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Fig. 1 · Structure
Cat. No.
A10531
CAS No.
1180-71-8
Formula
C26H30O8
Mol. Weight
470.5

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Limonin

Limonin is a limonoid, and a bitter, white, crystalline substance found in citrus and other plants. It is also known as limonoate D-ring-lactone and limonoic acid di-delta-lactone.

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Publications for Limonin

1 publication citing this product

  1. Hyungkuen Kim, .et al. , Journal of Animal Science and Technology, 2024, October PMID: 41695672
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Biological Activity

Bioactivity / Mechanism

Limonin interacted with ERK2 in a microscale thermophoresis assay using transfected-cell lysates (reported Kd 11.56 ± 2.93 μM). EGFP and a four-site ERK2 mutant served as negative binding controls. This binding constant is distinct from cellular treatment concentrations and does not establish kinase activation potency or broad target selectivity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
HIV protease

Cellular Effect

Cell Line Activity Value Description Reference
MCF7 IC50 4.3 μM Antiproliferative activity against human MCF7 cells incubated for 48 hrs by [3H]-thymidine incorporation assay [PMID: 33289552]
MDA-MB-435 IC50 26 μM Antiproliferative activity against human MDA-MB-435 cells incubated for 48 hrs by [3H]-thymidine incorporation assay [PMID: 33289552]
MOLT-3 CC50 201.56 μg/mL Cytotoxicity against human MOLT3 cells after 24 hrs by MTS assay [PMID: 21334901]
Neutrophil IC50 38.2 μM Immunomodulatory activity in polymorphoneutrophils assessed as inhibition of luminol-induced oxidative burst by chemiluminescence assay [PMID: 18950230]
PBMC CC50 451.91 μg/mL Cytotoxicity against PHA-stimutated human PBMC after 24 hrs by MTS assay [PMID: 21334901]

In Vitro Studies

In 3D4/31 porcine macrophages, 30 μM limonin reduced PMA-associated P2RY14, STAT1 and PTGS2 transcript levels, while ARG1 was not significantly reduced. With PMA plus 200 μM UDPG, limonin reduced P2RY14, RARB, STAT1, PTGS2 and ARG1 expression. These cellular responses are consistent with modulation of P2Y14-associated signaling; direct receptor binding and antagonist potency were not established. [2]

Inflammatory gene responses in porcine macrophages

Cell-based study · 3D4/31 porcine alveolar macrophage cell line, unstimulated or stimulated with PMA, with or without UDPG [2]

At 30 μM, limonin reduced P2RY14, STAT1 and PTGS2 expression under PMA stimulation; ARG1 was not significantly reduced in this PMA-only setting. With PMA plus 200 μM UDPG, limonin reduced P2RY14, RARB, STAT1, PTGS2 and ARG1 expression. These are transcript responses, not a receptor binding or antagonist potency assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
P2RY14, STAT1, PTGS2 and ARG1 mRNAqualitative change 30 μM reduced P2RY14, STAT1 and PTGS2; ARG1 not significantly reduced versus PMA-only cells.[2]
P2RY14, RARB, STAT1, PTGS2 and ARG1 mRNA after PMA/UDPGqualitative change Reduced with 30 μM limonin versus PMA plus 200 μM UDPG.[2]
Relative WST8 metabolic viability signalqualitative change 30 μM increased the WST8 signal with or without PMA. The tested 100 μM condition is marked ns versus zero-limonin control.[2]

Literature-Reported Treatment Conditions

Treatment concentration
Dose screening: 0, 1, 3, 30 and 100 μM for qPCR; selected limonin concentration 30 μM. WST8 also includes 10 μM.
Exposure duration
Limonin 24 h; PMA stimulation 4 h for qPCR (Figure 5B); PMA/UDPG stimulation 4 h for Figure 5C. WST8: limonin 24 h and PMA 24 h.
Method
Cell treatment; 2 nM PMA, with or without UDPG (100 or 200 μM in Figure 5C). Methods describe medium/treatment refresh before stimulation.
Vehicle
DMSO used for limonin stock.
Co-treatment
Inflammatory challenges: PMA alone or PMA plus UDPG; comparisons include untreated and stimulus-only cells.
Reported limits
Final DMSO concentration and explicit solvent matching of all qPCR controls are not specified in the inspected text/figure. No IC50 or direct P2Y14 binding measurement reported in the limonin experiments.
Methods and source locations

Compound reported in the paper: Limonin; Compound label in the paper: A10531

Evidence for the paper’s tested limonin material; no independent validation of the current Adooq lot.

