Arundic Acid
Based on 2 publication(s) in Google Scholar
Arundic Acid (ONO-2506; (R)-2-Propyloctanoic acid) is an orally active astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of astrocytic glutamate transporter EAAT1 by activating the ERK, Akt, and NF-κB pathways. Arundic Acid reduces retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid downregulates IL-1β, TNF-α, and ROS in a rat model of intracerebral hemorrhage, alleviating neuroinflammation, improving motor dysfunction, and reducing neuronal damage. Arundic Acid downregulates neuroinflammation and astrocyte dysfunction following status epilepticus in juvenile rats. Arundic Acid is used for research on Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage, and epilepsy.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Pureté : 98.0%
- CAS No.: 185517-21-9
- Formule: C11H22O2
- Masse moléculaire:186.29
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Stockage:Pure form -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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HY-107661R
Arundic Acid (Standard)Reference Standard -
HY-P1240
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TCS PrP Inhibitor 13PrP C Inhibitor -
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HY-P1038
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HY-107662R
TCS PrP Inhibitor 13 (Standard)Reference Standard
Publications Citing Use of MedChemExpress (MCE) Arundic Acid
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Activité biologique
Description
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COX-2 |
TNF-α |
IL-1β |
In Vitro
Arundic acid (0-100 μM; 3-24 h) enhances the promoter activity of EAAT1/EAAT2 in the human astrocytic H4 cell line[1].
Arundic acid (6.25-100 μM; 24 h) mediates the upregulation of EAAT1 promoter activity, mRNA and protein levels, and glutamate uptake function in human astrocytic H4 cells via the Akt, ERK and NF-κB pathways[1].
Arundic acid (50 μM; 3-24 h) activates the NF-κB pathway in human astrocyte H4 cells by reducing the cytoplasmic level of IκBα and inducing nuclear translocation of NF-κB p65[1].
Arundic acid (50 μM; 5 min-24 h) activates the Akt and ERK signaling pathways within 5 min of treatment[1].
Arundic acid (50 μM; 24 h) attenuates Mn-induced inhibition of EAAT1 expression by suppressing Mn-activated YY1 expression in human astrocyte H4 cells[1].
Arundic acid (100 μM; 14 days) enhances the glutamate uptake rate of primary cultured mouse Müller cells by increasing Vmax without altering glutamate affinity[2].
Arundic acid (0-100 μM; 14 days) upregulates the expression of GLAST mRNA in primary cultured mouse Müller cells[2].
Arundic acid modulates multiple astrocyte activation responses in cultured rat cerebral astrocytes, including inhibition of S-100β upregulation and pro-inflammatory gene expression, without altering GFAP levels[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Primary cultured mouse Müller cells
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Concentration:0, 12.5, 25, 50, 100 μM
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Incubation Time:14 days
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Result:Increased endogenous GLAST mRNA expression.
Detected GLAST mRNA induction as early as 24 h post-treatment.
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Cell Line:human astrocyte H4
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Concentration:0, 6.25, 12.5, 25, 50, 100 μM
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Incubation Time:24 h
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Result:Increased EAAT1 protein expression.
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Cell Line:human astrocyte H4
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Concentration:50 μM
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Incubation Time:0, 6, 12, 24 h
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Result:Enhanced NF-κB reporter gene activity and reduced IκBα levels in cytoplasmic components
In Vivo
Arundic acid (30 mg/kg; i.p.; 5 post-MPTP doses) protects dopaminergic neurons in mice from the neurotoxicity of MPTP (HY-W114750) in the MPTP-induced Parkinson's disease mouse model, maintains 52% of dopamine levels in the striatum and 44% of dopaminergic neurons in the substantia nigra, and ameliorates motor function deficits[3].
Arundic acid (0.02-20 μg/μL; i.c.v.; single dose) reduces the levels of S100B and GFAP in the striatum of healthy male Wistar rats[4].
A single intracerebroventricular (i.c.v.) dose of Arundic acid (2 μg/μL) reverses intracerebral hemorrhage (ICH)-induced neurological deficits, reduces striatal lesion volume, inhibits reactive astrogliosis, prevents neuronal apoptosis, normalizes central and peripheral S100B levels, and enhances early antioxidant defense capacity in male Wistar rats[4].
