浓度为 100、300 和 1000 µM 的二甲嗪会强烈抑制 HepG2 细胞活力 [1]。二甲嗪（3、10、30 µM；24 h）促进 HepG2 细胞的能量代谢从有氧三羧酸循环（TCA）和氧化磷酸化转变为无氧糖酵解[1]。在 HepG2 细胞中，异丙嗪（3、10、30 µM；24 小时）可抑制复合物 IV 活性 [1]。

三氯芬酸（46.3、139、417 mg/kg；口服；单次）在肾脏（18.64%）、脑（23.58%）、胃（21.94%）和肝脏（35.84%）中蓄积[1]。异丙嗪（46.3、139、417 mg/kg；口服；单剂量）比任何其他器官都更能提高小鼠肝脏和大脑中的 MDA 水平[1]。

RT-PCR[1]
细胞类型： HepG2 细胞
测试浓度： 3、10、30 µM
孵育时间： 24 小时
实验结果： 30 µM 时，乳酸脱氢酶 B (LDHB) 水平显着增加，6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶略有增加3（PFKFB3）。在 3、10 和 30 µM 噻嗪酮处理下，ATP 水平以浓度依赖性方式分别降低至载体对照水平的 91.3%、87.9 和 67.2%。乳酸水平显着增加。

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免疫荧光[1]
细胞类型： HepG2 细胞
测试浓度： 3、10、30 µM
孵育时间： 24 小时
实验结果： 在 3、10 和 30 ℃ 进行噻嗪酮处理后，复合物 IV 的活性显着抑制至载体对照水平的 82.2、69.2 和 63.4%分别为μM。

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细胞活力测定[1]
细胞类型： HepG2 细胞
测试浓度： 3、10、30 µM
<孵育时间： 24 小时
实验结果： 以不依赖浓缩物的方式显着提高细胞内 ROS 水平，并降低 mtDNA 含量。

Animal/Disease Models: Male C57BL/6 mice (6 to 8weeks old)[1].
Doses: 46.3, 139, 417 mg/kg
Route of Administration: Oral administration; single
Experimental Results: Tended to elevate the MDA level in all organs, and the most significant concentration-dependent increases were observed in the liver and brain. demonstrated the highest concentrations in the liver (35.84%) followed by the brain (23.58%), stomach (21.94%) and kidney (18.64%), while the levels in the mouse spleen and heart were below the limit of detection.

Absorption, Distribution and Excretion
(14)C-buprofezin (radiochemical purity >97%) administered by gavage to 5 rats/sex/dose at 10 and 100 mg/kg; in males, 90-91% of dose eliminated by 48 hr (20-21% in urine, 69-71% in feces); in females, 87-89% of dose eliminated by 48 hr (13-14% in urine, 73-76% in feces); elimination faster in males during 1st 24 hr, but equalized by 48 hr; <1% of dose remained in body by 7 days; > or =30% of male dose and > or =38% of female dose recovered in bile at 24 hr; chromatography of urine, bile, and feces indicated extensive conjugation; bile cannulation of 3M/3F revealed that fecal metabolites were likely of bile origin.
[(14)C-phenyl]-buprofezin (2 or 22.5 mCi/mmol; >97% radiochemical purity) suspended in 1 mL of olive oil was administered by gavage to fasted /rats/ at 10 and 100 mg/kg (number of animals varied with the experiment); over 90% of administered dose was excreted by 48 hr at both concentrations; by 96 hr at both concentrations, 70-74% of dose excreted in feces (though a delay at the high dose relative to the low dose was noted through 24 hr), 21-25% in urine, very low amounts excreted as expired (14)C-CO2; at 10 mg/kg, 12% of the parent compound was excreted into the feces; Cmax in blood occurred at 9 hr for both doses after which concentrations declined biphasically (t1/2 =13 and 60 hr); peak levels of radiolabel occurred in tissues at 5-9 hr post dose, after which tissue levels decreased biphasically with a t1/2 of 3.5-15 hr and 15-72 hr for the 2 phases; by 96 hr tissue residue levels were low.
Male rats /were/ fed diet containing buprofezin at 200 or 1000 ppm for up to 24 weeks; 3/dose were sacrificed on days 2 and 4 and on weeks 1, 2, 4, 8, 12, 16, and 24; buprofezin levels measured by gas-liquid chromatography after extraction from blood, brain, liver, kidney, adipose tissue, and muscle; detection limit: 0.1 ppm; 200 ppm: only adipose tissue attained levels high enough to consistently detect, remaining stable between 4 days and 24 weeks at a mean concentration of 0.43-1.10 ppm; an occasional animal showed detectable levels in liver, while kidney, muscle, and brain never showed detectable levels; 1000 ppm: adipose tissue peaked at 10.53 ppm on day 4, declining to 3.40 ppm at 24 weeks; liver retained a stable concentration of 0.21-0.96 over the entire period; kidneys were near or below the detection limit for 8 weeks and undetectable thereafter; brain was near or below the detection limit for 1 week and undetectable thereafter; muscle was near or below the detection limit for 2 weeks and undetectable thereafter (no measurement at 4 weeks); test article thus did not accumulate in any tissue at either concentration.

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Metabolism / Metabolites
[(14)C-phenyl]-buprofezin (2 or 22.5 mCi/mmol; >97% radiochemical purity) suspended in 1 mL of olive oil was administered by gavage to fasted /rats/ at 10 and 100 mg/kg (number of animals varied with the experiment); ... metabolite studies revealed hydroxylation of the phenyl ring, oxidation of sulfur, and cleavage of the thiadiazin ring, with evidence of glucuronic and sulfuric conjugation.
/In/ ruminants: 2-tert-butylimino-5-(4-hydroxyphenyl)-3-isopropyl-1,3,5- thiadiazinan-4-one (BF2) was the major residue identified in liver and kidney (residue in fat and muscle were < or =0.020 ppm) and N-(4-hydroxyphenyl)acetamide (BF23) was the major residue identified in milk from the ruminant metabolism study (all other residue were <10% total radioactive residue (TRR); 3.5x maximum theoretical dietary burden (MTDB)). ...The residues of concern in milk are buprofezin and BF23; ... the residues of concern in ruminant tissues are buprofezin and BF2.

[1]. Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism. J Hazard Mater. 2016 Dec 15;320:176-186.

[2]. Inhibition of chitin biosynthesis by buprofezin analogs in relation to their activity controlling Nilaparvata lugens Stål. Pestic Biochem Physiol, 1985, 24(3): 343-347.

Description
Buprofezin is a 2-(tert-butylimino)-5-phenyl-3-(propan-2-yl)-1,3,5-thiadiazinan-4-one in which the C=N double bond has Z configuration. It has a role as an insecticide and a member of homopteran inhibitor of chitin biosynthesis.

C16H23N3OS

305.44

305.156

69327-76-0

Buprofezin-d6;2140803-94-5

50367

White to off-white solid powder

1.18

273°C (12 torr)

104-106°C

176-178°C

1.52-1.522

4.185

61.21

0

3

3

21

408

0

PRLVTUNWOQKEAI-UHFFFAOYSA-N

InChI=1S/C16H23N3OS/c1-12(2)19-14(17-16(3,4)5)21-11-18(15(19)20)13-9-7-6-8-10-13/h6-10,12H,11H2,1-5H3

2-tert-butylimino-5-phenyl-3-propan-2-yl-1,3,5-thiadiazinan-4-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 100 mg/mL (327.40 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (8.18 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (8.18 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (8.18 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。