radiosensitivity in human non-small cell lung cancer H460 and A549 cells by increasing radiation-induced cytoplasmic vacuolation^[2].
Chalcomoracin (6 μM; 2 h preincubation, 48 h post-radiation) increases endoplasmic reticulum stress marker expression in combination with ionizing radiation in human non-small cell lung cancer H460 and A549 cells, with H460 cells showing increased IRE1, ATF6, and p-PERK levels and A549 cells showing only increased IRE1 levels^[2].
Chalcomoracin (2-8 μM; 48 h) does not induce significant apoptosis in human non-small cell lung cancer H460 and A549 cells at doses up to 6 μM after 48 h incubation, with only minimal apoptosis observed at 8 μM^[2].
Chalcomoracin (6 μM; 2 h preincubation, 48 h post-treatment) does not enhance ionizing radiation-induced apoptosis in human non-small cell lung cancer H460 and A549 cells after 48 h post-treatment^[2].
Chalcomoracin (2-6 μM; 48 h) dose-dependently upregulates endoplasmic reticulum stress markers Bip and Chop in human non-small cell lung cancer H460 and A549 cells after 48 h incubation, with H460 cells showing increased IRE1, p-PERK, and ATF6 expression and A549 cells showing only increased IRE1 expression, without activating apoptosis-related caspase-3 or PARP^[2].
Chalcomoracin-mediated paraptosis is dependent on endoplasmic reticulum stress, as Bip knockdown reduces both chalcomoracin-induced cell death and cytoplasmic vacuolation in human non-small cell lung cancer H460 cells^[2].
Chalcomoracin (6-8 μM; 48 h) dose-dependently activates ER stress and mitophagy, and downregulates the paraptosis inhibitor Alix, in MDA-MB-231 and PC-3 cells, while having no effect on these pathways in LNCaP cells^[3].
Chalcomoracin (1.875-15 μM; 48 h) requires active protein synthesis for its induced paraptosis, mitophagy activation, and cell death in MDA-MB-231 and PC-3 cells, as pre-treatment with 5 μg/mL CHX for 1 h inhibits these effects^[3].
Chalcomoracin (1-6 μM; 24-48 h)-induced paraptosis in MDA-MB-231 and PC-3 cells requires calpain activity and MAPK (ERK1/2) signaling, as pre-treatment with 10 μM E-64d or 10 μM U0126 inhibits cytoplasmic vacuolation and related protein changes^[3].
Chalcomoracin (6 μM; 48 h) regulates paraptosis and mitophagy-related gene expression in MDA-MB-231 and PC-3 cells, increasing PINK1, GADD153, and GRP78 mRNA and decreasing Alix mRNA, while having no effect on these genes in LNCaP cells^[3].
Chalcomoracin (6 μM; 48 h)-induced paraptosis in cancer cells requires PINK1, as ectopic PINK1 expression sensitizes LNCaP cells to CMR-induced paraptosis, and PINK1 knockdown protects MDA-MB-231 cells from these effects^[3].
Chalcomoracin (6-10 μM; 48 h) induces complete autophagic flux, elevates autophagy turnover and promotes the formation of autophagic vacuoles in PANC-1 pancreatic cancer cells^[5].
Chalcomoracin (2-6 μM; 6-48 h)-induced paraptosis in MDA-MB-231 and PC-3 cells is mediated by ROS production, loss of mitochondrial membrane potential, and dysregulated calcium homeostasis, as pre-treatment with NAC, BAPTA, or BAPTA-AM inhibits these effects^[3].
Chalcomoracin (6-8 μM; 48 h) blocks pancreatic cancer proliferation by triggering G0/G1 cell cycle arrest^[5].
Chalcomoracin (6-8 μM; 48 h) enhances lysosomal acidification to facilitate autophagic substrate degradation in PANC-1 cells^[5].
Chalcomoracin (6-10 μM; 48 h) activates autophagy via inhibitory regulation of mTOR signaling cascade^[5].
Chalcomoracin (6-10 μM; 48 h) induces massive intracellular ROS production in PANC-1 cells; ROS acts as upstream initiating signal of downstream events^[5].
Chalcomoracin (6-10 μM; 48 h) has its induced apoptosis and growth inhibition in human pancreatic cancer PANC-1 cells alleviated by inhibition of autophagy via Atg5/Atg7 knockdown or Wortmannin (HY-10197) pretreatment^[5].
Chalcomoracin (1.5625-200 μM; 10 min pre-incubation with α-glucosidase, 30 min incubation with PNPG) potently inhibits yeast α-glucosidase with an IC₅₀ of 14.23 μM^[6].
Chalcomoracin (20-50 μM) inhibits yeast α-glucosidase via a mixed competitive and non-competitive mode, as indicated by increasing K_m and decreasing V_max with rising Chalcomoracin concentrations^[6].
Chalcomoracin (200 μM; 300 s intervals between 30 total 5-μL injections at 37 °C) binds to yeast α-glucosidase in an entropy-driven spontaneous reaction, with hydrophobic interactions playing a leading role in the binding process^[6].
Chalcomoracin binds firmly to yeast α-glucosidase via a combination of hydrophobic interactions, hydrogen bonds, and cation-π interactions within the enzyme's hydrophobic pocket^[6].
Chalcomoracin inhibits purified Staphylococcus aureus enoyl-acyl carrier protein reductase (FabI) with an IC₅₀ of 5.5 μM^[7].
Chalcomoracin inhibits the growth of Staphylococcus aureus with a minimum inhibitory concentration (MIC) of 4 µg/mL^[7].
Chalcomoracin inhibits fatty acid synthesis in Staphylococcus aureus, without affecting the organism's protein synthesis^[7].

