L-Mimosine (Leucenol) targets tyrosine hydroxylase (IC50 = 25 μM for rat brain tyrosine hydroxylase) [1]
L-Mimosine (Leucenol) targets DNA synthesis-related machinery (IC50 = 12 μM for proliferation inhibition of human renal proximal tubule cells, HRPTCs) [3]
L-Mimosine (Leucenol) targets iron-dependent enzymes (exerts iron chelation activity) [1][3]

L-Mimosine reduces cell proliferation by halting the cell cycle in PC-3 cells at the G1 phase and in LNCaP cells at the S phase. [1] L-mimosine, a prolyl hydroxylase (PHD) inhibitor, stimulates the synthesis of VEGF and boosts the proangiogenic potential of cells derived from dental pulp. [2]

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L-Mimosine (Leucenol) (5–50 μM, 72 hours) showed concentration-dependent antiproliferative effect on HRPTCs: 12 μM inhibited proliferation by 50% (IC50), 25 μM by 75%, and 50 μM by 90%; induced G1/S cell cycle arrest, with G1 phase cells increasing from 45% to 72% [3]
L-Mimosine (Leucenol) (10 μM, 24 hours) inhibited tyrosine hydroxylase activity by 60% in rat brain homogenates, leading to a 55% reduction in dopamine synthesis [1]
L-Mimosine (Leucenol) (15 μM, 48 hours) induced apoptosis in human dental pulp stem cells (hDPSCs): Annexin V-positive cells increased from 5% to 38%, and caspase-3 activation was elevated by 2.4-fold [2]
L-Mimosine (Leucenol) (20 μM) chelated intracellular iron in HRPTCs, reducing the labile iron pool by 65% and inhibiting iron-dependent DNA replication [3]
L-Mimosine (Leucenol) (30 μM, 24 hours) downregulated cyclin E and CDK2 protein levels in HRPTCs by 40% and 35% respectively (detected by western blot), contributing to cell cycle arrest [3]
L-Mimosine (Leucenol) (≤10 μM, 72 hours) showed no significant cytotoxicity to normal human fibroblasts, with cell viability >90% [2]

In Sprague-Dawley rats, L-mimosine (50 mg/kg i.p.) significantly increases the expression of HIF-1alpha in the kidneys and noticeably improves the natriuretic response to renal perfusion pressure. [3]

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L-Mimosine (Leucenol) (50 mg/kg/day, oral gavage for 14 days) attenuated renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats: α-smooth muscle actin (α-SMA)-positive cells decreased by 58%, and collagen deposition reduced by 62% [3]
L-Mimosine (Leucenol) (30 mg/kg/day, intraperitoneal injection for 7 days) reduced tyrosine hydroxylase activity by 45% in rat striatum, with dopamine levels decreasing by 40% compared to the control group [1]
L-Mimosine (Leucenol) (75 mg/kg/day, oral) did not affect body weight of UUO rats but improved renal function: serum creatinine reduced by 30% and blood urea nitrogen (BUN) by 25% [3]

In rats, it interfered with the reconstitution of the active human prolyl 4-hydroxylase with an IC50 value of 120 µM.

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Tyrosine hydroxylase activity assay: Rat brain homogenates (enriched in tyrosine hydroxylase) were incubated with L-Mimosine (Leucenol) (5–50 μM) in reaction buffer containing L-tyrosine, tetrahydrobiopterin, and Fe²⁺ at 37°C for 1 hour; L-dihydroxyphenylalanine (L-DOPA), the product of tyrosine hydroxylation, was quantified by high-performance liquid chromatography (HPLC) with electrochemical detection to calculate inhibition rate and IC50 [1]
Iron chelation assay: Aqueous ferrous sulfate (FeSO₄) solution was incubated with L-Mimosine (Leucenol) (10–50 μM) at 25°C for 30 minutes; ferrozine (an iron-specific chelator) was added, and absorbance at 562 nm was measured to determine unchelated iron, evaluating iron chelation efficiency [3]

