K-80003 is a potent inhibitor of tRXRα-dependent Akt activation and cancer cell growth.

When MCF-7 cells are cotreated with K-80003, TNFα-induced colocalization of tRXRα with p85α in the cytoplasm is inhibited, resulting in tRXRα nuclear localization. Western blotting shows that K-80003-stabilized tetrameric form of tRXRα is found exclusively in the nuclear fraction, while tRXRα monomer is distributed both in the nuclear and cytoplasmic fractions^[2].

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.

K-80003 is a potent inhibitor of AKT activation by all-trans-retinoic acid. K-80003 displays enhanced efficacy in inhibiting tRXRα-dependent AKT activation and tRXRα tumor growth in animals. K-80003 has high affinity to RXRα but lacks COX inhibitory activity^[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.

336.40

C₂₂H₂₁FO₂

1292821-90-9

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 : 30 mg/mL (89.18 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。-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: ≥ 3 mg/mL (8.92 mM); Clear solution

  此方案可获得 ≥ 3 mg/mL (8.92 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 30.0 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

• [1]. Zhou H, et al. NSAID sulindac and its analog bind RXRalpha and inhibit RXRalpha-dependent AKT signaling. Cancer Cell. 2010 Jun 15;17(6):560-73.

  [2]. Chen L, et al. Modulation of nongenomic activation of PI3K signalling by tetramerization of N-terminally-cleaved RXRα. Nat Commun. 2017 Jul 17;8:16066.

MCF-7 cells cotransfected with Myc-RXRα, Myc-tRXRα, tRXRα/L433D and p85α are pretreated with or without K-80003 (5 μM) for 3 h before exposed to TNFα (10 ng/mL) for 30 min. Cells are immunostained with anti-Myc and anti-p85α antibody, and their subcellular localization revealed by confocal microscopy. HEK293T cells cotransfected with Myc-tRXRα are treated with or without K-80003 (5 μM) for 6 h. Nuclear (N) and cytoplasmic (C) fractions are prepared, subjected to BS3 crosslinking, and analysed by western blotting using anti-Myc antibody. The purity of fractions is examined by analysing the expression of nuclear PARP and cytoplasmic α-tubulin in non-crosslinked fractions. One of three similar experiments is shown^[2].

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]
Nude mice (BALB/c, 4-5-week old) are injected subcutaneously with 100 μL of cells (2×10⁶). For drug treatment, mice (n=6) are treated intraperitoneally after 7 days of transplantation with Corn oil, Sulindac (60 mg/kg), or K-80003 (60 mg/kg) once every other day (six injections). Body weight and tumor sizes are measured every 4 days.

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]. Zhou H, et al. NSAID sulindac and its analog bind RXRalpha and inhibit RXRalpha-dependent AKT signaling. Cancer Cell. 2010 Jun 15;17(6):560-73.

  [2]. Chen L, et al. Modulation of nongenomic activation of PI3K signalling by tetramerization of N-terminally-cleaved RXRα. Nat Commun. 2017 Jul 17;8:16066.