Arundic acid (10 mg/kg; i.p.; single injection; 6 h or 24 h post-SE induction) exerts neuroprotective effects on rats with lithium-pilocarpine-induced status epilepticus (SE) by alleviating hippocampal neuroinflammation, reversing astrocytic dysfunction, restoring glutamate homeostasis and improving glucose uptake, with administration at 24 h post-SE induction showing more stable efficacy across all endpoint indicators[5].
Arundic Acid (2 μg/μL; i.c.v.; single dose; administered immediately before ICH induction) attenuates neuroinflammation and prevents motor dysfunction in collagenase-induced intracerebral hemorrhage rats by reducing S100B, astrogliosis, microglial activation, pro-inflammatory cytokines, and ROS[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (backcrossed for ≥10 generations; GLAST heterozygous; postnatal day 22 to 35)[2]
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Dosage:10 mg/kg
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Administration:p.o.; daily; 14 days
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Result:Increased retinal GLAST mRNA levels relative to vehicle controls.
Increased retinal GLAST protein expression relative to vehicle controls.
Increased retinal glutamate uptake velocity by 1.23-fold relative to vehicle-treated GLAST+/- mice.
Increased GCL neuron count to 438 cells per retina, compared with 366 cells in vehicle-treated GLAST+/- mice.
Showed no effect on glutamate uptake in GLAST-/- mice.
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Animal Model:C57BL/6 (male, 10 weeks old, 22-28 g, MPTP-induced Parkinson’s disease)[3]
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Dosage:30 mg/kg
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Administration:i.p.; 5 doses at 1 minute, 6 h, 24 h, 48 h, 72 h after last MPTP injection
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Result:Preserved striatal dopamine levels at 52% of normal control values.
Preserved striatal DOPAC and HVA levels at 47% and 60% of normal control values, respectively.
Significantly reduced motor function deficits in the pole test (T-turn and T-LA) and catalepsy test.
Preserved the number of tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra pars compacta at 42% of normal control values 3 days after MPTP injection and 44% of normal control values 7 days after MPTP injection.
Induced earlier appearance of GFAP-positive reactive astrocytes (by 3 days post-MPTP) compared to MPTP-only mice, with GFAP immunoreactivity comparable to MPTP-only mice at 7 days.
Reduced S-100 immunoreactivity in the substantia nigra at 3 days and in the striatum at 7 days post-MPTP compared to MPTP-only mice.
Showed no significant effect on microglial activation relative to MPTP-only mice.
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Animal Model:Wistar rats (adult male, 90 days-old, 300-350 g)[4]
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Dosage:0.02 μg/μL; 0.2 μg/μL; 2 μg/μL; 20 μg/μL
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Administration:i.c.v.; single dose
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Result:Significantly reduced striatal S100B immunocontent at 0.2 μg/μL and 2 μg/μL doses compared to control groups.
Significantly reduced striatal GFAP immunocontent at 2 μg/μL dose compared to control groups.
Showed no inhibitory effect on either S100B or GFAP levels at 20 μg/μL dose.
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Animal Model:Wistar rats (adult male, 90 days-old, 300-350 g, intracerebral hemorrhage induced by intrastriatal injection of type-IV collagenase)[4]
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Dosage:2 μg/μL
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Administration:i.c.v.; single dose; administered immediately before ICH induction
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Result:Reversed motor dysfunction completely at 7 days post-injury, with neurological scores and significantly.
Reduced striatal lesion volume significantly at 7 days post-injury.
Lowered striatal GFAP and S100B fluorescence intensity and immunostained surface area significantly at 7 days post-injury.
Increased NeuN fluorescence intensity and number of NeuN-positive cells significantly at 7 days post-injury.
Decreased cleaved caspase-3 fluorescence intensity and number of cleaved caspase-3-positive cells significantly at 7 days post-injury.
Lowered striatal GFAP levels significantly at 7 days post-injury.
Lowered striatal S100B levels significantly at 7 days post-injury; lowered cerebrospinal fluid S100B levels significantly at 72 hours post-injury; lowered serum S100B levels significantly at 24 hours and 7 days post-injury.
Increased striatal GSH levels significantly at 24 hours post-injury.
Decreased striatal GS activity significantly at 24 hours post-injury.
