2. Metabolic Enzyme/Protease
  3. Amylases Glycosidase
  4. Lotusine

Lotusine is an orally active signaling pathway modulator and enzyme inhibitor, with an IC50 of 30.60 μg/mL against α-amylase and an IC50 of 36.15 μg/mL against α-glucosidase. Lotusine inhibits the EGFR-Akt-ERK signaling pathway by reducing the levels of phosphorylated EGFR, Akt and ERK. Lotusine induces apoptosis, triggers G0/G1 cell cycle arrest and inhibits cancer cell proliferation. Lotusine reduces lipid peroxidation and increases the activities of SOD, CAT and GPx. Lotusine is applicable to researches related to non-small cell lung cancer, type 2 diabetes and autism spectrum disorder.

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Lotusine

Lotusine Chemical Structure

CAS No. : 6871-67-6

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Lotusine Related Antibodies

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Description

Lotusine is an orally active signaling pathway modulator and enzyme inhibitor, with an IC50 of 30.60 μg/mL against α-amylase and an IC50 of 36.15 μg/mL against α-glucosidase. Lotusine inhibits the EGFR-Akt-ERK signaling pathway by reducing the levels of phosphorylated EGFR, Akt and ERK. Lotusine induces apoptosis, triggers G0/G1 cell cycle arrest and inhibits cancer cell proliferation. Lotusine reduces lipid peroxidation and increases the activities of SOD, CAT and GPx. Lotusine is applicable to researches related to non-small cell lung cancer, type 2 diabetes and autism spectrum disorder[1][2][3][4].

In Vitro

Lotusine (2, 4, 10 μM; 24, 48, 72 h) potently inhibits proliferation of EGFR-mutant HCC827 NSCLC cells and EGFR-wildtype A549 NSCLC cells in time- and concentration-dependent manners, with stronger activity against HCC827 cells (73% inhibition at 10 μM for 72 h)[1].
Lotusine (2.5, 5, 10 μM; 24 h) induces concentration-dependent apoptosis in EGFR-mutant HCC827 NSCLC cells, with 80% of cells undergoing apoptosis at 10 μM for 24 h[1].
Lotusine (2.5, 5, 10 μM; 24 h) disrupts mitochondrial membrane potential in EGFR-mutant HCC827 NSCLC cells in a concentration-dependent manner, as evidenced by reduced JC-1 fluorescence ratios at 2.5, 5, and 10 μM for 24 h[1].
Lotusine (2.5, 5, 10 μM; 72 h) induces concentration-dependent G0/G1 phase cell cycle arrest in EGFR-mutant HCC827 NSCLC cells, halting progression into the DNA synthesis phase[1].
Lotusine (2.5, 5, 10 μM; 24 h) inhibits the EGFR-Akt-ERK signaling pathway in EGFR-mutant HCC827 NSCLC cells in vitro in a concentration-dependent manner, reducing p-EGFR, p-Akt, and p-ERK levels most significantly at 10 μM for 24 h[1].
Lotusine (25-50 μM; 48-72 h) does not significantly reduce the viability of HepG2 cells when administered alone or in combination with 25 mM D-glucose, maintaining 85-90% cell viability[2].
Lotusine (25-50 μM; 48-72 h, co-treated with 25 mM D-glucose) reverses hyperglycemia-induced reductions in SOD, CAT, and GPx antioxidant enzyme activities and lowers elevated MDA levels in HepG2 cells[2].
Lotusine (1.56-200 μg/mL; 10 min) inhibits alpha-amylase activity with an IC50 of 30.60 μg/mL, and achieves 80.36% inhibition at a concentration of 200 μg/mL in a cell-free biochemical assay[2].
Lotusine (1.56-200 μg/mL; 20 min) inhibits alpha-glucosidase activity with an IC50 of 36.15 μg/mL, and achieves 82.6% inhibition at a concentration of 200 μg/mL in a cell-free biochemical assay[2].
Lotusine (10-1000 μM; 24 h) exhibits low cytotoxicity in H9c2 cells, with an IC50 of 701 μM, and concentrations of 10, 50, and 100 μM maintain cell viability near control levels[3].
Lotusine (10-100 μM) enhances endogenous antioxidant (SOD, CAT, GSH) levels in H9c2 cells exposed to doxorubicin, supporting protection against oxidative stress[3].
Lotusine (10-100 μM) significantly reduces doxorubicin-induced lipid peroxidation in H9c2 cells, with 50 μM showing the greatest reduction[3].
Lotusine (10-50 μM; 24 h pretreatment) prevents doxorubicin-induced morphological and nuclear abnormalities in H9c2 cells[3].
Lotusine (10-50 μM) completely inhibits doxorubicin-induced ROS generation in H9c2 cells[3].
Lotusine (10-50 μM) modulates apoptotic gene expression in H9c2 cells exposed to doxorubicin, upregulating Bcl-2 and downregulating Bax and Cas-3 to inhibit apoptosis[3].
Lotusine (10-50 μM; 24 h pretreatment) reduces doxorubicin-induced caspase-3/7 activity in H9c2 cells, with 50 μM showing activity comparable to control cells[3].
Lotusine (50 μM; 3 h) directly interacts with and stabilizes DRD1 protein in PC12 cells[4].
Lotusine (3.12-25 μM; 48 h following 1 h 38 mM PPA pretreatment) protects PC12 cells against PPA-induced cytotoxicity[4].

