Hordenine sulfate
Based on 2 publication(s) in Google Scholar
Hordenine sulfate (Ordenina sulfate; Peyocactine sulfate) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine sulfate inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine sulfate promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine sulfate inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine sulfate activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine sulfate activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine sulfate inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine sulfate limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine sulfate can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder.
For research use only. We do not sell to patients.
- CAS No.: 62493-39-4
- Formula: C10H17NO5S
- Molecular Weight:263.31
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) Hordenine sulfate
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Biological Activity
Description
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ERK1 |
ERK2 |
IL-6 |
IL-1β |
TNF-α |
iNOS |
COX-2 |
D3 Receptor 6.6 μM (EC50) |
D3 Receptor 6.9 μM (Ki) |
Alpha-2A adrenergic receptor 7.4 μM (EC50) |
Alpha-2A adrenergic receptor 11 μM (Ki) |
5-HT2A Receptor 3.1 μM (Ki) |
In Vitro
Hordenine (25-200 μM; 2 h) sulfate shows no cytotoxicity in EpH4-Ev cells at experimental concentrations of 2-100 μM, but affects cell viability at 200 μM[1].
Hordenine (100 μM; 0-8 h) sulfate activates the AMPK/Nrf2/HO-1 signaling cascade in EpH4-Ev cells[1].
Hordenine (0.5-100 μM; 1 h/5 days) sulfate inhibits melanin content in human epidermal melanocytes by downregulating the expression of MITF, tyrosinase, TRP-1, and TRP-2, and inhibiting CREB phosphorylation, reduces melanin levels in reconstructed epidermis, inhibits tyrosinase activity, and suppresses cAMP production[2].
Hordenine (12.5-200 μM; 48 h) sulfate promotes the proliferation of mouse primary dermal papilla cells in a dose-dependent manner[5].
Hordenine (25-50 μM; 10 consecutive days) sulfate significantly enhances the colony-forming ability of primary mouse dermal papilla cells at a concentration of 50 μM[5].
Hordenine (25-50 μM; 24 h) sulfate increases the proportion of proliferating (Ki67-positive) primary mouse dermal papilla cells, promotes nuclear translocation of β-catenin, elevates the gene expression of key DPC activity markers (ALP, Versican, and Wnt3a), activates the gene expression of the Wnt/β-catenin signaling pathway, and increases ALP protein expression[5].
Hordenine (2-50 μM; 24 h) sulfate dose-dependently activates DRD2 in live 293T-Tango-PB cells, with a maximum effective concentration of 50 μM[6].
Hordenine (0-90 μM; 15 min) sulfate inhibits cAMP production in HEK293T cells expressing DRD2, with an IC50 of 5.546 μM[6].
Hordenine (25-50 μM; 7 days) sulfate attenuates age-related α-synuclein accumulation in C. elegans strain NL5901 via a DRD2-dependent pathway[6].
Hordenine sulfate binds to multiple GPCRs with low micromolar affinity, exhibiting the highest affinity for the 5-HT2A receptor (Ki = 3.1 μM) and the D3 receptor (Ki = 6.9 μM)[7].
Hordenine sulfate binds to human SERT (Ki = 4.0 μM) with higher affinity than to human DAT (Ki = 30 μM)[7].
Hordenine sulfate acts as a potent partial agonist at D3R (EC50 = 6.6 μM; Emax = 70%), a weak partial agonist at α1A-AR (EC50 = 38 μM; Emax = 23%), and a neutral antagonist at 5-HT2A R (Emax < 5%)[7].
Hordenine sulfate is a full agonist of the α2A-adrenergic receptor (EC50 = 7.4 μM; Emax = 109%)[7].
Hordenine (25-100 μM; 2 h) sulfate attenuates LPS (HY-D1056)-induced inflammatory responses at the mRNA level in EpH4-Ev cells by decreasing pro-inflammatory cytokines and increasing anti-inflammatory cytokines, reduces the expression of the pro-inflammatory enzymes iNOS and COX-2, and alleviates the activation of the TLR4-MAPK/NF-κB inflammatory signaling pathway as well as oxidative stress[1].
Hordenine (50-75 μg/mL; 1 h pre-treatment) sulfate inhibits the secretion of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 macrophages, downregulates the mRNA expression of pro-inflammatory mediators, and upregulates M2 macrophage markers, inhibits the activation of AKT, NF-κB, and MAPK signaling pathways, and reduces the protein expression of iNOS and COX-2[3].
Hordenine (75 μg/mL; 1 h pretreatment) sulfate inhibits LPS-induced nuclear translocation of p65 in RAW264.7 macrophages[3].
