Colchicine is a tubulin inhibitor and a microtubule disrupting agent. Colchicine inhibits microtubule polymerization with an IC₅₀ of 3 nM^[1][2][3]. Colchicine is also a competitive antagonist of the α3 glycine receptors (GlyRs)^[4].

Microtubule/Tubulin^[1]

Exposure to 1μM Colchicine, a microtubule disrupting agent, triggered apoptosis in rat cerebellar granule cells (CGC). Colchicine treatment also causes alterations in Ca²⁺ responses to chemical depolarization and a moderate, but progressive, increase in the resting intracellular Ca²⁺ concentration^[1]. Colchicine exerts its biological effects through binding to the soluble tubulin heterodimer, the major component of the microtubule. The Colchicine binding abilities of tubulins from a variety of sources are summarized, and the mechanism of Colchicine binding to brain tubulin is explored in depth. The relationship between colchicinoid structure and tubulin binding activity provides insight into the structural features of Colchicine responsible for high affinity binding to tubulin and is reviewed for analogs in the Colchicine series. The thermodynamic and kinetic aspects of the association are described and evaluated in terms of the binding mechanism. Colchicine binding to tubulin results in unusual alterations in the low energy electronic spectra of Colchicine. The spectroscopic features of Colchicine bound to tubulin are discussed in terms of the nature of the Colchicine-tubulin complex. Attempts to locate the high affinity Colchicine binding site on tubulin are presented^[2]. Colchicine treatment inhibits indomethacin-induced small intestinal injury by 86% (1 mg/kg) and 94% (3 mg/kg) as indicated by the lesion index 24 h after indomethacin administration. Colchicine inhibits the protein expression of cleaved caspase-1 and mature IL-1β, without affecting the mRNA expression of NLRP3 and IL-1β^[3].

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

Vehicle or Colchicine (1 mg/kg) is administered orally 30 min prior to indomethacin administration. The lesions stained with Evans blue in the small intestine are smaller in Colchicine-treated mice than those in vehicle-treated mice 24 h after indomethacin administration. In addition, histological examination shows that Colchicine-treated mice have less mucosal inflammation and ulceration and a decrease in the size and numbers of lesions compared with vehicle-treated mice. Colchicine treatment significantly reduces the lesion index at doses of 1 mg/kg and 3 mg/kg (by 86% and 94%, respectively) compared with vehicle treatment. Colchicine treatment significantly inhibits the protein levels of mature IL-1β at doses of 1 mg/kg and 3 mg/kg (by 56% and 69%, respectively) without affecting those of pro-IL-1β. Colchicine treatment also significantly inhibits the protein levels of cleaved caspase-1 at doses of 1 mg/kg and 3 mg/kg (by 26% and 39%, respectively) without affecting those of pro-caspase-1^[3].

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

399.44

C₂₂H₂₅NO₆

64-86-8

秋水仙素；秋水仙碱

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 48 mg/mL (120.17 mM)

H₂O : ≥ 33.33 mg/mL (83.44 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。

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： PBS

  Solubility: 2.78 mg/mL (6.96 mM); Clear solution; Need ultrasonic and warming and heat to 60°C

• [1]. Bonfoco E, et al. Colchicine induces apoptosis in cerebellar granule cells. Exp Cell Res. 1995 May;218(1):189-200.

  [2]. Hastie SB. Interactions of colchicine with tubulin. Pharmacol Ther. 1991;51(3):377-401

  [3]. Otani K, et al. Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome. Sci Rep. 2016 Sep 2;6:32587.

  [4]. Carola Muñoz-Montesino, et al. Inhibition of the Glycine Receptor alpha 3 Function by Colchicine. Front Pharmacol. 2020 Jul 30;11:1143.

Mice^[3]
Specific-pathogen-free 8-week-old male mice are used. Wild-type C57BL/6 mice and NLRP3^−/− mice on a C57BL/6 background are used. To examine the effects of Colchicine on NSAID-induced small intestinal injury, vehicle or Colchicine (1 or 3 mg/kg) is administered orally 30 min prior to indomethacin administration. Mice received intraperitoneal injections of sterilized phosphate buffered saline or mouse recombinant IL-1β (0.1 μg/kg) 3 h after indomethacin treatment. Vehicle or Colchicine (1 or 3 mg/kg) is also administered to NLRP3^−/− mice before indomethacin administration. The lesion index is evaluated 24 h after indomethacin administration, and examined mRNA and protein expression of inflammasome components 6 h after indomethacin administration.

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

• [1]. Bonfoco E, et al. Colchicine induces apoptosis in cerebellar granule cells. Exp Cell Res. 1995 May;218(1):189-200.

  [2]. Hastie SB. Interactions of colchicine with tubulin. Pharmacol Ther. 1991;51(3):377-401

  [3]. Otani K, et al. Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome. Sci Rep. 2016 Sep 2;6:32587.

  [4]. Carola Muñoz-Montesino, et al. Inhibition of the Glycine Receptor alpha 3 Function by Colchicine. Front Pharmacol. 2020 Jul 30;11:1143.