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

Lotusine Related Antibodies

Cell Proliferation Assay[1]

Cell Line: human EGFR-mutant HCC827 NSCLC cells, human EGFR-wildtype A549 NSCLC cells
Concentration: 2.5, 5, 10 μM
Incubation Time: 24 h, 48 h, 72 h
Result: Inhibited approximately 73% of HCC827 cell proliferation at 10 μM for 72 h.
Inhibited approximately 52% of A549 cell proliferation at 10 μM for 72 h.
Exhibited time- and concentration-dependent inhibitory effects on both cell lines, with more pronounced activity in HCC827 cells.

Apoptosis Analysis[1]

Cell Line: human EGFR-mutant HCC827 NSCLC cells
Concentration: 2.5 μM (24 h); 5 μM (24 h); 10 μM (24 h)
Incubation Time: 24 h (2.5 μM); 24 h (5 μM); 24 h (10 μM)
Result: Induced a substantial increase in apoptosis relative to untreated cells at 2.5 μM for 24 h.
Induced apoptosis in more than 50% of HCC827 cells at 5 μM for 24 h.
Induced apoptosis in approximately 80% of HCC827 cells at 10 μM for 24 h.

Cell Cycle Analysis[1]

Cell Line: human EGFR-mutant HCC827 NSCLC cells
Concentration: 2.5 μM (72 h); 5 μM (72 h); 10 μM (72 h)
Incubation Time: 72 h (2.5 μM); 72 h (5 μM); 72 h (10 μM)
Result: Increased the proportion of cells in the G0/G1 phase in a concentration-dependent manner.
Decreased the S and G2/M phase cell populations in a concentration-dependent manner.

Western Blot Analysis[1]

Cell Line: human EGFR-mutant HCC827 NSCLC cells
Concentration: 2.5 μM (24 h); 5 μM (24 h); 10 μM (24 h)
Incubation Time: 24 h (2.5 μM); 24 h (5 μM); 24 h (10 μM)
Result: Reduced phosphorylated EGFR (p-EGFR) levels in a concentration-dependent manner.
Reduced phosphorylated Akt (p-Akt) levels in a concentration-dependent manner.
Reduced phosphorylated ERK (p-ERK) levels in a concentration-dependent manner.
Showed the highest inhibitory activity at 10 μM for 24 h.

Cell Viability Assay[2]

Cell Line: HepG2 cells
Concentration: 25 μM (alone; combined with 25 mM D-glucose); 50 μM (alone; combined with 25 mM D-glucose)
Incubation Time: 48 h (25 μM alone; 25 μM + 25 mM D-glucose); 72 h (50 μM alone; 50 μM + 25 mM D-glucose)
Result: Maintained 85-90% of HepG2 cell viability.
Showed no significant reduction in viability relative to control cells.

Cell Cytotoxicity Assay[3]

Cell Line: H9c2
Concentration: 10, 50, 100, 250, 500, 1000 μM
Incubation Time: 24 h
Result: Exhibited an IC50 value of 701 μM.
Maintained cell viability near control levels at 10, 50, and 100 μM.
Caused significant decreases in cell viability at concentrations from 250 to 1000 μM.

Cell Viability Assay[3]

Cell Line: H9c2
Concentration: 10, 50, 100 μM (pretreated prior to doxorubicin exposure)
Incubation Time: 24 h (pretreatment); 24 h (doxorubicin exposure)
Result: Maintained cell viability near control levels at 10 μM.
Induced cell proliferation at 50 μM, with viability values of 118.53 % (SRB assay) and 110.36 % (MTT assay).
Caused significantly reduced cell viability at 100 μM (84.41% in SRB assay, 79.84 % in MTT assay).

