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

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 can be used for the research of american trypanosomiasis (chagas' disease) and immobilization-related bone loss.

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Aminobutane bisphosphonate

Aminobutane bisphosphonate Chemical Structure

CAS No. : 32545-60-1

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Aminobutane bisphosphonate Related Antibodies

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Description

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 can be used for the research of american trypanosomiasis (chagas' disease) and immobilization-related bone loss[1][2].

In Vitro

Aminobutane bisphosphonate (Compound 8) inhibits purified Trypanosoma cruzi farnesyl pyrophosphate synthase activity with an IC50 of 30.77 μM[1].
Aminobutane bisphosphonate (up to 100 μM) does not inhibit proliferation of Trypanosoma cruzi epimastigote forms at concentrations up to 100 μM, resulting in an IC50 > 100 μM[1].
Aminobutane bisphosphonate (85 μM) inhibits only 13% of Trypanosoma cruzi amastigote proliferation at 85 μM, resulting in an IC50 > 85 μM[1].

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

Aminobutane bisphosphonate Related Antibodies
In Vivo

Aminobutane bisphosphonate (Compound 8) (0.01-1.0 mg P per kg; s.c.; 2 consecutive days prior to surgery) inhibits immobilization-induced bone loss in male Sprague-Dawley rats in a dose-dependent manner, with the 0.10 mg P per kg dose eliminating trabecular bone volume differences between intact and immobilized limbs at 20 days and reducing the percentage difference in femoral ash weight/length to 7.0%[2].

MedChemExpress (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.
Molecular Weight

233.10

Formula

C4H13NO6P2
CAS No.
SMILES

O=P(O)(C(CCC)(P(O)(O)=O)N)O
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Aminobutane bisphosphonate Related Classifications

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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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