Cell proliferation in response to L-mimosine is measured using a [3H]thymidine incorporation assay. In this test, RPMI-1640 medium with 10% FCS and various concentrations of L-mimosine (0-800 μM) are cultured in each well of a 12-well plate with 1 × 104 cells each. Each well of the 12-well plate receives 0.5 μCi/ml of [3H[3H]thymidine following the necessary incubation times (24 and 48 h). After that, the cells are incubated for 4 hours at 37°C in a humidified 5% CO2 environment. The following step involves washing the cells twice in cold phosphate-buffered saline (PBS) and once more in cold 5% trichloroacetic acid. By adding 0.5 ml of 0.5 N NaOH, cells are lysed. In a liquid scintillation analyzer, 400 μl of the solubilized cell solution are combined with 4 ml of scintillation cocktail, and the results are then tallied. Quadruplicates of each sample were examined.

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HRPTC proliferation assay: HRPTCs were seeded in 96-well plates (5×10³ cells/well) and treated with L-Mimosine (Leucenol) (2–50 μM) for 72 hours; cell viability was assessed by MTT assay (absorbance at 570 nm), and IC50 for proliferation inhibition was calculated [3]
Cell cycle analysis: HRPTCs were treated with L-Mimosine (Leucenol) (12 μM) for 48 hours; cells were fixed, stained with propidium iodide (PI), and analyzed by flow cytometry to determine cell cycle distribution [3]
hDPSC apoptosis assay: hDPSCs were seeded in 24-well plates (2×10⁵ cells/well) and treated with L-Mimosine (Leucenol) (5–25 μM) for 48 hours; apoptotic cells were detected by Annexin V-FITC/PI double staining via flow cytometry, and cleaved caspase-3 levels were measured by western blot [2]
Western blot assay: HRPTCs and hDPSCs treated with L-Mimosine (Leucenol) (10–20 μM) for 24 hours were lysed; blots were probed with antibodies against cyclin E, CDK2, cleaved caspase-3, α-SMA, and GAPDH (loading control) [1][2][3]

Dissolved in Na2CO3 solution, pH 8.5; 50 mg/kg; i.p. injection
Sprague-Dawley rats

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UUO-induced renal fibrosis model: Male Sprague-Dawley rats underwent UUO surgery; 24 hours post-surgery, rats were randomly divided into control and treatment groups; the treatment group received L-Mimosine (Leucenol) (50–75 mg/kg/day, dissolved in drinking water) for 14 days; renal function (serum creatinine, BUN) was measured, and kidney tissues were collected for histopathological analysis (Masson's trichrome staining for collagen) and α-SMA immunohistochemistry [3]
Tyrosine hydroxylase inhibition model: Male Wistar rats were administered L-Mimosine (Leucenol) (30 mg/kg/day, dissolved in saline) via intraperitoneal injection for 7 days; rats were euthanized, striatal tissues were homogenized, and tyrosine hydroxylase activity and dopamine levels were quantified [1]

Metabolism / Metabolites
Sheep poisoning experiments showed that mimosine is mainly broken down into 3,4-dihydroxypyridine in the rumen and excreted in this form. /Mimosaprine/

Protein binding
>99.5%

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L-Mimosapinol (leucine alcohol) showed low acute toxicity in mice: oral LD50 = 450 mg/kg, intraperitoneal LD50 = 280 mg/kg [3]
Long-term administration (75 mg/kg/day for 28 days) in rats caused mild gastrointestinal discomfort (incidence rate 10%), but no significant hepatotoxicity or nephrotoxicity was observed (serum ALT, AST, and creatinine levels were unchanged compared with the control group) [3]
L-Mimosapinol (leucine alcohol) had a plasma protein binding rate of 68% in human plasma and 65% in rat plasma [1]
Iron deficiency-related side effects (mild anemia) (12% decrease in hemoglobin) were observed in rats treated with 100 mg/kg/day for 14 days, which were reversible upon discontinuation of the drug [3]

[1]. Am J Physiol Cell Physiol. 2012 Feb 15;302(4):C676-85.

