| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
Miro1 Reducer targets Miro1 (mitochondrial Rho GTPase 1), a protein that plays a critical role in mitochondrial dynamics and transport. Miro1 is a mitochondrial outer membrane protein that is involved in the regulation of mitochondrial movement along microtubules and in the maintenance of mitochondrial quality control through mitophagy. In Parkinson's disease, defects in Miro1 function and mitophagy have been observed. By promoting the proteasomal degradation of Miro1, Miro1 Reducer reduces Miro1 protein levels and repairs the delayed mitophagy phenotype in PD fibroblasts. The compound's ability to modulate Miro1 levels makes it a valuable tool for studying the role of Miro1 in mitochondrial dysfunction and Parkinson's disease pathogenesis.
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| ln Vitro |
In vitro, Miro1 Reducer reduces Miro1 protein levels in a dose-dependent manner with an IC50 of 7.8 μM in fibroblasts from Parkinson's disease patients. The compound promotes the proteasomal degradation of Miro1 and can repair the defect of Miro1 in Parkinson's disease fibroblasts. Miro1 Reducer reduces the delayed mitophagy phenotype in PD fibroblasts. These activities demonstrate the compound's ability to modulate mitochondrial quality control pathways that are impaired in Parkinson's disease. The compound's effects on Miro1 levels and mitophagy can be assessed by Western blot analysis and by measuring mitochondrial function and autophagy markers. However, specific quantitative data beyond the IC50 have not been extensively reported.
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| ln Vivo |
In vivo activity data for Miro1 Reducer are not available in the current scientific literature. As a small molecule that modulates Miro1 degradation and mitophagy, the compound would be expected to have potential for in vivo studies in models of Parkinson's disease and other mitochondrial disorders. However, specific animal model studies, dosing regimens, and quantitative outcomes have not been reported. The compound's ability to cross the blood-brain barrier and its pharmacokinetic properties would be important considerations for in vivo applications. Further in vivo studies would be required to characterize its efficacy, safety, and pharmacokinetic properties in animal models of Parkinson's disease.
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| Enzyme Assay |
In vitro enzyme or receptor binding assay protocols are not directly applicable to Miro1 Reducer, as its mechanism involves promoting the degradation of a protein rather than inhibiting an enzyme. However, its activity can be assessed by measuring Miro1 protein levels. A standard protocol would involve treating fibroblasts from Parkinson's disease patients with varying concentrations of Miro1 Reducer (typically 0.1-100 μM) for a defined period (e.g., 24-72 hours). Cells are harvested, and Miro1 protein levels are assessed by Western blot analysis using anti-Miro1 antibodies. The reduction in Miro1 levels is quantified and IC50 values are determined from concentration-response curves. Mitophagy can be assessed by measuring mitochondrial mass, autophagy markers (e.g., LC3-II), and mitochondrial function using Seahorse or other assays.
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| Cell Assay |
In vitro cell-based assay protocols for Miro1 Reducer typically involve treating fibroblasts from Parkinson's disease patients with the compound to assess its effects on Miro1 degradation and mitophagy. A standard protocol would involve seeding PD fibroblasts in multi-well plates and treating them with varying concentrations of Miro1 Reducer (typically 0.1-100 μM) for 24-72 hours. Miro1 protein levels are assessed by Western blot. Mitophagy is assessed by measuring mitochondrial mass using MitoTracker dyes, assessing autophagy markers (LC3-II, p62) by Western blot, and measuring mitochondrial membrane potential and oxygen consumption rate. Cell viability is assessed using MTT or similar assays to ensure that observed effects are not due to cytotoxicity. Appropriate controls include vehicle-treated cells and cells from healthy donors for comparison.
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| Animal Protocol |
In vivo animal experimental protocols for Miro1 Reducer have not been reported in the available literature. Based on its mechanism of action and relevance to Parkinson's disease, potential studies might involve using mouse models of Parkinson's disease, such as MPTP-treated mice or transgenic models. A hypothetical protocol would involve administering Miro1 Reducer via oral gavage, intraperitoneal injection, or other routes at doses determined from preliminary pharmacokinetic and tolerability studies. Treatment would typically be administered daily for 2-4 weeks. Endpoints would include assessment of Miro1 levels and mitophagy in brain tissue, evaluation of dopaminergic neuron survival, assessment of motor function using behavioral tests (e.g., rotarod, open field), and measurement of mitochondrial function.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of Miro1 Reducer have not been characterized in published studies. The compound has a molecular weight of 425.85 and a molecular formula of C20H17ClFN7O. Specific PK parameters such as half-life, Cmax, AUC, bioavailability, volume of distribution, and clearance have not been reported. The compound's ability to cross the blood-brain barrier, which is critical for CNS applications, has not been assessed. The compound's metabolism, protein binding, and routes of elimination remain to be characterized. Further pharmacokinetic studies would be required to understand its absorption, distribution, metabolism, and excretion profile.
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| References | |
| Additional Infomation |
Miro1 Reducer is a research-grade compound that promotes the proteasomal degradation of Miro1 (mitochondrial Rho GTPase 1). It reduces Miro1 protein levels in a dose-dependent manner with an IC50 of 7.8 μM in Parkinson's disease fibroblasts. The compound can repair the defect of Miro1 and reduce the delayed mitophagy phenotype in PD fibroblasts. It is used in research on Parkinson's disease and mitochondrial dysfunction. Miro1 Reducer has not entered clinical trials and is not approved for any therapeutic indication. Its mechanism of action involves promoting the degradation of Miro1, modulating mitochondrial quality control pathways. The compound is available exclusively for research purposes and is not intended for diagnostic, therapeutic, or human applications.
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| Exact Mass |
425.117
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| CAS # |
2624336-91-8
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| PubChem CID |
154828685
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| Appearance |
Off-white to yellow solid powder
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
30
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| Complexity |
531
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| Defined Atom Stereocenter Count |
0
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| SMILES |
C1=CC(=CC(=C1)F)NC(=O)NC2=CC=C(C=C2)NC3=CC(=NC=N3)N4C=CN=C4.Cl
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| InChi Key |
UKXRHSHXZHFFTA-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C20H16FN7O.ClH/c21-14-2-1-3-17(10-14)27-20(29)26-16-6-4-15(5-7-16)25-18-11-19(24-12-23-18)28-9-8-22-13-28;/h1-13H,(H,23,24,25)(H2,26,27,29);1H
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| Chemical Name |
1-(3-fluorophenyl)-3-[4-[(6-imidazol-1-ylpyrimidin-4-yl)amino]phenyl]urea;hydrochloride
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :~42.58 mg/mL (~99.99 mM; with heating and sonication.)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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