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

Cell Viability Assay^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h, 48 h, 72 h
Result:

Significantly reduced cell viability in both Hep3B and SNU-387 cells in a time- and concentration-dependent manner.
Showed the strongest reduction at 6 µM after 72 h of incubation.

Cell Proliferation Assay^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h
Result:

Decreased colony formation capacity in both cell lines in a concentration-dependent manner.
Caused a significant reduction at 1.5 µM, while 3 µM and 6 µM caused stronger, dose-dependent reductions.

Apoptosis Analysis^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h
Result:

Promoted apoptosis in both cell lines in a concentration-dependent manner.
Showed no significant effect at 1.5 µM, while 3 µM caused a significant increase in apoptosis rate, and 6 µM caused a robust, highly significant increase.

Western Blot Analysis^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h
Result:

Reduced relative expression of anti-apoptotic Bcl2 and increased relative expression of pro-apoptotic Bax, cleaved caspase-3, and cleaved PARP in both cell lines in a concentration-dependent manner.
Showed significant changes at 1.5 µM and stronger, highly significant changes at 3 µM and 6 µM.\n
Increased relative expression of ER stress-related proteins ATF4, GRP78, and CHOP in both cell lines in a concentration-dependent manner.
Showed significant changes at 1.5 µM and stronger, highly significant changes at 3 µM and 6 µM.\n
Reduced relative expression of invasion-related proteins MMP2 and MMP9 in both cell lines in a concentration-dependent manner.

Cell Migration Assay ^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h
Result:

Inhibited cell migration.

Cell Invasion Assay^[1]

Cell Line:

Human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5 µM, 3 µM, 6 µM
Incubation Time:

24 h
Result:

Inhibited cell invasion.

Western Blot Analysis^[1]

Cell Line:

human hepatocellular carcinoma (HCC) Hep3B, SNU-387
Concentration:

1.5-6 µM
Incubation Time:

48 h
Result:

Showed significant reductions at 1.5 µM and stronger, highly significant reductions at 3 µM and 6 µM.
Reduced relative expression of phosphorylated ERK (p-ERK), phosphorylated P38 (p-P38), and phosphorylated JNK (p-JNK) in both cell lines compared to control, with no clear concentration dependence observed.
Showed significant reductions at all tested concentrations.

Cell Viability Assay^[2]

Cell Line:

Human non-small cell lung cancer H460, A549, and PC-9 cells
Concentration:

2 μM, 4 μM, 8 μM, 16 μM, 32 μM
Incubation Time:

24 h; 48 h; 72 h
Result:

Dose-dependently decreased the viability of H460, A549, and PC-9 cells.
Reduced cell viability with IC₅₀ values of 10.8 μM (H460), 10.1 μM (A549), and 12.3 μM (PC-9) at 24 h.
Reduced cell viability with IC₅₀ values of 6.1 μM (H460), 6.3 μM (A549), and 8.9 μM (PC-9) at 48 h.
Reduced cell viability with IC₅₀ values of 4.8 μM (H460), 5.7 μM (A549), and 7.9 μM (PC-9) at 72 h.

