Ligusticum cyprolactin (LIGc) (2.5-10 μM; 2 h) dose-dependently inhibited the production of LPS-induced pro-inflammatory mediators (NO, TNF-α, IL-1β) in RAW264.7 mouse macrophages and promoted the secretion of anti-inflammatory cytokines (IL-4, IL-10) [1]. Ligusticum cyprolactin (2.5-10 μM; 2 h) dose-dependently decreased the expression of LPS-induced pro-inflammatory proteins (CD86, iNOS, COX-2) in RAW264.7 mouse macrophages and increased the expression of anti-inflammatory protein (CD206) [1]. Ligusticum cyprolactin (10 μM; 2 h) inhibited the expression of LPS-induced pro-inflammatory genes (cd86, Nos2) in RAW264.7 mouse macrophages [1]. Ligusticum cyprolactin (LIGc) (10 μM; 2 h) can reduce the expression of the pro-inflammatory marker CD86 in LPS-induced mouse primary microglia[1]. Ligusticum cyprolactin (10 μM; 2 h) can regulate the transcriptional profile of LPS-stimulated RAW264.7 mouse macrophages, significantly downregulate the expression of the pro-inflammatory gene Fpr1 and enrich anti-inflammatory signaling pathways[1]. Ligusticum cyprolactin (10 μM; 2 h) can inhibit the expression of FPR1 protein in LPS-induced RAW264.7 mouse macrophages[1]. Ligusticum cyprolactin (10 μM; 2 h) can inhibit the expression of NLRP3 protein in LPS-induced RAW264.7 mouse macrophages and mouse primary microglia[1]. Ligusticum cyprolactin (10 μM; 2 h) exerted anti-inflammatory effects on LPS-stimulated RAW264.7 mouse macrophages and primary mouse microglia by downregulating the FPR1/NLRP3 signaling pathway, while FPR1 overexpression reversed these effects [1]. Ligusticum cyprolactin (20-80 μM; 36 h) reduced uric acid-induced NRK-52E cell damage by inhibiting the TLR4/NF-κB signaling pathway, thereby reducing inflammation and fibrosis [2]. Ligusticum cyprolactin (2.5-40 μM; 24 h) had no cytotoxic effect on BV2 microglia at concentrations up to 20 μM, but reduced cell viability at 40 μM [3]. Ligusticum cyprolactin (5-20 μM; 1 h) dose-dependently reduced LPS-induced NO production in BV2 microglia, with the strongest inhibitory effect at 10 μM [3]. Ligusticum cyprolactin (5-20 μM; 1 h) dose-dependently reduced LPS-induced TNF-α and IL-1β secretion in BV2 microglia [3]. Ligusticum cyprolactin (10 μM; 1 h) inhibited LPS-induced NF-κB pathway activation in BV2 microglia by reducing the phosphorylation levels of IκBα, IKKα+β and NF-κB p65 [3]. Ligusticum cyprolactin (10 μM; 1 h) protected HT22 hippocampal neurons from LPS-activated neurotoxicity induced by BV2 microglia conditioned medium and restored the viability of HT22 cells [3]. Ligusticum cyprolactin (10 μM; 1 h) can attenuate LPS-activated BV2 microglia-induced apoptosis of HT22 hippocampal neurons by restoring the Bcl2/Bax ratio and reducing the expression of BID and CytC [3]. In cell-free molecular docking experiments, ligusticum cyprolactin (LIGc) can bind directly to purified FXR protein [4].

Ligusticum chuanxiong cyprolactin (LIGc) (20 and 60 mg/kg; orally; once daily for 4 days) can reduce neuroinflammation in mice induced by lipopolysaccharide (LPS) by inhibiting the activation of pro-inflammatory microglia/macrophages and regulating the FPR1/NLRP3 signaling pathway [1]. Ligusticum chuanxiong cyprolactin (20 and 60 mg/kg; orally; 1, 24 and 48 hours after ischemia/reperfusion) can dose-dependently reduce the infarct volume and improve the neurological function of tMCAO mice [1]. Ligusticum chuanxiong cyprolactin (20-80 mg/kg; orally; once daily for 3 weeks) can improve hyperuricemic nephropathy in mice by inhibiting the TLR4/NF-κB pathway, reducing uric acid levels, kidney inflammation and fibrosis [2].

ELISA detection [1]
Cell Types: LPS-stimulated RAW264.7 mouse macrophages
Tested Concentrations: 2.5; 5; 10 μM
Incubation Duration: 2 hours
Experimental Results: Dose-dependently inhibited LPS-induced production of NO, TNF-α and IL-1β. Enhanced the secretion of IL-4 and IL-10, with the best effect at 10 μM. All changes were statistically significant compared with the LPS-only group.

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Western Blot Analysis [1]
Cell Types: LPS-stimulated RAW264.7 mouse macrophages
Tested Concentrations: 2.5; 5; 10 μM
Incubation Duration: 2 hours
Experimental Results: The LPS-induced upregulation of CD86, iNOS and COX-2 protein expression was attenuated in a dose-dependent manner, while CD206 protein expression was increased, with significant differences at all test concentrations compared to the LPS-only group.

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Western Blot Analysis [1]
Cell Types: LPS-stimulated RAW264.7 mouse macrophages
Tested Concentrations: 10 μM (pretreatment for 2 hours); 100 ng/mL LPS (co-treatment for 12 hours)
Incubation Duration: 2 hours (pretreatment); 12 hours (co-treatment)
Experimental Results: Compared with the LPS-only group, LPS-induced FPR1 protein expression was significantly inhibited.

