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].
For research use only. We do not sell to patients.
- 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.
All Calcium Channel Isoforms
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Biological Activity
Description
In Vitro
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. Further protocols information, click here.
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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.
In Vivo
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.
Protocols
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Trophoblast Invasion Assay
The trophoblast invasion assay is commonly based on the Matrigel-coated Transwell invasion system, in which invasive cells migrate through a reconstituted basement membrane matrix toward a chemoattractant gradient, thereby modeling extracellular matrix (ECM) penetration and invasive behavior in vitro. The readout is typically the number of cells that traverse the Matrigel barrier and attach to the lower surface of a porous membrane, reflecting invasive capacity through ECM-like substrates and basement membrane components. This system was originally developed to quantify invasive cell behavior using Matrigel as a basement membrane analog in a Boyden chamber format.
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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CCK-8/WST-8 Cell Proliferation Assay
The CCK-8/WST-8 assay is based on the reduction of the water-soluble tetrazolium salt WST-8 to a water-soluble formazan product by cellular dehydrogenases in metabolically active cells, where the generated formazan amount is proportional to the number of living cells and is quantified by measuring absorbance in the visible range, providing a colorimetric readout for cell viability and proliferation assessment. This class of tetrazolium-based assays improves upon earlier MTT-based systems by producing a water-soluble formazan, eliminating the need for organic solubilization steps and enabling direct spectrophotometric measurement in culture medium.
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Acute Systemic Toxicity Study
Acute systemic toxicity studies evaluate adverse effects occurring after a single exposure, or repeated exposure within a short acute window, and the main in vivo readouts are mortality, moribund condition, clinical signs, body-weight change, and gross pathological findings; acute oral toxicity methods were developed to replace classical LD50 testing with reduced-animal designs such as fixed-dose procedure, acute toxic class method, and up-and-down procedure. The fixed-dose procedure classifies acute toxicity by administering predefined dose levels and observing evident toxicity rather than using death as the primary endpoint, whereas the acute toxic class method uses sequential groups of three animals per step and the up-and-down procedure doses animals sequentially to estimate an LD50 with fewer animals than conventional LD50 testing.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Protocol for Fluorescence In Situ Hybridization (FISH)
Fluorescence in situ hybridization detects specific DNA or RNA sequences inside fixed cells or tissue sections by hybridizing fluorescently labeled nucleic-acid probes to complementary target sequences, allowing the target’s copy number, chromosomal position, spatial distribution, or transcript abundance to be visualized microscopically. DNA-FISH detects genomic loci, chromosomal gains/losses, amplifications, deletions, and rearrangements, while RNA-FISH detects RNA molecules or transcript localization; in cancer cells, mouse tumors, neurons, organoids, macrophages, or drug-screening samples, the readout is fluorescent puncta, fusion/split signals, or localized RNA signal interpreted relative to validated controls.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
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)