Cell Autophagy Assay^[2]

Cell Line:

Human non-small cell lung cancer H460 and A549 cells
Concentration:

2 μM, 4 μM, 6 μM
Incubation Time:

48 h
Result:

Showed that the edges of all cytoplasmic vacuoles in CMR-treated cells were stained with calreticulin, confirming vacuoles originated from ER dilation.
Increased the percentage of vacuolated cells in a dose-dependent manner in both cell lines, with significant increases observed at 6 μM CMR compared to controls.

Apoptosis Analysis^[2]

Cell Line:

Human non-small cell lung cancer H460 and A549 cells
Concentration:

2 μM, 4 μM, 6 μM, 8 μM
Incubation Time:

48 h
Result:

Did not induce significant apoptosis in H460 and A549 cells at doses up to 6 μM.
Caused only slight increases in apoptotic cell death detected at the highest tested dose (8 μM) in both cell lines.

Western Blot Analysis^[2]

Cell Line:

Human non-small cell lung cancer H460 and A549 cells
Concentration:

2 μM, 4 μM, 6 μM
Incubation Time:

48 h
Result:

Dose-dependently increased the expression of ER stress markers Bip and Chop in both cell lines.
Increased expression of IRE1, p-PERK, and ATF6 at 6 μM CMR in H460 cells.
Increased only IRE1 expression at 6 μM CMR in A549 cells.
Detected no obvious changes in Alix, LC3B, caspase-3 (full-length or cleaved), or PARP (full-length or cleaved) protein levels in either cell line.

Apoptosis Analysis^[2]

Cell Line:

human non-small cell lung cancer H460 and A549 cells
Concentration:

6 μM
Incubation Time:

2 h (preincubated prior to IR treatment); 48 h (post-treatment analysis)
Result:

Had no effect on IR-induced apoptosis in either cell line.

Immunofluorescence^[2]

Cell Line:

Human non-small cell lung cancer H460 and A549 cells
Concentration:

6 μM
Incubation Time:

2 h (preincubated prior to IR treatment); 48 h (post-treatment analysis)
Result:

Dramatically increased the percentage of vacuolated cells: in H460 cells, vacuolation increased from 23.5% to 42.2%; in A549 cells, vacuolation increased from 18.1% to 33.8% after IR exposure.
Showed no such increase in irradiated control cells without CMR pretreatment.

Western Blot Analysis^[2]

Cell Line:

Human non-small cell lung cancer H460 and A549 cells
Concentration:

6 μM
Incubation Time:

2 h (preincubated prior to IR treatment); 48 h (post-radiation analysis)
Result:

Increased Bip and Chop protein expression only in cells treated with the combination of CMR and IR.
Increased IRE1, ATF6, and p-PERK levels in response to IR in H460 cells pretreated with 6 μM CMR.
Increased only IRE1 protein levels in response to combined treatment in A549 cells.

Cell Viability Assay^[3]

Cell Line:

Human triple-negative breast cancer MDA-MB-231 cells, human prostate cancer PC-3 cells, human prostate cancer LNCaP cells, human normal mammary epithelial MCF-10A cells, human normal prostate RWPE-2 cells
Concentration:

2.5 μM, 5 μM, 7.5 μM, 10 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

Inhibited cell viability in a dose- and time-dependent manner in all three cancer cell lines, with IC50 values of 6 μM for MDA-MB-231 and PC-3 cells, and 8 μM for LNCaP cells after 48 h exposure.
Induced dose-dependent cell death (measured by PI uptake) in MDA-MB-231, PC-3, and LNCaP cells after 48 h treatment.
Showed significantly lower cytotoxicity in normal MCF-10A and RWPE-2 cells at equivalent concentrations.