Hordenine (0.5-1.0 mg/mL; 48 h) sulfate inhibits quorum sensing in Pseudomonas aeruginosa PAO1 in a concentration-dependent manner by reducing the production of the signaling molecules C4-HSL and 3-oxo-C12-HSL, with an inhibition rate of up to 79% for C4-HSL at 1.0 mg/mL[4].
Hordenine (0.5-1.0 mg/mL; 24 h) sulfate reduces biofilm formation in Pseudomonas aeruginosa PAO1 by up to 31% at subinhibitory concentrations without affecting planktonic cell viability[4].
Hordenine (0.5-1.0 mg/mL; 24 h) sulfate significantly inhibits the production of QS-related virulence factors (protease, elastase, pyocyanin, rhamnolipid, alginate, and pyoverdine) in Pseudomonas aeruginosa PAO1 in a concentration-dependent manner[4].
Hordenine (0.5-1.0 mg/mL; 24 h) sulfate inhibits swimming and swarming motility of Pseudomonas aeruginosa PAO1 in a concentration-dependent manner[4].
Hordenine (1.0 mg/mL; 24 h) sulfate inhibits the expression of key QS-related genes (lasI, lasR, rhlI, rhlR) in Pseudomonas aeruginosa PAO1, with the most significant effect being a 60% downregulation of lasR[4].
Hordenine (25-50 μM; 9 days) sulfate alleviates 6-OHDA (HY-B1081A)-induced locomotor deficits in C. elegans strain N2[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:EpH4-Ev mouse mammary epithelial cells
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Concentration:25, 50, 100, 200 μM
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Incubation Time:2 h pretreatment; 24 h LPS stimulation
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Result:Exerted a notable impact on cell viability at 200 μM.
Showed no cytotoxic effect at 25, 50, and 100 μM.
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Cell Line:EpH4-Ev mouse mammary epithelial cells
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Concentration:25, 50, 100 μM
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Incubation Time:2 h pretreatment; 24 h LPS stimulation
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Result:Suppressed the LPS-induced increase in mRNA levels of TNF-α, IL-1β, and IL-6.
Further increased the level of IL-10.
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Cell Line:EpH4-Ev mouse mammary epithelial cells
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Concentration:25, 50, 100 μM
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Incubation Time:2 h pretreatment; 24 h LPS stimulation
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Result:Alleviated the LPS-triggered elevation of iNOS and COX-2 expression.\nDose-dependently reduced the expression of TLR4 and phosphorylated expression of p65 and IκBα.
Alleviated the phosphorylation levels of p38, JNK, and ERK.
Alleviated p65 nuclear translocation.
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Cell Line:EpH4-Ev mouse mammary epithelial cells
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Concentration:100 μM
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Incubation Time:0, 1, 2, 4, 8 h
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Result:Enhanced activation of the AMPK/Nrf2/HO-1 pathway after 2-4 h pretreatment.
Promoted Nrf2 translocation into the nucleus.
AMPK inhibitor compound C inhibited AMPK phosphorylation, Nrf2 upregulation, and HO-1 expression.
Nrf2 inhibitor retinoic acid inhibited Nrf2 activation, HO-1 expression, the decrease in MDA content, and the increase in CAT activity and GSH/GSSG ratio.
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Cell Line:human epidermal melanocytes (Cascade Biologics)
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Concentration:0.5, 5, 50, 100 μM
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Incubation Time:1 h
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Result:Inhibited cAMP production in a concentration-dependent manner.
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Cell Line:human epidermal melanocytes (Cascade Biologics)
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Concentration:0.5, 5, 50, 100 μM
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Incubation Time:1 h and 5 days
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Result:Suppressed CREB phosphorylation.
Decreased MITF expression significantly in a concentration-dependent manner.
Inhibited the production of tyrosinase, TRP-1, and TRP-2.
At 100 μM, tyrosinase/β-actin, TRP-1/β-actin, and TRP-2/β-actin ratios were reduced to approximately 0.35, 0.4, and 0.35, respectively.
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Cell Line:LPS-stimulated RAW264.7 macrophages
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Concentration:50, 75 μg/mL
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Incubation Time:1 h (pre-treatment); 12 h (LPS stimulation)
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Result:Suppressed the LPS-induced increases in TNF-α, IL-6, and IL-1β protein levels.
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Cell Line:LPS-stimulated RAW264.7 macrophages
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Concentration:50, 75 μg/mL
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Incubation Time:1 h (pre-treatment); LPS stimulation
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Result:Reduced the LPS-induced mRNA expression of IL-6, TNF-α, iNOS, and COX-2.
Promoted the expression of M2 macrophage marker genes Arg-1, Ym-1, and CD206.
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Cell Line:LPS-stimulated RAW264.7 macrophages
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Concentration:50, 75 μg/mL
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Incubation Time:1 h (pre-treatment); 1 h (LPS stimulation)
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Result:Reduced the LPS-induced increases in iNOS and COX-2 protein levels.
