2. Metabolic Enzyme/Protease
  3. Farnesyl Transferase
  4. Aminobutane bisphosphonate

Aminobutane bisphosphonate 是一种克氏锥虫 (Trypanosoma cruzi) 法尼基焦磷酸合酶 (FPPS) 抑制剂，对克氏锥虫的 IC50 为 30.77 μM。Aminobutane bisphosphonate 可抑制细胞内无鞭毛体期克氏锥虫的增殖，且对非感染性上鞭毛体期无活性。Aminobutane bisphosphonate 可降低破骨细胞性骨吸收、类骨质表面积以及每毫米骨表面的破骨细胞数量。Aminobutane bisphosphonate 可改变大鼠完整腿部的矿物质沉积速率，抑制制动诱导的骨丢失，并增加大鼠的小梁骨体积。Aminobutane bisphosphonate 可用于美洲锥虫病 (恰加斯病) 和制动相关性骨丢失的研究。

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Aminobutane bisphosphonate

Aminobutane bisphosphonate Chemical Structure

CAS No. : 32545-60-1

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Aminobutane bisphosphonate 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Aminobutane bisphosphonate is a Trypanosoma cruzi farnesyl pyrophosphate synthase (FPPS) inhibitor with an IC50 of 30.77 μM against Trypanosoma cruzi. Aminobutane bisphosphonate inhibits proliferation of intracellular amastigote Trypanosoma cruzi and lacks activity against non-infective epimastigote forms. Aminobutane bisphosphonate reduces osteoclastic bone resorption, osteoid surface extent, and osteoclast number per mm of bone surface.Aminobutane bisphosphonate alters mineral apposition rate in intact legs, inhibits immobilization-induced bone loss, and increases trabecular bone volume in Sprague-Dawley rats. Aminobutane bisphosphonate can be used for the research of american trypanosomiasis (chagas' disease) and immobilization-related bone loss[1][2].

体外研究
(In Vitro)

Aminobutane bisphosphonate 可抑制纯化的克氏锥虫法尼基焦磷酸合酶的活性，其 IC50 为 30.77 μM[1]。
Aminobutane bisphosphonate (最高 100 μM) 在最高 100 μM 的浓度下不会抑制克氏锥虫上鞭毛体的增殖，其 IC50 > 100 μM[1]。
Aminobutane bisphosphonate (85 μM) 仅能抑制 13%的克氏锥虫无鞭毛体增殖，其 IC50 > 85 μM[1]。

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

Aminobutane bisphosphonate 相关抗体:
体内研究
(In Vivo)

Aminobutane bisphosphonate (0.01-1.0 mg P/kg；皮下注射；术前连续 2 天给药) 可呈剂量依赖性抑制雄性 Sprague-Dawley 大鼠制动诱导的骨丢失，其中 0.10 mg P per kg 剂量可在 20 天时消除完整肢体与制动肢体之间的骨小梁体积差异，并将股骨灰重/长度的百分比差异降至 7.0%[2]。

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

Animal Model: Sprague-Dawley (male, 250-280 g, immobilization-induced bone loss via unilateral sciatic neuroctomy)[2]
Dosage: 0.01 mg P per kg; 0.10 mg P per kg; 1.0 mg P per kg
Administration: s.c.; 2 consecutive days prior to surgery
Result: Increased femoral ash weight in both intact and immobilized limbs in a dose-dependent manner at 10 and 20 days post-surgery (p < 0.05) compared to vehicle controls.
Abolished the immobilization-induced decrease in femoral ash weight at 10 days with 0.10 mg P per kg dose.
Reduced the percentage difference in femoral ash weight/length between intact and immobilized limbs from 11.5% in vehicle controls to 7.0% with 0.10 mg P per kg and 4.8% with 1.0 mg P per kg at 20 days.
Reduced femoral length in both limbs from 36.6 mm to 35.6 mm (intact) and 36.4 mm to 35.6 mm (immobilized) at 20 days with 1.0 mg P per kg dose (p < 0.05).
Increased trabecular bone volume to 52.1% (intact) and 41.0% (immobilized) at 10 days with 0.10 mg P per kg dose, compared to 17.9% (intact) and 7.9% (immobilized) in vehicle controls (p < 0.05).
Increased trabecular bone volume in a dose-dependent manner at 20 days: 22.9% (intact) and 15.5% (immobilized) with 0.01 mg P per kg; 37.6% (intact) and 35.4% (immobilized) with 0.10 mg P per kg; 71.6% (intact) and 68.1% (immobilized) with 1.0 mg P per kg (all p < 0.05 vs vehicle).
Eliminated the difference in trabecular bone volume between intact and immobilized limbs at 20 days with 0.10 and 1.0 mg P per kg doses.
Reduced osteoclast number per mm trabecular surface in both limbs at 20 days with all doses compared to vehicle controls (p < 0.05), eliminating the difference between intact and immobilized limbs seen in vehicle controls.
Reduced eroded surface in both limbs at 20 days with 0.01 mg P per kg (12.1% intact, 12.3% immobilized) and 1.0 mg P per kg (16.1% intact, 15.8% immobilized), and in immobilized limbs with 0.10 mg P per kg (17.7%) compared to vehicle controls (p < 0.05).
Reduced osteoid surface to 0.4% (intact) and 0.1% (immobilized) at 10 days with 0.10 mg P per kg dose, compared to 6.0% (intact) and 2.4% (immobilized) in vehicle controls (p < 0.05).
Decreased osteoid surface in a dose-dependent manner at 20 days: 1.3% (intact) with 0.01 mg P per kg; 0.2% (intact) and 0.3% (immobilized) with 0.10 mg P per kg; 0.2% (intact) and 0.1% (immobilized) with 1.0 mg P per kg (all p < 0.05 vs vehicle).
Reduced mineral apposition rate in intact limbs by 14% (0.82 μm/day and 0.83 μm/day, respectively) with 0.10 and 1.0 mg P per kg doses compared to vehicle controls (0.97 μm/day; p < 0.05), but did not further reduce rates in immobilized limbs.
分子量

233.10

Formula

C4H13NO6P2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

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纯度 & 产品资料
参考文献

Aminobutane bisphosphonate 相关分类

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Keywords:

Aminobutane bisphosphonate32545-60-1Farnesyl TransferaseFtasefarnesyl pyrophosphate synthasetrabecular bone volumeTrypanosoma cruziSprague-Dawley ratsosteoclastic bone resorptionamerican trypanosomiasisepimastigotechagas' diseaseosteoid surface extentintracellular amastigoteInhibitorinhibitorinhibit

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