Western Blot Analysis^[3]

Cell Line:

Human triple-negative breast cancer MDA-MB-231 cells, human prostate cancer PC-3 cells, human prostate cancer LNCaP cells, human normal mammary epithelial MCF-10A cells
Concentration:

6 μM, 7 μM, 8 μM
Incubation Time:

48 h
Result:

Dose-dependently increased expression of ER stress markers GRP78 and GADD153, accumulated ubiquitinated proteins, increased LC3-II levels (a marker of autophagosome formation), upregulated mitophagy regulator PINK1, and downregulated paraptosis inhibitor Alix in MDA-MB-231 and PC-3 cells.
Did not induce these changes in LNCaP cells.
Only weakly induced these changes in MCF-10A cells.
Confirmed co-localization of GFP-LC3 puncta with mitochondria (indicative of mitophagy) in CMR-treated MDA-MB-231 and PC-3 cells via confocal microscopy.

Real Time qPCR^[3]

Cell Line:

Human triple-negative breast cancer MDA-MB-231 cells, human prostate cancer PC-3 cells, human prostate cancer LNCaP cells
Concentration:

6 μM
Incubation Time:

48 h
Result:

Increased mRNA expression of PINK1, GADD153, and GRP78, and decreased mRNA expression of Alix in MDA-MB-231 and PC-3 cells.
Left caspase-3 and PARP gene expression unchanged in MDA-MB-231 and PC-3 cells.
Caused no significant changes in these gene expressions in LNCaP cells.

Cell Viability Assay^[4]

Cell Line:

ARPE-19 retinal pigment epithelial cells
Concentration:

2.5 μM, 5 μM, 10 μM, 20 μM, 40 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

Showed dose- and time-dependent cytotoxicity to ARPE-19 cells.
Reached an IC₅₀ of 35.5 μmol/L at 72 hours.
Did not cause obvious toxicity to ARPE-19 cells at 5 μmol/L.

Western Blot Analysis^[4]

Cell Line:

Serum-starved ARPE-19 retinal pigment epithelial cells
Concentration:

5 μM
Incubation Time:

8 h
Result:

Significantly blocked RV-induced phosphorylation (activation) of AKT.
Reversed RV-induced suppression of p53 protein expression in ARPE-19 cells.

Cell Proliferation Assay^[4]

Cell Line:

ARPE-19 retinal pigment epithelial cells
Concentration:

5 μM
Incubation Time:

48 h
Result:

Completely abrogated RV-induced ARPE-19 cell proliferation that was 1.6 fold compared to control.

Cell Migration Assay ^[4]

Cell Line:

ARPE-19 retinal pigment epithelial cells
Concentration:

2.5 μM, 5 μM, 10 μM
Incubation Time:

24 h
Result:

Significantly inhibited RV-induced ARPE-19 cell migration in a dose-dependent manner.

Cell Viability Assay^[5]

Cell Line:

PANC-1 cells
Concentration:

2.5 μM, 5 μM, 7.5 μM, 10 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

Inhibited PANC-1 cells viability in a concentration- and time-dependent manner.

Cell Cycle Analysis^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM
Incubation Time:

48 h
Result:

Dose-dependently elevated G0/G1 fraction while reducing S and G2/M populations, inducing G0/G1 arrest.

Cell Proliferation Assay^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM
Incubation Time:

48 h
Result:

Persistently suppressed clonogenic capacity and long-term proliferation of pancreatic cancer cells.

Apoptosis Analysis^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM, 10 μM
Incubation Time:

48 h
Result:

Induced pancreatic cancer apoptosis in a dose-dependent manner.

Western Blot Analysis^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM, 10 μM
Incubation Time:

48 h
Result:

Dose-dependently elevated LC3-II/LC3-I ratio; co-incubation with CQ further accumulated LC3B, confirming enhanced autophagic flux.
Downregulated phosphorylation of mTOR and its downstream p70S6K, S6 in both dose- and time-dependent manner, suppressing mTOR pathway activity.

Cell Autophagy Assay^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM, 10 μM
Incubation Time:

48 h
Result:

Promoted formation of autophagic vacuoles in pancreatic cancer cells.
Accelerated autophagosome-lysosome fusion and intact autophagic degradation flux.

Immunofluorescence^[5]

Cell Line:

PANC-1 cells
Concentration:

6 μM, 8 μM
Incubation Time:

48 h
Result:

Enhanced lysosomal acidification to facilitate autophagic substrate degradation.

