2. Metabolic Enzyme/Protease Cytoskeleton Cell Cycle/DNA Damage PI3K/Akt/mTOR Apoptosis Autophagy Immunology/Inflammation NF-κB MAPK/ERK Pathway
  3. Herbicide Microtubule/Tubulin PI3K Akt Apoptosis Autophagy Reactive Oxygen Species (ROS) NF-κB p38 MAPK
  4. Ethalfluralin

Ethalfluralin is a dinitroaniline herbicide and microtubule inhibitor. Ethalfluralin blocks nuclear division and cytokinesis of parasites by inhibiting intranuclear spindle formation. Ethalfluralin activates the phosphorylation levels of NF-κB and P38 MAPK, inhibits the PI3K/AKT signaling pathway, impairs mitochondrial function, and induces apoptosis, endoplasmic reticulum stress, autophagy, and ROS production. Ethalfluralin is applicable to research related to toxoplasmosis.

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Ethalfluralin

Ethalfluralin Chemical Structure

CAS No. : 55283-68-6

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Ethalfluralin Related Antibodies

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Description

Ethalfluralin is a dinitroaniline herbicide and microtubule inhibitor. Ethalfluralin blocks nuclear division and cytokinesis of parasites by inhibiting intranuclear spindle formation. Ethalfluralin activates the phosphorylation levels of NF-κB and P38 MAPK, inhibits the PI3K/AKT signaling pathway, impairs mitochondrial function, and induces apoptosis, endoplasmic reticulum stress, autophagy, and ROS production. Ethalfluralin is applicable to research related to toxoplasmosis[1][2][3].

In Vitro

Ethalfluralin (2-20 μM; 48 h) reduces the viability of pLE and pTr cells[1].
Ethalfluralin (20 μM; 48 h) inhibits the expression of the proliferation marker PCNA in pLE and pTr cells[1].
Ethalfluralin (20 μM; 4 h) impairs the migratory capacity of pLE and pTr cells[1].
Ethalfluralin (5-20 μM; 48 h) induces cell cycle arrest in pLE and pTr cells, resulting in an increase in the sub-G1 cell population and a decrease in the S-phase cell population[1].
Ethalfluralin (5-20 μM; 48 h) induces apoptotic cell death in pLE and pTr cells, increases the late apoptotic cell population in both cell lines, and elevates the early apoptotic cell population in pTr cells[1].
Ethalfluralin (5-20 μM; 48 h) reduces cytoplasmic calcium levels in pLE and pTr cells[1].
Ethalfluralin (5-20 μM; 48 h) reduces mitochondrial matrix calcium levels in pLE and pTr cells[1].
Ethalfluralin (5-20 μM; 48 h) disrupts the mitochondrial membrane potential of pLE and pTr cells[1].
Ethalfluralin (20 μM; 20 h) impairs mitochondrial respiratory function in pLE and pTr cells, reduces basal respiration, maximal respiration, spare respiratory capacity and ATP production in pLE cells, and decreases maximal respiration, spare respiratory capacity and ATP production in pTr cells[1].
Ethalfluralin (20 μM; 24 h) downregulates the mRNA expression of genes encoding subunits of mitochondrial respiratory complexes I-V in pLE and pTr cells[1].
Ethalfluralin (5-20 μM; 48 h) activates endoplasmic reticulum stress and autophagy pathways in pLE and pTr cells, upregulates the expression levels of GRP78, phosphorylated eIF2α, GADD153, phosphorylated ULK1 and phosphorylated P62, and promotes LC3B II/I conversion[1].
Ethalfluralin (5-20 μM; 48 h) activates the P38 MAPK and NF-κB signaling pathways, and inhibits the PI3K/AKT signaling pathway in pLE and pTr cells[1].
Ethalfluralin (20 μM; 48 h) impairs autophagic flux and reduces mitochondrial mass in pLE and pTr cells[1].
Ethalfluralin potently inhibits the replication of tachyzoites of Toxoplasma gondii RH strain in human primary foreskin fibroblasts, with an IC50 of 100 nM[3].
Ethalfluralin (0.5 μM; 36 h) exerts no significant inhibitory effect on the invasion of primary human foreskin fibroblasts by tachyzoites of Toxoplasma gondii RH strain, but causes severe morphological abnormalities in intracellular parasites[3].
Ethalfluralin (1 μM; 0-24 h) ablates the plaque-forming ability of tachyzoites of Toxoplasma gondii RH strain in primary human foreskin fibroblasts within 8-12 h, but has no effect on the viability of extracellular tachyzoites treated for 12 h[3].
Ethalfluralin (1 μM; 0-24 h) acts for up to 24 h but does not inhibit nucleic acid synthesis of tachyzoites of the Toxoplasma gondii RH strain in primary human foreskin fibroblasts, even though it completely abolishes parasite activity[3].
Ethalfluralin (1 μM; 20 h) blocks nuclear division of tachyzoites of the Toxoplasma gondii RH strain in primary human foreskin fibroblasts by inhibiting intranuclear spindle formation, while preserving their subpellicular microtubules and causing expansion of the endomembrane compartment[3].
Ethalfluralin (1 μM) inhibits the release of tachyzoites of Toxoplasma gondii RH strain induced by calcium ionophores in primary human foreskin fibroblasts, and simultaneously causes shrinkage of the vacuolar space and increased refractivity of treated parasites after ionophore treatment[3].

