DIM-C-pPhOCH₃ is a Nur77 agonist. Nerve growth factor-induced Bα (NGFI-Bα, Nur77) is an orphan nuclear receptor.

Nur77^[1]

DIM-C-pPhOCH₃ decreases survival and induces apoptosis in RKO colon cancer cells, and this is accompanied by induction of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) protein. DIM-C-pPhOCH₃ also induces Nur77-independent apoptosis. DIM-C-pPhOCH₃ (10 μM) inhibits cell growth after treatment for 24, 48, or 72 h, and the maximum inhibitory response is observed after 72 h, where there is considerable cell detachment and dead cells. The growth-inhibitory effects observed for DIM-C-pPhOCH₃ after 72 h are also accompanied by several markers of apoptosis, including PARP cleavage and cleavage of caspase-3, caspase-9, and caspase-8. PARP cleavage is also observed after treatment of RKO cells for 48 h with DIM-C-pPhOCH₃^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

DIM-C-pPhOCH₃ (25 mg/kg/d) also inhibits tumor growth in athymic nude mice bearing RKO cell xenografts. The effects of DIM-C-pPhOCH₃ (25 mg/kg/d) on colon tumor growth are also investigated in athymic nude mice bearing RKO cell xenografts. Treatment with the DIM-C-pPhOCH₃ significantly decreases tumor volumes and final tumor weights compared with corn oil controls^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

352.43

C₂₄H₂₀N₂O

33985-68-1

Room temperature in continental US; may vary elsewhere.

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

In Vitro: 

DMSO : ≥ 33.3 mg/mL (94.49 mM)

* “≥” means soluble, but saturation unknown.

*

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。-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: ≥ 2.5 mg/mL (7.09 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (7.09 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 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: ≥ 2.5 mg/mL (7.09 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (7.09 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 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

• [1]. Cho SD, et al. Nur77 agonists induce proapoptotic genes and responses in colon cancer cells through nuclear receptor-dependent and nuclear receptor-independent pathways. Cancer Res. 2007 Jan 15;67(2):674-83.

RKO cells are treated with DMSO or 12.5 μM DIM-C-pPhOCH₃ for 2 and 6 h. RNA is isolated for the reverse transcription-PCR (RT-PCR) experiment and analyzed for gene expression, and three replicates are determined for each time point and the DMSO control. The microarray data are analyzed^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Mice^[1]
Male athymic nude mice (Foxn1^nu, ages 7-8 weeks) are used. The mice are housed and maintained in laminar flow cabinets under specific pathogen-free conditions. A xenograft is established by s.c. injection of in vitro cultured RKO cells (5×10⁶ per 150 μL) into the flanks of individual mice. Tumors are allowed to grow for 4 days until tumors are palpable. Mice are then randomized into two groups of six mice per group and dosed by oral gavage with either corn oil or 25 mg/kg/d DIM-C-pPhOCH₃ for 21 days. The mice are weighed, and tumor size is measured^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Cho SD, et al. Nur77 agonists induce proapoptotic genes and responses in colon cancer cells through nuclear receptor-dependent and nuclear receptor-independent pathways. Cancer Res. 2007 Jan 15;67(2):674-83.