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Animal Model:Wistar rats (male, postnatal day 27)[5]
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Dosage:10 mg/kg (6 h post-SE induction); 10 mg/kg (24 h post-SE induction)
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Administration:i.p.; single injection
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Result:Partially reversed elevated hippocampal IL-1β levels, abolished elevated hippocampal TLR4 protein expression, partially reversed elevated hippocampal COX2 protein expression, increased hippocampal TGF-β levels, and did not alter TNF-α, RAGE, or Iba1 levels at 6 h post-SE.
Prevented elevated hippocampal IL-1β levels, decreased hippocampal TNF-α levels, prevented elevated hippocampal RAGE and TLR4 protein expression, completely abolished elevated hippocampal COX2 protein expression, partially reversed elevated hippocampal Iba1 levels, and increased hippocampal TGF-β levels at 24 h post-SE.
Prevented elevated hippocampal GFAP levels at 6 h and 24 h post-SE.
Partially reversed elevated hippocampal S100B levels, reversed reduced hippocampal connexin-43 (Cx-43) protein expression, partially reversed elevated CSF S100B levels, and partially reversed reduced serum S100B levels at 6 h post-SE.
Abolished elevated hippocampal S100B levels, and did not alter reduced hippocampal Cx-43 levels or CSF/serum S100B levels at 24 h post-SE.
Reversed reduced hippocampal GLAST protein expression, partially reversed reduced hippocampal GLT1 protein expression, reversed increased hippocampal glutamate uptake, did not alter reduced hippocampal GSH levels, partially reversed reduced hippocampal glutamine synthetase (GS) activity, and reversed reduced hippocampal GS protein expression at 6 h post-SE.
Partially reversed reduced hippocampal GLAST protein expression, partially reversed reduced hippocampal GLT1 protein expression, reversed increased hippocampal glutamate uptake, prevented reduced hippocampal GSH levels, did not alter reduced hippocampal GS activity, and reversed reduced hippocampal GS protein expression at 24 h post-SE.
Abolished reduced hippocampal glucose uptake, and did not alter hippocampal GLUT1 protein expression at 6 h and 24 h post-SE.
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Animal Model:Wistar (male, approximately 90 days old, 300-350 g)[6]
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Dosage:2 μg/μL; dose weight × 0.005
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Administration:i.c.v. injection into the left lateral ventricle; single; immediately before ICH induction
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Result:At 72 h, right forelimb and hindlimb placement error percentages were lower and forelimb/hindlimb step scores were higher than in ICH.
At 7 days, forelimb and hindlimb error deficits were reversed relative to ICH, with step quality better than ICH and similar to VEH.
In the grip strength test, no loss of forelimb strength occurred at 72 h and values remained similar to VEH; at 7 days, both ICH groups showed recovery with no difference between groups.
At 72 h, GFAP increased in both ICH groups versus VEH with no difference between groups; S100B increased in both ICH groups versus VEH but was lower than in ICH.
At 7 days, GFAP and S100B remained elevated in ICH but were reduced to levels similar to VEH.
CD11b increased in both ICH groups at 72 h versus VEH and was lower than in ICH; at 7 days, CD11b remained elevated in ICH but was lower and similar to VEH.
TNF-α did not differ at 24 h or 72 h; at 7 days, ICH increased TNF-α versus VEH, and TNF-α was reduced versus ICH to a level similar to control.
IL-1β did not differ at 24 h; at 7 days, IL-1β increased in ICH but not in the other ICH group, which remained similar to VEH.
DCF oxidation did not increase at 24 h; at 72 h, both ICH groups increased ROS versus VEH; at 7 days, only ICH increased ROS, while ROS was reduced versus ICH and was similar to VEH.
