10-Hydroxydecanoic acid significantly and dose-dependently inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW264 murine macrophages, with inhibition observed at concentrations between 0.5 and 5 mM over a 24-hour period.[1]
10-Hydroxydecanoic acid (5 mM) inhibited LPS-induced NO production in a time-dependent manner over 8 to 24 hours.[1]
10-Hydroxydecanoic acid (5 mM) did not affect LPS-induced production of tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6).[1]
10-Hydroxydecanoic acid markedly decreased LPS-induced iNOS mRNA expression, as shown by semi-quantitative RT-PCR, with peak inhibition observed at 12 hours post-stimulation.[1]
10-Hydroxydecanoic acid significantly and dose-dependently inhibited LPS-induced activation of the iNOS gene promoter in a luciferase reporter assay.[1]
10-Hydroxydecanoic acid did not decrease LPS-induced mRNA expression of various cytokines and chemokines, including TNF-α, IL-6, IP-10, MCP-1, MIP-1α, and MIP-2.[1]
10-Hydroxydecanoic acid (2–5 mM) significantly inhibited LPS-induced activation of an interferon-stimulated response element (ISRE)-dependent reporter gene but did not affect NF-κB-dependent reporter gene activation.[1]
10-Hydroxydecanoic acid (5 mM) did not reduce, and even slightly increased, LPS-induced interferon-β (IFN-β) mRNA expression.[1]
10-Hydroxydecanoic acid (5 mM) abolished NO production induced by recombinant IFN-β stimulation.[1]
10-Hydroxydecanoic acid (5 mM) did not affect LPS-induced phosphorylation of STAT1 at Tyr701 and Ser727 or STAT2 at Tyr689 but markedly inhibited the de novo synthesis of interferon regulatory factor-1 (IRF-1) protein.[1]
10-Hydroxydecanoic acid (5 mM) did not inhibit the increase in total IRF-1 mRNA levels after LPS stimulation but significantly decreased the level of IRF-1 mRNA present in the polysomal (actively translating) fraction.[1]
10-Hydroxydecanoic acid (5 mM) also decreased the polysomal mRNA level of IP-10 but not of TNF-α, IFN-β, MCP-1, or MIP-1α.[1]
10-Hydroxydecanoic acid (5 mM) inhibited LPS-induced phosphorylation of Akt at Ser473.[1]
10-Hydroxydecanoic acid (5 mM) inhibited LPS-induced hyperphosphorylation of 4E-BP1 (decrease in γ isoform, increase in β isoform) and reduced phosphorylation at Ser65, Thr70, and Thr37/46 residues.[1]

For nitrite determination (a measure of NO production), RAW264 cells were seeded in 96-well plates. Cells were preincubated with or without various concentrations of 10-Hydroxydecanoic acid for 30 minutes, followed by stimulation with LPS (100 ng/mL) or IFN-β for indicated periods (up to 24 hours). The culture supernatant was then mixed with an equal volume of Griess reagent. The nitrite concentration was determined by measuring absorbance at 540 nm.[1]
For semi-quantitative RT-PCR analysis of gene expression, RAW264 cells were cultured in multi-well plates, pretreated with or without 5 mM 10-Hydroxydecanoic acid for 30 minutes, and then stimulated with LPS for various time periods. Total RNA was extracted, reverse transcribed into cDNA, and amplified using gene-specific primers. PCR products were analyzed by agarose gel electrophoresis with ethidium bromide staining. Hypoxanthine phosphoribosyltransferase (HPRT) was used as a housekeeping control.[1]
For reporter gene assays, RAW264 cells seeded in 96-well plates were transfected with luciferase reporter constructs (piNOS-luc1974, pISRE-TA-luc, or pNF-κB-TA-luc) along with a control Renilla luciferase plasmid. After 24 hours, cells were pretreated with 10-Hydroxydecanoic acid for 30 minutes and then stimulated with LPS for another 24 hours. Cells were lysed, and luciferase activities were measured using a dual-luciferase assay system. Firefly luciferase activity was normalized to Renilla luciferase activity.[1]
For immunoblotting (Western blot) analysis, RAW264 cells were pretreated with or without 5 mM 10-Hydroxydecanoic acid for 30 minutes and stimulated with LPS for indicated time points. Cells were harvested and lysed. Cytoplasmic proteins were separated by SDS-PAGE, transferred to a membrane, and probed with specific primary antibodies against target proteins (e.g., phospho-STAT1, STAT1, phospho-STAT2, STAT2, IRF-1, phospho-Akt, total 4E-BP1, phospho-4E-BP1 at specific residues). Detection was performed using horseradish peroxidase-conjugated secondary antibodies and a chemiluminescent substrate.[1]
For polysome fractionation analysis, RAW264 cells were pretreated with or without 5 mM 10-Hydroxydecanoic acid for 30 minutes and stimulated with LPS for 3 hours. Cells were then treated briefly with cycloheximide to freeze ribosomes. Lysates were prepared and layered onto a continuous sucrose density gradient (20–50%). After ultracentrifugation, fractions were collected while monitoring absorbance at 260 nm. Polysome-containing fractions were pooled, and RNA was extracted for subsequent RT-PCR analysis to assess mRNA levels in the actively translating pool.[1]