Western Blot Analysis[4]

Cell Line: rat pheochromocytoma PC12 cells
Concentration: 6.25 μM
Incubation Time: 48 h (following 1 h 38 mM PPA pretreatment)
Result: Restored PPA-induced reductions in DRD1, c-fos, GluA1, p-GluA1 Ser 845, and p-GluA1 Ser 831 protein levels.
Had its rescue effect abolished when co-treated with the DRD1 antagonist SCH23390.
In Vivo

Lotusine (50 mg/kg bw; diet supplementation; daily; 4 weeks) restores antioxidant vitamin levels and liver protein content, improves growth performance, and normalizes relative organ weight in streptozotocin-induced diabetic rats[2].
Lotusine (5-20 mg/kg; p.o.; daily; 5 days) ameliorates propionic acid-induced ASD-like social deficits and cognitive impairments in mice, with 10 and 20 mg/kg doses also restoring mPFC neuronal activity and AMPA receptor function via upregulation of c-fos and phosphorylated GluA1 levels[4].

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

Animal Model: Wistar (Sprague Dawley) (male, 160 ± 20 g, streptozotocin-induced diabetes mellitus)[2]
Dosage: 50 mg/kg bw
Administration: diet supplementation; daily; 4 weeks
Result: Restored serum, liver, and pancreatic vitamin C and E concentrations to near-normal values (liver vitamin C: 160 mg/100g; liver vitamin E: 2990 mg/100g).
Increased liver cell protein content to 11.6 mg/g.
Enhanced body weight gain by 45% compared to untreated diabetic rats (final body weight: 225.5 g; body weight gain: 65.3 g).
Reduced feed conversion ratio to 1.45, matching the ratio of non-diabetic control rats.
Lowered relative organ weight to 2.49%, a level comparable to non-diabetic control rats.
Maintained 100% survival rate.
Animal Model: C57BL/6J (male, 6-8 weeks old, 20 ± 2 g, intracerebroventricular injection of propionic acid to induce ASD-like behavior)[4]
Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: p.o.; daily; 5 days
Result: Significantly increased interaction time with a stranger mouse in the sociability test and with a novel stranger mouse in the social novelty test reversing PPA-induced social deficits.
Significantly increased the percentage of spontaneous alternations in the Y-maze test.
Significantly reversed the PPA-induced reduction in miniature excitatory postsynaptic current frequency in the medial prefrontal cortex at 10 mg/kg, with no effect on amplitude.
Significantly increased c-fos protein levels in the mPFC, reversing PPA-induced reductions.
Reversed PPA-induced reductions in p-GluA1 Ser845 protein levels in the mPFC; reversed PPA-induced reductions in p-GluA1 Ser831 protein levels in the mPFC .
Molecular Weight

314.40

Formula

C19H24NO3
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

C[N+]1(C)[C@H](CC2=CC=C(O)C=C2)C3=C(C=C(O)C(OC)=C3)CC1
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : ≥ 100 mg/mL (318.07 mM)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.1807 mL 15.9033 mL 31.8066 mL
5 mM 0.6361 mL 3.1807 mL 6.3613 mL
View the Complete Stock Solution Preparation Table

* 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.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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  • Dilution Calculator

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In Vivo Dissolution Calculator
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This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).
Purity & Documentation
References

Complete Stock Solution Preparation Table

* 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.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
H2O 1 mM 3.1807 mL 15.9033 mL 31.8066 mL 79.5165 mL
5 mM 0.6361 mL 3.1807 mL 6.3613 mL 15.9033 mL
10 mM 0.3181 mL 1.5903 mL 3.1807 mL 7.9517 mL
15 mM 0.2120 mL 1.0602 mL 2.1204 mL 5.3011 mL
20 mM 0.1590 mL 0.7952 mL 1.5903 mL 3.9758 mL
25 mM 0.1272 mL 0.6361 mL 1.2723 mL 3.1807 mL
30 mM 0.1060 mL 0.5301 mL 1.0602 mL 2.6506 mL
40 mM 0.0795 mL 0.3976 mL 0.7952 mL 1.9879 mL
50 mM 0.0636 mL 0.3181 mL 0.6361 mL 1.5903 mL
60 mM 0.0530 mL 0.2651 mL 0.5301 mL 1.3253 mL
80 mM 0.0398 mL 0.1988 mL 0.3976 mL 0.9940 mL
100 mM 0.0318 mL 0.1590 mL 0.3181 mL 0.7952 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Lotusine6871-67-6AmylasesGlycosidaseEGFR-Akt-ERK signalingtype 2 diabetes mellitusA549 NSCLC cellsautism spectrum disorderHepG2 cellsHCC827 NSCLC cellsα-glucosidasenon-small cell lung cancerporcine α-amylasedoxorubicin-induced cardiotoxicityInhibitorinhibitorinhibit

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