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Chemical Information
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CAS No. 185517-21-9
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Appearance Liquid (Density: 0.908 g/cm3)
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Masse moléculaire 186.29
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Formule C11H22O2
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Color Colorless to light yellow
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SMILES
CCCCCC[C@H](C(O)=O)CCC
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Synonyms
ONO-2506; (R)-2-Propyloctanoic acid
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Pure form -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (2)
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Journal Impact Factor
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Most Recent
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Int Immunopharmacol
2021 Aug:97:107792. PMID: 34051593 -
Behav Brain Res
Overexpression of S100B promotes depressive-like behaviors in stroke-induced rats by modulating the PI3K/AKT/NF-κB pathway. [Abstract]2025 Jun 25:488:115597. PMID: 40250529
Solvant et solubilité
In Vitro:
DMSO : 100 mg/mL (536.80 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 3.75 mg/mL (20.13 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 3.75 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (37.5 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 3.75 mg/mL (20.13 mM); Clear solution
This protocol yields a clear solution of ≥ 3.75 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (37.5 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Pureté et documentation
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Fiche technique (300 KB)
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SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
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- Italian - IT (396 KB)
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- Portuguese - PT (396 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Karki P, et al. Arundic Acid Increases Expression and Function of Astrocytic Glutamate Transporter EAAT1 Via the ERK, Akt, and NF-κB Pathways. Mol Neurobiol. 2018;55(6):5031-5046. [Content Brief]
[2]. Yanagisawa M, et al. Arundic acid attenuates retinal ganglion cell death by increasing glutamate/aspartate transporter expression in a model of normal tension glaucoma. Cell Death Dis. 2015;6(3):e1693. Published 2015 Mar 19. [Content Brief]
[3]. Kato H, et al. Arundic acid, an astrocyte-modulating agent, protects dopaminergic neurons against MPTP neurotoxicity in mice. Brain Res. 2004;1030(1):66-73. [Content Brief]
[4]. Cordeiro JL, et al. Arundic Acid (ONO-2506), an Inhibitor of S100B Protein Synthesis, Prevents Neurological Deficits and Brain Tissue Damage Following Intracerebral Hemorrhage in Male Wistar Rats. Neuroscience. 2020 Aug 1;440:97-112. [Content Brief]
[5]. Vizuete AFK, et al. Arundic acid (ONO-2506) downregulates neuroinflammation and astrocyte dysfunction after status epilepticus in young rats induced by Li-pilocarpine. Prog Neuropsychopharmacol Biol Psychiatry. 2023;123:110704. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 5.3680 mL | 26.8399 mL | 53.6797 mL | 134.1994 mL |
| 5 mM | 1.0736 mL | 5.3680 mL | 10.7359 mL | 26.8399 mL | |
| 10 mM | 0.5368 mL | 2.6840 mL | 5.3680 mL | 13.4199 mL | |
| 15 mM | 0.3579 mL | 1.7893 mL | 3.5786 mL | 8.9466 mL | |
| 20 mM | 0.2684 mL | 1.3420 mL | 2.6840 mL | 6.7100 mL | |
| 25 mM | 0.2147 mL | 1.0736 mL | 2.1472 mL | 5.3680 mL | |
| 30 mM | 0.1789 mL | 0.8947 mL | 1.7893 mL | 4.4733 mL | |
| 40 mM | 0.1342 mL | 0.6710 mL | 1.3420 mL | 3.3550 mL | |
| 50 mM | 0.1074 mL | 0.5368 mL | 1.0736 mL | 2.6840 mL | |
| 60 mM | 0.0895 mL | 0.4473 mL | 0.8947 mL | 2.2367 mL | |
| 80 mM | 0.0671 mL | 0.3355 mL | 0.6710 mL | 1.6775 mL | |
| 100 mM | 0.0537 mL | 0.2684 mL | 0.5368 mL | 1.3420 mL |
Arundic Acid Related Classifications
HY-107661 Related Classifications
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Keywords
- Arundic Acid
- 185517-21-9
- ONO-2506
- (R)-2-Propyloctanoic acid
- ONO2506
- ONO 2506
- ERK
- Akt
- NF-κB
- EAAT
- COX
- Reactive Oxygen Species (ROS)
- TNF Receptor
- Interleukin Related
- Extracellular signal regulated kinases
- PKB
- Protein kinase B
- Nuclear factor-κB
- Nuclear factor-kappaB
- Excitatory amino acid transporter
- Glutamate transporter
- Cyclooxygenase
- Tumor Necrosis Factor Receptor
- TNFR
- IL
- astrocyte function modulator
- neuroprotective agent
- Parkinson's disease
- cerebral ischemia
- glaucoma
- intracerebral hemorrhage
- epilepsy
- H4 cell
- C57BL/6J mice
- Wistar rats
- Inhibitor
- inhibitor
- inhibit