Picolinafen
Picolinafen is a pyridine-class herbicide that acts as a phytoene desaturase (PDS) inhibitor. Picolinafen effectively controls broadleaf weeds and disrupts carotenoid biosynthesis. Picolinafen exhibits cytotoxicity to porcine trophectoderm (pTr) and luminal epithelial (pLE) cells. Picolinafen induces (ROS accumulation, calcium depletion, and activates (MAPK and PI3K signaling pathways, leading to decreased cell viability, increased apoptosis, impaired migration, and altered expression of implantation-related genes. Picolinafen has an LD50 value of 2.7 mg/kg in mammals and 7 μg/L in fish. Picolinafen exhibits toxic effects during zebrafish embryogenesis[1][2].
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- CAS No.: 137641-05-5
- Formula: C19H12F4N2O2
- Molecular Weight:376.30
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Picolinafen (0.2-6 μM, 48 h) decreases cell viability and alters cell cycle progression in pTr and pLE cells[1].
Picolinafen (1-4 μM, 48 h) induces apoptosis, impairs self-assembly of cell spheroids and interferes with mitochondrial integrity and calcium homeostasis in pTr and pLE cells[1].
Picolinafen (1-4 μM, 2-48 h) causes ROS accumulation and disrupts intracellular Ca2+ regulation in pTr and pLE cells[1].
Picolinafen (4 μM, 15-24 h) inhibits pTr cell migration and alters the transcriptional regulation of genes involved in apoptosis and implantation[1].
Picolinafen (1-4 μM, 3 h) activates the MAPK and PI3K/AKT signaling pathways in pTr and pLE cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:pTr and pLE cells
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Concentration:1, 2, 4 μM
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Incubation Time:48 h
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Result:Increased G1 phase in pLE cells.
Decreased both G1 and S phases in pTr cells.
Reduced the ratio of cells in the G2/M phase by approximately 0.65- and 0.6-fold in pTr and pLE cells, respectively.
Increased the ratio of cells in the G1 phase by approximately 5.68- and 4.03-fold in pTr and pLE cells, respectively.
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Cell Line:pTr and pLE cells
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Concentration:0.2, 0.5, 1, 2, 4, 5, 6 μM
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Incubation Time:48 h
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Result:Decreased the viability of pTr cells (IC50 = 4.33 μM) and pLE cells (IC50 = 5.54 μM).
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Cell Line:pTr and pLE cells
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Concentration:1, 2, 4 μM
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Incubation Time:48 h
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Result:Increased early apoptosis by 3.23 and 1.5 fold in pTr and pLE cells, respectively.
Increased late apoptosis by 3.1 and 1.73 fold in pTr and pLE cells, respectively.
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Cell Line:pTr cells
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Concentration:4 μM
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Incubation Time:15 h
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Result:Decreased the percentage of wound closure in pTr cells by 0.31 fold.
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Cell Line:pTr and pLE cells
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Concentration:4 μM
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Incubation Time:24 h
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Result:Increased BAX by 1.31 fold, BAK1 by 1.3 fold, and CASP3 by 1.4 fold in pTr cells.
Increased BAX by 1.72 fold, BAK1 by 1.34 fold in pLE cells.
Increased the expression level of the cytochrome P450 enzyme-coding gene CYP1A1 in pTr cells.
Reduced the expression of FOLR1 and ITGAV, which are involved in implantation in pTr cells.
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Cell Line:pTr and pLE cells
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Concentration:1, 2, 4 μM
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Incubation Time:3 h
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Result:Increased the abundance of phosphorylated ERK1/2, JNK, and p38 and the expression levels of PI3K/AKT in pTr cells.
Increased the abundance of phosphorylated JNK and p38 in pLE cells.
Suppressed p-ERK1/2 levels by U0126 (HY-12031A) and Adezmapimod (SB203580) (HY-10256) treatments in pTr and pLE cells.
Reduced p-JNK by SP600125 (HY-12041), Wortmannin (HY-10197) and U0126 in pTr and pLE cells.
Restored the levels of p-p38 and SP203580, whereas SP600125 increased the phosphorylation of p38 in pLE cells.
Down-regulated phospho-AKT levels following treatment with Wortmannin and SB203580, whereas only Wortmannin inhibited p-AKT in pLE cells.
Inhibited the phosphorylation of p70S6K by Wortmannin, U0126, and SB203580 in both cell lines.
Inhibited S6 by wortmannin and U0126 in pTr cells, whereas this target was significantly down-regulated by all four inhibitors in pLE cells.
Picolinafen (0.1-100 μM, incubation, 0-5 days) exhibits an LC50 of 10 μM at 3 days and 5 μM at 5 days in zebrafish embryos[2].
Picolinafen (1-10 μM, incubation, 24-72 h) exhibits toxic effects during zebrafish embryogenesis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Zebrafish embryo[2]
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Dosage:1, 5, 10 μM
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Administration:Incubation for 24, 48 and 72 h
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Result:Caused embryo hatching at 48 h, with “dead hatched embryos” observed and reduced “live embryos” to 30%, with only 22% surviving self-hatching at 10 μM at 72 h.
Impaired early embryogenesis evidenced by the larger eyes and brain, the smaller yolk sac and heart and a tail curvature reduction from 180° to 89° at 10 μM.
Increased the apoptotic cells localized in the eyes and tail region of zebrafish embryo.
Destroyed DNA and induced cell death especially in the eyes and yolk-sac of zebrafish embryos.
Reduced oxidative stress during embryogenesis at 5 μM.
Decreased the amount of angiogenesis in the trunk of zebrafish embryos at 5 μM.
Chemical Information
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CAS No. 137641-05-5
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Molecular Weight 376.30
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Formula C19H12F4N2O2
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SMILES
O=C(C1=NC(OC2=CC(C(F)(F)F)=CC=C2)=CC=C1)NC3=CC=C(C=C3)F
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Synonyms
AC 900001
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Park W, et al. ROS accumulation and calcium depletion, leading to apoptosis in porcine embryonic trophectoderm and uterine luminal epithelial cells during the peri-implantation period. Theriogenology. 2023 Apr 15;201:12-23. [Content Brief]
[2]. Lee JY, et al. Picolinafen exerts developmental toxicity via the suppression of oxidative stress and angiogenesis in zebrafish embryos. Pestic Biochem Physiol. 2021 Jan;171:104734. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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