Figure 5A-C; Results: Limonin suppresses UDPG-induced proinflammatory gene expression; Drugs and treatment; qRT-PCR; Statistical analysis

P2RY14, STAT1, PTGS2 and ARG1 mRNA: qRT-PCR normalized to RPS29, 2^(-ΔΔCt); Figure 5B n = 3; mean ± SD under general statistics. — Figure 5B; qRT-PCR and Statistical analysis

P2RY14, RARB, STAT1, PTGS2 and ARG1 mRNA after PMA/UDPG: qRT-PCR normalized to RPS29; Figure 5C displays three points per group; general statistics specify at least 3 independent biological experiments and mean ± SD. Exact n is not separately stated in panel C caption. — Figure 5C; limonin Results; qRT-PCR and Statistical analysis

Relative WST8 metabolic viability signal: WST8 assay; n = 3; Figure 5A. Signal is not a direct cell-number or long-term safety measurement. — Figure 5A; Quantification of cell viability and proliferation; Statistical analysis

ERK2 binding measured by microscale thermophoresis

Biochemical assay · 293T cell lysates expressing wild-type ERK2-EGFP, four-site mutant ERK2-EGFP or EGFP control [1]

Limonin bound wild-type ERK2-EGFP with a reported Kd of 11.56 ± 2.93 μM. EGFP control and ERK2 carrying Y34A/V37A/K52A/C164A did not show comparable binding curves. This lysate binding endpoint does not establish kinase activation potency or selectivity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Limonin binding to wild-type ERK2-EGFPKd 11.56 ± 2.93 μM[1]
Binding to EGFP alone or four-site ERK2 mutantqualitative change EGFP did not generate a binding curve; four-site mutant did not exhibit the wild-type binding response.[1]

Literature-Reported Treatment Conditions

Treatment concentration
A 1 mM limonin starting solution was serially diluted 1:1 across 16 concentrations; at least 12 concentration points used for fitting.
Exposure duration
Binding incubation 30 min at room temperature.
Method
MST in lysates of transfected 293T cells; ERK2-EGFP compared with EGFP alone and four-site mutant ERK2-EGFP.
Vehicle
PBS-T (0.05% Tween-20, pH 7.2) used for lysate dilution; Compounds section describes limonin in distilled water containing 25% HS15.
Co-treatment
No combination drug; fluorescent fusion-protein controls.
Reported limits
MST-specific final HS15/solvent fraction and replicate n for the Kd are not separately specified. General statistics use mean ± SEM; the Kd sentence does not separately define its ± term.
Methods and source locations

Compound reported in the paper: Limonin; Compound label in the paper: Lim

Parent limonin research evidence using a different supplier; no Adooq lot validation.

Figure 4F-H; Results: ERK2 is a direct target of limonin; Plasmid transfection; Microscale thermophoresis; Compounds; Statistical analysis

Limonin binding to wild-type ERK2-EGFP: MST in 293T lysates; fitted binding curve; ± is preserved as reported, with mean ± SEM stated globally but no fit-specific definition. — ERK2 is a direct target of limonin, Kd sentence; Figure 4F; MST; Statistical analysis

Binding to EGFP alone or four-site ERK2 mutant: MST; mutant Y34A, V37A, K52A and C164A. Negative controls support the interaction assignment within this assay. — Figure 4F-H; ERK2-target Results; Plasmid transfection; MST

In Vivo Studies

In male C57BL/6 mice, oral limonin at 40 or 80 mg/kg once daily for four days, beginning three days before renal ischemia/reperfusion, reduced serum creatinine and BUN measured 24 h after injury. The 80 mg/kg group also showed less tubular injury and lower renal injury and inflammatory markers. The findings concern short-term pretreatment in one ischemic injury model. [1]

Oral limonin pretreatment in ischemic acute kidney injury

Animal study · Male C57BL/6 mice, 8–10 weeks; bilateral renal ischemia/reperfusion injury; sham and injury/vehicle controls [1]

