Kaempferitrin is a natural flavonoid, possesses antinociceptive, anti-inflammatory, anti-diabetic, antitumoral and chemopreventive effects, and activates insulin signaling pathway.

Insulin Receptor^[1]

Kaempferitrin activates insulin signaling pathway. Kaempferitrin causes survival rates higher than 90% at 1-20 μM in matured 3T3-L1 adipocyte, and the survival rates decline rapidly at 25 and 50 μM. Kaempferitrin (15 μM) increases insulin receptor beta tyrosine phosphorylation and tyrosine phosphorylation of the insulin receptor substrate 1, and such effects are similar to that of 10 nM insulin. Kaempferitrin (15 μM) also stimulates akt phosphorylation on ser473, and the stimulation can be blocked by a PI3-K inhibitor wortmannin. Kaempferitrin potently exerts the translocation of GLUT4 to the membrane of adipocytes at 15 μM, and this is suppressed by wortmannin. In addition, Kaempferitrin increases the total levels of Glu4 protein in differentiated cells and secreted adiponectin in mature 3T3-L1 adipocytes^[1]. Kaempferitrin is cytotoxic to human cancer cells such as HeLa and MDA-MB231 cells, with IC₅₀s of 45 ± 2.6 and 65 ± 2.6 μM, and shows low toxic effects on non-tumorigenic cells. Kaempferitrin (45 μM) induces apoptosis of HeLa cells after treatment for 24 and 48 h, and causes reactive oxygen species (ROS) generation in HeLa cells. Furthermore, Kaempferitrin (45 μM) exerts G1 arrest, causes the expression of proteins associated with intrinsic pathway of apoptosis and activates caspase 3 in HeLa cells^[2].

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

Kaempferitrin (2.5, 10 and 25 mg/kg, i.p.) markedly suppresses the growth of tumor by 40%, 87% and 97%, and decreases tumor weight by 37%, 81% and 95%, respectively in nu/nu mice bearing HeLa tumor. Kaempferitrin also inhibits cell proliferation and extends life span in mice bearing tumor^[2].

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

578.52

C₂₇H₃₀O₁₄

482-38-2

山奈苷

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

In Vitro: 

DMSO : 25 mg/mL (43.21 mM; Need ultrasonic)

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.08 mg/mL (3.60 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (3.60 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.08 mg/mL (3.60 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (3.60 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.08 mg/mL (3.60 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (3.60 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Tzeng YM, et al. Kaempferitrin activates the insulin signaling pathway and stimulates secretion of adiponectin in 3T3-L1 adipocytes. Eur J Pharmacol. 2009 Apr 1;607(1-3):27-34.

  [2]. Alonso-Castro AJ, et al. Kaempferitrin induces apoptosis via intrinsic pathway in HeLa cells and exerts antitumor effects. J Ethnopharmacol. 2013 Jan 30;145(2):476-89.

Viability assay is carried out by MTT assay. Preconfluent 3T3-L1 preadipocytes are seeded to reach confluence. Kaempferitrin is added in replacement of insulin immediately after confluence (day 0), and the viability is measured 3 h after addition of the compound. Another cell viability assay is performed at day 8. For kaempferitrin combined with insulin treatment, various concentrations of kaempferitrin are added simultaneously with 0.2 nM insulin from day 0 to day 8. Cells without insulin or kaempferitrin treatment during differentiation (day 0 to day 8) are used as control. Finally, to verify the cell viability in matured 3T3-L1 cells treated with insulin or kaempferitrin for 24-48 h, MTT are incubated for 3 h at the end of the 24 h and 48 h period of compound treatments, and survival rates calculated and compared to that without insulin or kaempferitrin^[1].

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

The nu/nu mice are injected subcutaneously in their backs with HeLa cells (1.5 × 10⁶). Four hours after tumor implantation, groups of five mice receive doses of Kaempferitrin between 2.5 to 25 mg/kg, dissolved in 0.1 mL of 0.9% saline solution, cisplatin (CDDP) 1 mg/kg or paclitaxel (PCX) 1 mg/kg injected intraperitoneally daily over a period of 32 days. The animal control group received 0.1 mL of vehicle solution. Tumors are measured using a vernier caliper, and their size in mm³ is calculated Tumor volume = lenght × width × height². At the end of the experiments, animals are sacrificed and their tumors are excised and weighed^[2].

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

• [1]. Tzeng YM, et al. Kaempferitrin activates the insulin signaling pathway and stimulates secretion of adiponectin in 3T3-L1 adipocytes. Eur J Pharmacol. 2009 Apr 1;607(1-3):27-34.

  [2]. Alonso-Castro AJ, et al. Kaempferitrin induces apoptosis via intrinsic pathway in HeLa cells and exerts antitumor effects. J Ethnopharmacol. 2013 Jan 30;145(2):476-89.