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

Ethalfluralin Related Antibodies

Cell Viability Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 2, 5, 10, 20 μM
Incubation Time: 48 h
Result: Suppressed pLE cell viability to 42% and pTr cell viability to 43% relative to vehicle-treated cells at 20 μM.

Immunofluorescence[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 48 h
Result: Markedly reduced relative green fluorescence (PCNA expression) in both pLE and pTr cells compared to vehicle-treated cells.

Cell Migration Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 4 h
Result: Reduced wounded area closure to 9.1% in pLE cells and 10.9% in pTr cells, compared to 27.4% and 30% in vehicle-treated cells, respectively.

Cell Cycle Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased the sub-G1 population up to 3.3-fold in pLE cells and 2.2-fold in pTr cells.
Decreased the S phase population by 46% in pLE cells and 63% in pTr cells relative to vehicle-treated cells.

Apoptosis Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased the late apoptotic cell population up to 2.7-fold in pLE cells at 20 μM.
Increased the early apoptotic population to 198% at 10 μM and 321% at 20 μM, and increased the late apoptotic population by over 2-fold in pTr cells.

Real Time qPCR[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Downregulated mRNA expression of all tested mitochondrial respiratory complex I-V subunit genes (including NDUFS3, SDHB, UQCRC2, MT-CO1, and MT-ATP6) in both pLE and pTr cells.

Western Blot Analysis[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 5, 10 and 20 μM
Incubation Time: 48 h
Result: Increased GRP78 protein levels by 2.9-fold in pLE cells and 2.8-fold in pTr cells at 20 μM.
Increased phosphorylated eIF2α by 1.7-1.8-fold in pLE cells and up to 2-fold in pTr cells at 20 μM.
Increased GADD153 by 2.4-fold in pLE cells and up to 2-fold in pTr cells at 20 μM.
Increased phosphorylated ULK1, phosphorylated P62, and LC3B I to LC3B II conversion ratio by 2-4-fold in both cell lines at 20 μM.\nIncreased phosphorylated p38 MAPK by over 4-fold in pLE cells and 2.2-fold in pTr cells at 20 μM.
Increased phosphorylated NF-κB by over 2-fold in both cell lines at 20 μM.
Reduced phosphorylated AKT by almost half in both cell lines at 20 μM.
Reduced phosphorylated S6 in both cell lines at 20 μM.

Cell Autophagy Assay[1]

Cell Line: porcine luminal epithelial (pLE) cells, porcine trophectoderm (pTr) cells
Concentration: 20 μM (with 10 μM Chloroquine (HY-17589A) pretreatment for 3 h)
Incubation Time: 48 h
Result: Markedly increased p-p62 levels in both cell lines, did not further increase LC3B II/I conversion ratio compared to chloroquine alone, and reduced mitochondrial mass significantly in pLE cells (with a similar trend in pTr cells).
In Vivo

Ethalfluralin (6-12 mg/L; aqueous immersion; daily continuous; 96 hours) induces dose-dependent developmental toxicity in zebrafish embryos, including reduced survival, impaired morphological development, increased apoptosis and ROS production, inhibited angiogenesis, and elevated inflammation, with an LC50 of 18.49 mg/L[2].

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

Animal Model: wild-type, fli1a:eGFP and flk1:eGFP transgenic lines[2]
Dosage: 6 mg/L, 9 mg/L, 12 mg/L
Administration: aqueous immersion; daily continuous; 96 hours
Result: Reduced survival rate, hatching rate and heart rate.
Led to edema of the heart and yolk sac, shortened body length, and spinal cord deformity.
Induced cell apoptosis, oxidative stress and verification.
Inhibited of angiogenesis.
Molecular Weight

333.26

Formula

C13H14F3N3O4
CAS No.
SMILES

O=[N+]([O-])C1=C(N(CC)CC(C)=C)C([N+]([O-])=O)=CC(C(F)(F)F)=C1
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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Ethalfluralin Related Classifications

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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.

Keywords:

Ethalfluralin55283-68-6HerbicideMicrotubule/TubulinPI3KAktApoptosisAutophagyReactive Oxygen Species (ROS)NF-κBp38 MAPKPhosphoinositide 3-kinasePKBProtein kinase BNuclear factor-κBNuclear factor-kappaBzebrafishpLE cellsP38 MAPKprimary human foreskin fibroblastsautophagyToxoplasma gondiiapoptosispTr cellsPI3K/AKT signaling pathwayInhibitorinhibitorinhibit

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