Oral limonin pretreatment at 40 or 80 mg/kg reduced serum creatinine and BUN at 24 h after renal injury compared with vehicle. At 80 mg/kg, fewer injured tubules and lower renal injury/inflammation markers were reported. This is a short-term prophylactic model, not treatment begun after established injury.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Serum creatinine and blood urea nitrogen at 24 h after injuryqualitative change Both 40 and 80 mg/kg groups lower than injury/vehicle. Exact concentrations not transcribed from plots.[1]
Injured tubules and kidney injury/inflammation markers at 80 mg/kgqualitative change Fewer injured tubules; reduced KIM-1, NGAL, IL-6, TNF-α and CD68-positive macrophage readouts versus injury/vehicle.[1]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Once daily
Treatment course
Four consecutive days beginning 3 days before injury; assessed 24 h after injury
Vehicle
Distilled water containing 25% HS15
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Limonin 40 mg/kgInjury + 25% HS15 vehicle; sham reference groupLower serum creatinine and BUN versus injury/vehicle.[1]
Limonin 80 mg/kgInjury + 25% HS15 vehicle; sham reference groupLower serum creatinine and BUN versus injury/vehicle. Histology and injury/inflammatory markers were additionally assessed at 80 mg/kg.[1]
Limonin 40 mg/kg
Model: Male C57BL/6 mice, 8–10 weeks, renal ischemia/reperfusion
Reported limits: Exact group-specific n for serum endpoints not specified beyond n = 5–11. No post-injury-only dosing arm.
Limonin 80 mg/kg
Model: Male C57BL/6 mice, 8–10 weeks, renal ischemia/reperfusion
Reported limits: Exact group-specific n for serum endpoints not specified beyond n = 5–11. No post-injury-only dosing arm.
Methods and source locations

Compound reported in the paper: Limonin; Compound label in the paper: Lim

Parent limonin research evidence using a different supplier; no Adooq lot validation.

Figure 1A-M; Results: Limonin mitigates ischemic AKI; Compounds; Mouse models; Renal function assessment; Kidney histology; Statistical analysis

Serum creatinine and blood urea nitrogen at 24 h after injury: Automatic chemistry analyzer; Figure 1B-C n = 5–11; mean ± SEM. Figure annotations indicate P < 0.01 comparisons for both doses versus injury/vehicle. — Figure 1B-C and caption; Renal function assessment; Mouse models; Statistical analysis

Injured tubules and kidney injury/inflammation markers at 80 mg/kg: PAS morphology, immunoblotting and immunohistochemistry; Figure 1D-M n = 5 for quantitative endpoints; mean ± SEM; no curve-derived exact values. — Figure 1D-M; Limonin mitigates ischemic AKI; Kidney histology; Statistical analysis

Limonin 40 mg/kg · Figure 1A-C; Mouse models; Discussion (daily dosing)

Limonin 80 mg/kg · Figure 1A-C; 1D-M; Mouse models; Discussion (daily dosing)

Specifications

Manufacturer Adooq Bioscience
CAS Number 1180-71-8
Formula C26H30O8
Molecular Weight 470.5
SMILES
C[C@@]12CC[C@H]3[C@]([C@@]14[C@H](O4)C(=O)O[C@H]2C5=COC=C5)(C(=O)C[C@@H]6[C@@]37COC(=O)C[C@@H]7OC6(C)C)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 40 mg/mL (85.01 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Xianke Zhou, Yadie Xiang, Dier Li, et al. Limonin, a natural ERK2 agonist, protects against ischemic acute kidney injury International Journal of Biological Sciences (2023). PMID: 37324945 DOI: 10.7150/ijbs.82417 Source material
  2. [2] Hyungkuen Kim, Hyun Sik Jun, Ki-Duk Song, et al. Aporocactus flagelliformis water extract and limonin suppresses P2Y purinoceptor 14-mediated proinflammatory features in 3D4/31 porcine alveolar macrophages Journal of Animal Science and Technology (2026). PMID: 41695672 DOI: 10.5187/jast.2024.e103 Source material

Publications

1 publication citing this product

  1. Hyungkuen Kim, .et al. , Journal of Animal Science and Technology, 2024, October PMID: 41695672

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