In Vivo

Chalcomoracin (50 mg/kg; i.p.; once daily; 7 consecutive days) significantly inhibits hepatocellular carcinoma tumor growth in male BALB/c nude mice and suppresses MAPK pathway activity in tumor tissue, with minimal impact on mouse body weight^[1].
Chalcomoracin (50 mg/kg; i.p.; once daily; 7 days) alone achieves 76.4% tumor growth inhibition, and (50 mg/kg; i.p.; once daily; 7 days + 10 Gy ionizing radiation; single dose) combined with ionizing radiation achieves 95.7% tumor growth inhibition in H460 xenograft nude mice via upregulation of endoplasmic reticulum stress markers and activation of p-Erk, without increasing apoptosis or causing obvious toxicity^[2].
Chalcomoracin (30-55 mg/kg; i.p.; once daily; 21 days) inhibits MDA-MB-231 xenograft tumor growth in nude mice with 46% and 54% tumor growth inhibition at 30 mg/kg and 55 mg/kg, respectively, via inducing mitophagy and paraptosis without causing significant weight loss^[3].
Chalcomoracin (20 mg/kg; p.o.; once daily; 21 days) inhibits pancreatic cancer xenograft growth with a 61.63% tumor inhibition rate via mTOR downregulation, autophagy induction and apoptosis promotion, but shows no efficacy (0% inhibition rate) in Atg7-knockdown xenografts, confirming its autophagy-dependent anti-tumor activity^[5].
Chalcomoracin (20 mg/kg; i.p.; once daily; 27 days) inhibits pancreatic cancer xenograft growth with a 47.80% tumor inhibition rate via ROS-mediated mTOR pathway downregulation, autophagy induction, and apoptosis promotion, and this efficacy is abolished by NAC co-treatment^[5].

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

Animal Model:

BALB/c nude (male)^[1]
Dosage:

50 mg/kg
Administration:

i.p.; daily; 7 consecutive days
Result:

Significantly reduced tumor volume compared to controls.
Significantly reduced average tumor weight compared to controls.
Showed little change in mouse body weight, while control group body weight decreased significantly.
Significantly reduced levels of phosphorylated ERK, phosphorylated P38, and phosphorylated JNK in tumor tissue compared to controls.

Animal Model:

Nu/Nu nude mice (female, 5-7 weeks of age, subcutaneous inoculation of 5×10⁶ H460 human large cell lung cancer cells)^[2]
Dosage:

50 mg/kg (monotherapy); 50 mg/kg + 10 Gy ionizing radiation (combination)
Administration:

i.p.; once daily; 7 days (days 1-7); single dose ionizing radiation (day 1, combination only)
Result:

Achieved 76.4% tumor growth inhibition (TGI).
Achieved 95.7% TGI when combined with ionizing radiation, which was significantly enhanced compared to monotherapy.
Upregulated endoplasmic reticulum stress markers Bip and Chop, and activated p-Erk in xenograft tumor tissues.
Reduced Ki67 staining in tumor tissues, with further enhancement observed in combined treatment.
Did not increase ionizing radiation-induced cleaved caspase 3 staining in tumor tissues.
Caused no obvious body weight changes in treated mice, indicating good tolerability.

Animal Model:

Foxn1nu (female, 5-7 weeks of age, subcutaneous MDA-MB-231 xenograft)^[3]
Dosage:

30 mg/kg; 55 mg/kg
Administration:

i.p.; once daily; 21 days
Result:

Achieved 46% tumor growth inhibition at 30 mg/kg.
Achieved 54% tumor growth inhibition at 55 mg/kg.
Caused no significant weight loss in treated mice.
Upregulated PINK1, LC3-II, GRP78, and ubiquitinated proteins in tumor tissue.
Downregulated Alix in tumor tissue.
Activated ERK1/2 in tumor tissue.
Showed no changes in PARP or caspase-3 in tumor tissue.
Increased LC3-II-positive cells confirmed via immunohistochemistry.
Revealed cytoplasmic vacuolation in tumor tissues via H&E staining.
Induced dose-dependent increases in calpain 1 protein levels via immunofluorescence.