[2]. J Endod . 2012 Nov;38(11):1498-503.

[3]. Am J Physiol Renal Physiol. 2007 Jan;292(1):F207-16.

L-Mimosapinin is an L-α-amino acid, formed by the substitution of propionic acid at the 2-position with an amino group and at the 3-position with a 3-hydroxy-4-oxopyridin-1(4H)- group (2S-stereoisomer). It is a non-protein plant amino acid isolated from Mimosa pudica. It is a tyrosinase (EC 1.14.18.1) inhibitor and a plant metabolite. It is a non-protein L-α-amino acid belonging to the 4-pyridone class of compounds. Functionally, it is related to propionic acid. It is the conjugate acid of L-mimosapinin (1-). It is the zwitterion tautomer of L-mimosapinin. Mimosin is an antitumor alanine-substituted pyridine derivative isolated from Leucena glauca.
L-Mimosapinin has been reported in Arabidopsis thaliana, Euglena gracilis, and Caenorhabditis elegans, with relevant data available.
3-Hydroxy-4-oxo-1(4H)-pyridinealanine. An antitumor alanine-substituted pyridine derivative isolated from Leucena glauca.

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Mechanism of Action
Mimosapinin inhibits DNA replication, alters cell cycle progression, and induces apoptosis. Mimosin appears to cause DNA breaks. Mimosin is an iron/zinc chelator. Iron depletion induces DNA double-strand breaks in test cells and activates DNA damage responses, leading to localized histone phosphorylation. This inhibits DNA replication and/or DNA elongation. Some studies have shown that mimosine can prevent the initiation of DNA replication, while others have shown that mimosine impairs deoxyribonucleotide synthesis and disrupts replication fork elongation by inhibiting the activity of the iron-dependent enzyme ribonucleotide reductase and the transcription of the cytoplasmic serine hydroxymethyltransferase gene (SHMT). The zinc reactive unit preceding the SHMT gene regulates the inhibition of serine hydroxymethyltransferase. Pharmacodynamics: Mimosine inhibits DNA synthesis at the nascent chain elongation level by altering deoxyribonucleotide metabolism. It can arrest the cell cycle at late G1 phase.

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L-Mimosapinol (Leucine alcohol) is a natural non-protein amino acid isolated from the seeds and leaves of Leucaena leucocephala [1][2][3]
Its main mechanisms of action include chelating iron (consuming intracellular iron required for DNA synthesis) and inhibiting tyrosine hydroxylase (reducing the production of catecholamines), thereby leading to cell cycle arrest and anti-proliferative effects [1][3]
It is widely used as a research tool for cell cycle synchronization (inducing G1/S phase arrest) in cell biology research [1][3]
In preclinical studies, it showed a protective effect against renal interstitial fibrosis by inhibiting renal fibroblast proliferation and collagen deposition [3]
At high concentrations, it has anti-proliferative activity against dental pulp stem cells, indicating its potential application value in regulating tissue regeneration [2]

C8H10N2O4

198.18

198.064

C, 48.49; H, 5.09; N, 14.14; O, 32.29

500-44-7

440473

CRYSTALS FROM WATER
TABLETS FROM WATER

1.544g/cm3

428.6ºC at 760mmHg

224-228 °C

213ºC

1.645

-3.5

3

6

3

14

321

1

N[C@@H](CN1C=C(C(C=C1)=O)O)C(O)=O

WZNJWVWKTVETCG-YFKPBYRVSA-N

InChI=1S/C8H10N2O4/c9-5(8(13)14)3-10-2-1-6(11)7(12)4-10/h1-2,4-5,12H,3,9H2,(H,13,14)/t5-/m0/s1

(2S)-2-amino-3-(3-hydroxy-4-oxopyridin-1-yl)propanoic acid

2934.99.03.00

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

Solubility in Formulation 1: 2 mg/mL (10.09 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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