[1]. Inhibitory effect of 10-hydroxydecanoic acid on lipopolysaccharide-induced nitric oxide production via translational downregulation of interferon regulatory factor-1 in RAW264 murine macrophages. Biomed Res. 2013 Aug;34(4):205-14.

10-Hydroxydecanoic acid is a 10-carbon ω-hydroxy fatty acid that has been shown to be the major hydroxylation product of decanoic acid in biological systems (along with the 9-hydroxy isomer) and has been used as a standard for lipid assays; it has been reported to have cytotoxic effects. It is a straight-chain saturated fatty acid and also an ω-hydroxy medium-chain fatty acid. It is functionally related to decanoic acid. It is the conjugate acid of 10-hydroxydecanoic acid. 10-Hydroxydecanoic acid has been reported in trypanosoma brucei, and there are relevant data. 10-Hydroxydecanoic acid is a saturated medium-chain fatty acid and is also a major lipid component of royal jelly at high concentrations (>100 mM). [1] The motivation for this study is that 10-hydroxydecanoic acid is structurally similar to 10-hydroxy-trans-2-decenoic acid (10H2DA), another component of royal jelly, which has previously been shown to have anti-inflammatory effects. [1]
10-Hydroxydecanoic acid (10-HHDC) inhibits LPS-induced NO production by downregulating the translation of IRF-1 mRNA without affecting its total mRNA level. This translational repression is associated with the inhibition of the Akt/4E-BP1 signaling pathway. [1]
The mechanism involves the inhibition of LPS-induced Akt phosphorylation and subsequent hyperphosphorylation/inactivation of the translational repressor 4E-BP1, thereby enhancing the binding of 4E-BP1 to eIF4E and inhibiting cap-dependent translation of specific mRNAs such as IRF-1 and IP-10. [1]
Downregulation of IRF-1 translation leads to reduced activation of the iNOS gene promoter (via ISRE), ultimately resulting in reduced NO production. [1]
This study proposes a novel anti-inflammatory mechanism based on gene-specific translational repression rather than transcriptional regulation, namely the mechanism of action of 10-HHDC. [1]
10-Hydroxydecanoic acid is considered a potential immunomodulatory candidate, particularly for diseases affected by IRF-1-dependent genes. Interferon-stimulated genes. [1]

C10H20O3

188.2640

188.141

1679-53-4

74300

White to off-white solid powder

1.0±0.1 g/cm3

330.8±15.0 °C at 760 mmHg

75-77 °C(lit.)

168.1±16.9 °C

0.0±1.6 mmHg at 25°C

1.466

1.96

2

3

9

13

123

0

YJCJVMMDTBEITC-UHFFFAOYSA-N

InChI=1S/C10H20O3/c11-9-7-5-3-1-2-4-6-8-10(12)13/h11H,1-9H2,(H,12,13)

10-hydroxydecanoic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~265.59 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: ≥ 1.25 mg/mL (6.64 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 1.25 mg/mL (6.64 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 1.25 mg/mL (6.64 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)