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Western Blot Analysis [2]
Cell Types: NRK-52E cells
Tested Concentrations: 20; 40; 80 μM
Incubation Duration: 36 hours
Experimental Results: Effectively reversed the upregulation of uric acid-induced inflammatory and fibrotic markers (such as Nlrp3, IL-1β, Fn1, and Tgfb1) transcription levels. Reduced the levels of KIM-1, NLRP3, IL-1β, VCAM1, FN, and α-SMA proteins, while enhancing the expression of E-cadherin.

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ELISA detection [3]
Cell Types: LPS-stimulated mouse BV2 microglia
Tested Concentrations: 5; 10; 20 μM
Incubation Duration: 1 hour
Experimental Results: At concentrations of 5, 10, and 20 μM, LPS-induced increases in TNF-α and IL-1β secretion were significantly attenuated. At a concentration of 10 μM, the strongest inhibitory effect was observed on both cytokines.

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Cell viability assay [3]
Cell Types: BV2 microglia
Tested Concentrations: 2.5; 5; 10; 20; 40 μM
Incubation Duration: 24 hours
Experimental Results: At concentrations up to 20 μM, the assay showed cytotoxic effects on BV2 microglia. At 40 μM, cell viability was reduced.

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Animal/Disease Models:Adult male Kunming mice (8-10 weeks old, 24 g)[1]
Doses: 20; 60 mg/kg
Route of Administration: Oral; once daily; 4 days
Experimental Results: Improved LPS-induced changes in open field parameters, including increased activity distance, central region dwell distance, central region dwell time and activity time, while reducing corner dwell time and rest time. Reduced the number of Iba1+CD86+ pro-inflammatory microglia/macrophages in the cerebral cortex. At a dose of 20 mg/kg, suppressed the levels of pro-inflammatory markers TNF-α, IL-1β, CD86, iNOS and COX-2 in the cerebral cortex, while increasing the levels of anti-inflammatory markers IL-4, IL-10 and CD206. Similar and more pronounced effects were observed at a dose of 60 mg/kg, including significant inhibition of FPR1 and NLRP3 protein expression in the cerebral cortex.

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Animal/Disease Models:Adult male Kunming mice (8-10 weeks old, 24 g) tMCAO model [1]
Doses: 20; 60 mg/kg
Route of Administration: Gavage; 1, 24 and 48 hours after I/R
Experimental Results: The volume of cerebral infarction decreased in a dose-dependent manner, with the 60 mg/kg dose group showing a more significant reduction. Neurological function was significantly improved, as evidenced by a decrease in Longa score, a reduced tendency to turn to the right in the corner test, and an increased use of the affected forelimb in the cylinder test. The number of Iba1+CD86+ pro-inflammatory microglia/macrophages in the cerebral cortex around the infarct was reduced, the expression of pro-inflammatory markers TNF-α, IL-1β, CD86, iNOS and COX-2 was inhibited, and the expression of anti-inflammatory markers IL-4, IL-10 and CD206 was increased. At a dose of 60 mg/kg, the expression of FPR1 and NLRP3 proteins in the cerebral cortex was significantly reduced.

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Animal/Disease Models:Male C57BL/6J mice (8 weeks old) with hyperuricemic nephropathy induced by hypoxanthine and potassium oxychloride [2]
Doses: 20, 40, 80 mg/kg
Route of Administration: Gavage; daily; for 3 weeks
Experimental Results: Reduced elevated serum uric acid levels and hepatic xanthine oxidase (XOD) activity. Reduced renal index, serum creatinine, blood urea nitrogen and 24-hour urinary albumin. Improved renal histological damage. Dose-dependently reduced macrophage infiltration (F4/80 positive staining) and downregulated the mRNA/protein expression of inflammatory markers (F4/80, Icam-1, IL-6, Ccl2, Nlrp3, IL-1β, MCP-1, NLRP3, IL-1β). It reduces renal collagen deposition and downregulates fibrosis markers (Fn1, Col4a1, Tgfb1, Timp1, FN, α-SMA) while increasing E-cadherin expression. It reverses the dysregulation of renal uric acid transporters (upregulating Abcg2, Oat3, Oct2 mRNA and OAT1 protein, downregulating Glut9 mRNA and URAT1, GLUT9 protein). It inhibits the TLR4/NF-κB signaling pathway.

[1]. A Novel Compound Ligusticum Cycloprolactam Alleviates Neuroinflammation After Ischemic Stroke via the FPR1/NLRP3 Signaling Axis. CNS Neurosci Ther. 2024;30(12):e70158.

[2]. Ligusticum cycloprolactam ameliorates hyperuricemic nephropathy through inhibition of TLR4/NF-κB signaling. J Nutr Biochem. 2025;139:109864.

[3]. Mechanism of ligusticum cycloprolactam against neuroinflammation based on network pharmacology and experimental verification. Clin Exp Pharmacol Physiol. 2023;50(8):647-663.

[4]. IDDF2024-ABS-0318 Ligusticum cycloprolactam (LIGc), a novel FXR agonist: target activation of FXR ameliorate metabolic associated fatty liver disease. Gut 2024;73(Suppl 2):A1-A398.

C15H21NO2

247.33

2283387-37-9

Typically exists as solids at room temperature

O=C1C2=C(C(N1C3CC3)(CCCC)O)CCC=C2

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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