Art. -Nr.: HY-107661

Arundic Acid

(Synonyms: ONO-2506; (R)-2-Propyloctanoic acid)

2 Cited Publications

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Based on 2 publication(s) in Google Scholar

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates 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 is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.

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Reinheit: 98.0%
CAS. Nr.: 185517-21-9
Formel: C₁₁H₂₂O₂
Molecular Weight:186.29

Speicherung:

Pure form -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

Arundic Acid Chemical Structure

CAS. Nr.: 185517-21-9

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Biologische Aktivität
- Beschreibung
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (2)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Bioz

Biologische Aktivität

Beschreibung

Alle ERK Isoform-spezifische Produkte anzeigen :

Alle Akt Isoform-spezifische Produkte anzeigen :

Alle NF-κB Isoform-spezifische Produkte anzeigen :

Alle EAAT Isoform-spezifische Produkte anzeigen :

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 V_max 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.

Real Time qPCR^[2]

Cell Line:

Primary cultured mouse Müller cells
Concentration:

0, 12.5, 25, 50, 100 μM
Incubation Time:

14 days
Result:

Increased endogenous GLAST mRNA expression.
Detected GLAST mRNA induction as early as 24 h post-treatment.

Western Blot Analysis^[1]

Cell Line:

human astrocyte H4
cell
Concentration:

0, 6.25, 12.5, 25, 50, 100 μM
Incubation Time:

24 h
Result:

Increased EAAT1 protein expression.

Western Blot Analysis^[1]

Cell Line:

human astrocyte H4
cell
Concentration:

50 μM
Incubation Time:

0, 6, 12, 24 h
Result:

Enhanced NF-κB reporter gene activity and reduced IκBα levels in cytoplasmic components

In Vivo

Arundic acid (10 mg/kg; p.o.; daily; 14 days) upregulates retinal GLAST expression, enhances glutamate uptake, and increases the retinal ganglion cell count by approximately 19.7% in GLAST heterozygous mice with normal-tension glaucoma-like degeneration^[2].
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].

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

Animal Model:

C57BL/6J (backcrossed for ≥10 generations; GLAST heterozygous; postnatal day 22 to 35)^[2]
Dosage:

10 mg/kg
Administration:

p.o.; daily; 14 days
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.

Animal Model:

C57BL/6 (male, 10 weeks old, 22-28 g, MPTP-induced Parkinson’s disease)^[3]
Dosage:

30 mg/kg
Administration:

i.p.; 5 doses at 1 minute, 6 h, 24 h, 48 h, 72 h after last MPTP injection
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.

Animal Model:

Wistar rats (adult male, 90 days-old, 300-350 g)^[4]
Dosage:

0.02 μg/μL; 0.2 μg/μL; 2 μg/μL; 20 μg/μL
Administration:

i.c.v.; single dose
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.

Animal Model:

Wistar rats (adult male, 90 days-old, 300-350 g, intracerebral hemorrhage induced by intrastriatal injection of type-IV collagenase)^[4]
Dosage:

2 μg/μL
Administration:

i.c.v.; single dose; administered immediately before ICH induction
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.

Animal Model:

Wistar rats (male, postnatal day 27)^[5]
Dosage:

10 mg/kg (6 h post-SE induction); 10 mg/kg (24 h post-SE induction)
Administration:

i.p.; single injection
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.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS. Nr. 185517-21-9
Appearance Liquid (Density: 0.908 g/cm³)
Molecular Weight 186.29
Formel C₁₁H₂₂O₂
Color Colorless to light yellow
SMILES

CCCCCC[C@H](C(O)=O)CCC
Synonyms

ONO-2506; (R)-2-Propyloctanoic acid
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

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

Int Immunopharmacol

Glycolipid toxicity induces osteogenic dysfunction via the TLR4/S100B pathway. [Abstract]

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 Apr 16:115597. PMID: 40250529

Lösungsmittel & Löslichkeit

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)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

5.3680 mL

26.8399 mL

53.6797 mL

5 mM

1.0736 mL

5.3680 mL

10.7359 mL

10 mM

0.5368 mL

2.6840 mL

5.3680 mL

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.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

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.

Protocol 1

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.

Protocol 2

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.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 3.75 mg/mL (20.13 mM); Clear solution

This protocol yields a clear solution of ≥ 3.75 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (37.5 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
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

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (288 KB)
SDS (396 KB)
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COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
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OR (2659 KB)
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Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[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]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

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

2 Cited Publications

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Arundic Acid

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Publications Citing Use of MedChemExpress (MCE) Arundic Acid

Alle ERK Isoform-spezifische Produkte anzeigen

Alle Akt Isoform-spezifische Produkte anzeigen

Alle NF-κB Isoform-spezifische Produkte anzeigen

Alle EAAT Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Publications (2)

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

Arundic Acid Related Classifications

Art. -Nr.: HY-107661