Alleviated the increased phosphorylation levels of AKT, p65, IκB, p38, ERK1/2, and JNK induced by LPS.
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Cell Line:LPS-stimulated RAW264.7 macrophages
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Concentration:75 μg/mL
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Incubation Time:1 h (pre-treatment); 12 h (LPS stimulation)
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Result:Inhibited the LPS-induced nuclear translocation of p65.
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Cell Line:primary mouse dermal papilla cells (DPCs)
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Concentration:0, 12.5, 25, 50, 100, 200 μM
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Incubation Time:48 h
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Result:Showed safety at 200 μM.
Significantly increased cell proliferation at 12.5, 25, 50, and 100 μM, with the highest increase observed at 50 μM.
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Cell Line:primary mouse dermal papilla cells (DPCs)
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Concentration:0, 25, 50 μM
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Incubation Time:24 h
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Result:Increased the percentage of Ki67-positive DPCs in a dose-dependent manner, with counts rising from 10 (control) to 28 (25 μM) and 39 (50 μM) per 100 cells.\nGreatly promoted the nuclear entrance of β-catenin in DPCs compared with the controls.
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Cell Line:primary mouse dermal papilla cells (DPCs)
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Concentration:0, 25, 50 μM
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Incubation Time:24 h
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Result:Markedly upregulated the mRNA levels of ALP, Versican, and Wnt3a in a dose-dependent manner.\nMarkedly upregulated the mRNA expression of β-catenin, Lef-1, Axin2, and Cyclin D1 in a dose-dependent manner.
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Cell Line:primary mouse dermal papilla cells (DPCs)
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Concentration:0, 25, 50 μM
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Incubation Time:24 h
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Result:Markedly upregulated the protein levels of ALP in a dose-dependent manner.\nSignificantly increased the protein levels of p-GSK3β, β-catenin, Lef-1, Axin2, and Cyclin D1.
In Vivo
Hordenine (10-15 mg/kg; i.p.; single administration; 1 h before LPS modeling) sulfate attenuates LPS-induced acute lung injury in mice in a dose-dependent manner by inhibiting inflammation and the production of inflammatory cytokines[3].
Hordenine (1-2 mM; topical application; daily; 25 days) sulfate accelerates the entry into the hair follicle anagen phase and hair regeneration in a depilation-induced mouse alopecia model by activating the Wnt/β-catenin signaling pathway[5].
Hordenine (30-100 mg/kg/day; p.o.; daily; 12 days) sulfate significantly ameliorates MPTP (HY-15608)-induced motor deficits and gait abnormalities in mice, rescues 44.4% of the climbing time, and restores multiple gait parameters[6].
Hordenine (100 mg/kg; p.o.; daily; 22 days) sulfate significantly ameliorates motor deficits in the 6-OHDA-induced hemiparkinsonian mouse model, reducing climbing time by 22.2% and traversal time by 34.2%[6].
Hordenine (50 mg/kg; i.p.; once daily; for 4 consecutive days) sulfate attenuates persistent alcohol intake in mice and prophylactically reduces relapse behavior after withdrawal[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (25-30 g, 7-8 weeks old, female)[1]
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Dosage:50 mg/kg/day
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Administration:p.o.; daily; 14 days
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Result:Reduced histopathological scores in mammary tissue from 3.75 to 1.75.
Attenuated the LPS-induced increase in MPO activity.
Reduced levels of pro-inflammatory mediators (IL-6, TNF-α, IL-1β, COX-2, iNOS) while elevating the anti-inflammatory cytokine IL-10.
Restored the integrity of the blood-milk barrier by upregulating the expression of tight junction proteins ZO-1, occludin, and claudin-3.
Inhibited the LPS-induced phosphorylation of key proteins in the TLR4-MAPK/NF-κB pathway while activating the AMPK/Nrf2/HO-1 antioxidative pathway.
Mitigated the LPS-induced increase in MDA content and restored decreased CAT activity, GSH/GSSG ratio, and SOD activity.
Altered the composition of intestinal microbiota, increasing the abundance of Lactobacillaceae, S24-7, and Prevotellaceae at the family level and Lactobacillus at the genus level, while decreasing Bacteroidaceae, Desulfovibrionaceae, Lachnospiraceae, and Ruminococcaceae at the family level and Bacteroides, Desulfovibrio, Oscillospira, and Blautia at the genus level.\nReduced histopathological damage in recipient mice.
Reduced MPO activity, IL-1β, IL-6, TNF-α, iNOS, and COX-2 levels, and elevated IL-10 levels.
Enhanced expression of tight junction proteins ZO-1 (fold change ~2.0), occludin (fold change ~1.8), and claudin-3 (fold change ~4.0) compared to the FN group.