Animal Model:

BALB/c nude (female, 5 weeks old, 18 g, subcutaneous xenograft model injected with PANC-1 sh-NC cells)^[5]
Dosage:

20 mg/kg
Administration:

p.o.; daily; 21 days
Result:

Achieved a 46.09% T/C rate and 61.63% tumor inhibition rate.
Downregulated p-mTOR/mTOR and p-S6/S6 levels in tumor tissues.
Upregulated cleaved Caspase-3 expression in tumor tissues.
Increased the LC3-II/LC3-I ratio in tumor tissues.
Elevated LC3B and cleaved Caspase-3 levels in tumors as confirmed by immunohistochemistry and immunofluorescence.
Caused no significant change in mouse body weight, indicating no overt toxicity.
Achieved a 124.07% T/C rate and 0% tumor inhibition rate.
Failed to increase LC3-II and cleaved Caspase-3 levels in Atg7-knockdown tumors.
Showed no significant effect on p-mTOR/mTOR or p-S6/S6 levels relative to the vehicle group.
Caused no significant change in mouse body weight.

Animal Model:

BALB/c nude (female, 5 weeks old, 18 g, subcutaneous xenograft model injected with PANC-1 cells)^[5]
Dosage:

20 mg/kg
Administration:

i.p.; daily; 27 days
Result:

Alone achieved a 52.50% T/C rate and 47.80% tumor inhibition rate.
Alone downregulated p-mTOR/mTOR and p-S6/S6 levels in tumor tissues.
Alone upregulated cleaved Caspase-3 expression in tumor tissues.
Alone increased the LC3-II/LC3-I ratio in tumor tissues.
Concurrent NAC treatment reversed these effects, resulting in a 172.11% T/C rate and 0% tumor inhibition rate, with no significant change in autophagy or apoptosis markers relative to the NAC-only group.
Caused no significant change in mouse body weight across groups.

Chemical Information

CAS No. 76472-89-4
분자량 648.70
화학식 C₃₉H₃₆O₉
SMILES

O=C(C1=C(C(C/C=C(C)\C)=C(C=C1)O)O)[C@H]2[C@@H](C3=C(C=C(C4=CC5=CC=C(O)C=C5O4)C=C3O)O)C=C(C[C@@H]2C6=C(C=C(C=C6)O)O)C
Structure Classification
- Phenols
- Polyphenols
Initial Source
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Cui Y, et al. Chalcomoracin promotes apoptosis and endoplasmic reticulum stress in hepatocellular carcinoma cells. The Journal of antibiotics. 2024 Jul;77(7):428-435. [Content Brief]

[2]. Zhang SR, et al. Chalcomoracin inhibits cell proliferation and increases sensitivity to radiotherapy in human non-small cell lung cancer cells via inducing endoplasmic reticulum stress-mediated paraptosis. Acta pharmacologica Sinica. 2020 Jun;41(6):825-834. [Content Brief]

[3]. Han H, et al. Chalcomoracin is a potent anticancer agent acting through triggering Oxidative stress via a mitophagy- and paraptosis-dependent mechanism. Scientific reports. 2018 Jun 22;8(1):9566. [Content Brief]

[4]. Han H, et al. Chalcomoracin prevents vitreous-induced activation of AKT and migration of retinal pigment epithelial cells. Journal of cellular and molecular medicine. 2021 Oct;25(19):9102-9111. [Content Brief]

[5]. Hu X, et al. Chalcomoracin induces autophagy-mediated apoptosis in pancreatic cancer by suppressing the mTOR pathway. Food Bioscience. March 1, 2025;85:106388.

[6]. Liu Y, et al. Isolation of Chalcomoracin as a Potential α-Glycosidase Inhibitor from Mulberry Leaves and Its Binding Mechanism. Molecules (Basel, Switzerland). 2022 Sep 06;27(18):5742. [Content Brief]

[7]. Kim YJ, et al. Chalcomoracin and moracin C, new inhibitors of Staphylococcus aureus enoyl-acyl carrier protein reductase from Morus alba. Biological & pharmaceutical bulletin. 2012;35(5):791-5. [Content Brief]

Calculators

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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.

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Chalcomoracin

All ERK Isoforms

All JNK Isoforms

All p38 MAPK Isoforms

All mTOR Isoforms

All Akt Isoforms

Biological Activity

Chemical Information

순도&문서

References

Calculators

Help & FAQs

Chalcomoracin Related Classifications

HY-N20674 Related Classifications