2. MAPK/ERK Pathway PI3K/Akt/mTOR Membrane Transporter/Ion Channel Neuronal Signaling Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Apoptosis
  3. p38 MAPK PI3K Calcium Channel Reactive Oxygen Species (ROS) Apoptosis Cytochrome P450
  4. Picolinafen

Picolinafen  (Synonyms: 氟吡酰草胺; AC 900001)

目录号: HY-W711035
产品使用指南 技术支持

Picolinafen 是一种八氢番茄红素去饱和酶 (PDS) 抑制型吡啶类除草剂。Picolinafen 可控制阔叶杂草的生长并且干扰类胡萝卜素生物合成。Picolinafen 对猪胚胎滋养外胚层细胞 (pTr) 和子宫腔上皮细胞 (pLE) 具有细胞毒性。 Picolinafen 可通过诱导 ROS 积累、钙耗竭，激活 MAPK 和 PI3K 信号通路，导致细胞活力下降、凋亡 (apoptosis) 增加、迁移能力受损以及着床相关基因表达改变。Picolinafen 对哺乳动物的 LD50 值为 2.7 mg/kg，对鱼类为 7 μg/L。Picolinafen 在斑马鱼胚胎发育过程中表现出毒性效应[1][2]。

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Picolinafen

Picolinafen Chemical Structure

CAS No. : 137641-05-5

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Picolinafen 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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].

体外研究
(In Vitro)

Picolinafen (0.2-6 μM, 48 h) 降低猪胚胎滋养外胚层细胞 (pTr) 和子宫腔上皮细胞 (pLE) 的细胞活力并改变细胞周期进程[1]。

Picolinafen (1-4 μM, 48 h) 诱导 pTr 和 pLE 细胞凋亡，破坏细胞球体的自我组装能力，并且干扰 pTr 和 pLE 细胞的线粒体完整性和钙稳态[1]。

Picolinafen (1-4 μM, 2-48 h) 导致 pTr 和 pLE 细胞中 ROS 积累并破坏细胞内 Ca2+ 调控[1]。

Picolinafen (4 μM, 15-24 h) 抑制 pTr 细胞迁移并改变与凋亡和着床相关基因的转录调控[1]。

Picolinafen (1-4 μM, 3 h) 激活 pTr 和 pLE 细胞中的 MAPK 和 PI3K/AKT 信号通路[1]。

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

Picolinafen 相关抗体:

Cell Cycle Analysis[1]

Cell Line: pTr and pLE cells
Concentration: 1, 2, 4 μM
Incubation Time: 48 h
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.

Cell Viability Assay[1]

Cell Line: pTr and pLE cells
Concentration: 0.2, 0.5, 1, 2, 4, 5, 6 μM
Incubation Time: 48 h
Result: Decreased the viability of pTr cells (IC50 = 4.33 μM) and pLE cells (IC50 = 5.54 μM).

Apoptosis Analysis[1]

Cell Line: pTr and pLE cells
Concentration: 1, 2, 4 μM
Incubation Time: 48 h
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.

Cell Migration Assay [1]

Cell Line: pTr cells
Concentration: 4 μM
Incubation Time: 15 h
Result: Decreased the percentage of wound closure in pTr cells by 0.31 fold.

Real Time qPCR[1]

Cell Line: pTr and pLE cells
Concentration: 4 μM
Incubation Time: 24 h
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.

Western Blot Analysis[1]

Cell Line: pTr and pLE cells
Concentration: 1, 2, 4 μM
Incubation Time: 3 h
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.
体内研究
(In Vivo)

Picolinafen (0.1-100 μM，孵育，0-5 天) 在斑马鱼胚胎中 3 天时 LC50 为 10 μM，5 天时 LC50 为 5 μM[2]。

Picolinafen (1-10 μM，孵育，24-72 h) 在斑马鱼胚胎发育过程中表现出毒性效应[2]。

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

Animal Model: Zebrafish embryo[2]
Dosage: 1, 5, 10 μM
Administration: Incubation for 24, 48 and 72 h
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.
分子量

376.30

Formula

C19H12F4N2O2
CAS 号
中文名称

氟吡酰草胺
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Picolinafen 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

Picolinafen137641-05-5AC 900001氟吡酰草胺AC900001AC-900001p38 MAPKPI3KCalcium ChannelReactive Oxygen Species (ROS)ApoptosisCytochrome P450Phosphoinositide 3-kinaseCa2+ channelsCa channelsCYPsMAPKROSPI3K/AKTapoptosiszebrafishpTr cellspLE cellsInhibitorinhibitorinhibit

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