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Animal Model:BALB/c mice (Male, 6-8 weeks old, LPS-induced)[3]
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Dosage:10, 15 mg/kg
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Administration:i.p.; single dose; 1 h before LPS modeling
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Result:Reduced lung histopathological injury score in a dose-dependent manner, with the 15 mg/kg dose showing greater alleviation than the 10 mg/kg dose.
Decreased the lung wet-dry (W/D) weight ratio.
Reduced mRNA expression levels of Il6, Il1β, Tnfa, iNOS, Cox2, and Mpo in lung tissues.
Reduced protein secretion of IL-6, IL-1β, and TNF-α in bronchoalveolar lavage fluid (BALF).
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Animal Model:C57BL/6 (female, 7-week-old)[5]
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Dosage:1 mM; 2 mM
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Administration:topical application; daily; 25 days
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Result:Accelerated anagen entry and hair regrowth.
Significantly increased the rate of hair regeneration at both 1 mmol/L and 2 mmol/L.
Markedly promoted hair follicles to enter a state of active growth at day 6.
Markedly increased the protein levels of β-catenin, p-GSK3β, and Axin2, and greatly increased the expression of downstream target genes Lef-1 and Cyclin D1 at both mRNA and protein levels.
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Animal Model:C57BL/6 (male, 12-week-old, 20-25 g, MPTP-induced)[6]
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Dosage:30, 100 mg/kg/day
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Administration:p.o.; daily; 12 days
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Result:Reduced turning and climbing time in the pole test, rescuing 44.4% of climbing time.
Improved locomotor speed, step size, and preserved shorter run duration in Catwalk gait analysis.
Rescued shortened bilateral print positions and recovered stride length of four limbs.
Presented similar or better effect than PPX on swing speed and relieved prolonged standing time and step cycle time.
Increased TH-immunopositive fiber fluorescence intensity in the striatum but did not change TH-immunopositive cells in the SNpc.
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Animal Model:C57BL/6 (male, 12-week-old, 20-25 g, 6-OHDA-induced)[6]
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Dosage:100 mg/kg
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Administration:p.o.; daily; 22 days
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Result:Reduced climbing time by 22.2% in the pole test compared to the 6-OHDA-lesioned group.
Spent 34.2% less time to cross the beam in the balance beam test.
Regained almost 30% locomotion activity compared to the 6-OHDA group.
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Animal Model:C57BL/6 J mice (Male, 8 weeks old, 26 g)[7]
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Dosage:50 mg/kg
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Administration:i.p.; once a day; 4 days
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Result:Reduced ongoing alcohol consumption on the first treatment day and the second day after treatment, with a significant decrease in the 6-day average alcohol consumption.
Decreased the 6-day average alcohol preference and total intake.
Reduced alcohol consumption on the first, third, and fourth days of reinstatement, with a significant decline in the 4-day average consumption and preference during withdrawal.
Had no effect on alcohol consumption during relapse, but significantly decreased alcohol preference on the third reinstatement day and in the 4-day average analysis.
Chemical Information
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CAS No. 62493-39-4
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Molecular Weight 263.31
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Formula C10H17NO5S
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SMILES
OC1=CC=C(CCN(C)C)C=C1.O=S(O)(O)=O
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Synonyms
Ordenina sulfate; Peyocactine sulfate
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (2)
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Journal Impact Factor
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Most Recent
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J Agric Food Chem
Chemoproteomic Profiling of Cobalamin-Independent Methionine Synthases in Plants with a Covalent Probe. [Abstract]2020 Jul 29;68(30):8050-8056. PMID: 32618189
Purity & Documentation
References
[2]. Kim SC, et al. Hordenine, a single compound produced during barley germination, inhibits melanogenesis in human melanocytes. Food chemistry. 2013 Nov 01;141(1):174-81. [Content Brief]
[6]. Li H, et al. Hordenine improves Parkinsonian-like motor deficits in mice and nematodes by activating dopamine D2 receptor-mediated signaling. Phytotherapy research : PTR. 2023 Aug;37(8):3296-3308. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Hordenine sulfate Related Classifications
HY-N0113A Related Classifications
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Keywords
- Hordenine
- 62493-39-4
- Ordenina
- Peyocactine
- Bacterial
- p38 MAPK
- JNK
- ERK
- Akt
- Interleukin Related
- TNF Receptor
- NO Synthase
- COX
- Reactive Oxygen Species (ROS)
- Microphthalmia Associated Transcription Factor (MITF)
- Wnt
- β-catenin
- Dopamine Receptor
- Adrenergic Receptor
- 5-HT Receptor
- Serotonin Transporter
- Dopamine Transporter
- α-synuclein
- TRP-1
- tyrosinase
- MITF
- cAMP
- Nrf2
- HO-1
- TLR4
- NF-κB
- AMPK
- MAPK
- Inhibitor
- inhibitor
- inhibit