MDL 72394
MDL 72394 (FMMT) is an orally active, blood-brain barrier-penetrant amino acid-based prodrug compound. MDL 72394 is decarboxylated by aromatic L-amino acid decarboxylase to generate the active metabolite MDL 72392 (HY-182727), which is a covalent irreversible MAO inhibitor. MDL 72394 is transported into the brain and synaptosomes via the L-neutral amino acid transport system and the norepinephrine transporter. MDL 72394 selectively inhibits MAO in noradrenergic and dopaminergic neurons without inhibiting serotonergic neurons. MDL 72394 increases hypothalamic extracellular 5-HT, tissue 5-HT, and pineal melatonin biosynthesis, and decreases 5-HIAA. MDL 72394 can be used in research related to MAO-mediated diseases, such as depression.
For research use only. We do not sell to patients.
- CAS No.: 99630-95-2
- Formula: C10H10FNO3
- Molecular Weight:211.19
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All 5-HT Receptor Isoforms
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Biological Activity
Description
In Vitro
MDL 72394 (FMMT) is stereoselectively decarboxylated by AADC in porcine kidney and intact rat brain synaptosomes to form (E)-β-fluoromethylene-m-tyramine, which is a potent, time-dependent, irreversible inhibitor of rat brain MAO, with approximately 10-fold selectivity for MAO type A[3].
MDL 72394 (0.75-7.5 μM; 15 min) is actively transported into rat brain synaptosomes via an amino acid carrier, as leucine dose-dependently attenuates FMMT-mediated MAO inhibition in intact synaptosomes but not in sonicated synaptosomes[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MDL 72394 (0.003-0.1 mg/kg; oral; once daily; 7 days) in combination with Carbidopa (HY-B0311) enhances the preference for MAO inhibition within noradrenergic and dopaminergic neurons, with ED50 values of 0.016 and 0.010 mg/kg, respectively[1].
MDL 72394 (0.05-0.1 mg/kg; oral; 24 h) in combination with the selective NA uptake inhibitor CPP 199 antagonizes the preferential inhibition of MAO within noradrenergic neurons by FMMT, indicating that this preference is due to the accumulation of the active metabolite by the NA transporter[1].
MDL 72394 (0.5-2 mg/kg; intraperitoneal injection; single administration) produced the greatest increase in hypothalamic extracellular 5-HT, but even after L-tryptophan it failed to induce 5-HT behavioral syndrome, whereas MAO-A inhibition alone at 0.5 mg/kg was insufficient to elevate extracellular 5-HT or behavior[2].
MDL 72394 (FMMT) (0.5 mg/kg; intraperitoneal injection) inhibits MAO in vivo, but this effect is abolished by pretreatment with MFMD to inhibit AADC, confirming that FMMT requires decarboxylation by AADC to inhibit MAO[3].
MDL 72394 (0.1-0.5 mg/kg; intraperitoneal injection) is actively transported into the brain in vivo, as high-dose leucine attenuates its MAO inhibitory effect in the brain, but not in peripheral tissues[3].
MDL 72394 (0.1 mg/kg; oral) in combination with carbidopa produced significantly less MAO inhibition in the 6-OHDA-lesioned striatum than in the intact striatum, indicating that FMMT is decarboxylated within dopamine-containing neurons of the nigrostriatal bundle; moreover, the MAO A inhibitory effect on the MFMD-infused side of the striatum was significantly reduced, confirming that neuronal AADC is essential for FMMT activation and neuronal selectivity[3].
MDL 72394 (0.015-1 mg/kg; oral; daily; 5 days) in combination with Carbidopa produced brain MAO inhibition (-76%) and monoamine elevation comparable to higher doses of FMMT alone, but with significantly reduced tyramine potentiation, indicating that combination with a peripheral AADC inhibitor can reduce adverse tyramine interactions[3].
MDL 72394 (MDL) (0.5 mg/kg; intraperitoneal injection; single administration) administered systemically stimulated melatonin biosynthesis in the rat pineal gland, increasing melatonin to 1.49 ng/pineal gland, most likely due to selective MAO-A inhibition caused by the decarboxylation product of MDL 72394, MDL 72392[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley rats (male, 180-220 g)[1]
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Dosage:0.1, 0.25, 0.5, 1 mg/kg
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Administration:s.c.; single injection
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Result:Inhibited [14C]5-HT deamination with ED50 0.42 mg/kg s.c. outside and 0.50 mg/kg s.c. inside serotonergic neurons in the hypothalamus.
Inhibited NA deamination with ED50 0.24 mg/kg s.c. inside and 0.40 mg/kg s.c. outside noradrenergic neurons.
Inhibited DA deamination with ED50 0.20 mg/kg s.c. inside and 0.25 mg/kg s.c. outside dopaminergic neurons in the striatum.
Had no effect on neuronal uptake of the biogenic amines studied.
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Animal Model:Sprague-Dawley rats (male, 180-220 g)[1]
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Dosage:0.025, 0.05, 1 mg/kg (5-HT)
0.003, 0.01, 0.025, 0.05 mg/kg (NA, DA) -
Administration:p.o.; once daily; 7 days
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Result:Inhibited 5-HT deamination with ED50 0.027 mg/kg p.o. outside and 0.048 mg/kg p.o. inside serotonergic neurons.
Inhibited MAO within noradrenergic and dopaminergic neurons with ED50 0.016 and 0.010 mg/kg p.o., respectively, and outside these neurons with ED50 0.035 and 0.020 mg/kg p.o., respectively.
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Animal Model:Sprague-Dawley rats (male, 180-220 g)[1]
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Dosage:0.05, 0.1 mg/kg
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Administration:p.o.; single dose
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Result:In control rats, produced 38% inhibition inside and 20% inhibition outside NA neurons at 0.05 mg/kg p.o.; produced 65% inhibition inside and 37% inhibition outside NA neurons at 0.1 mg/kg p.o.
In CPP 199-pretreated rats, produced 17% inhibition inside and 23% inhibition outside NA neurons at 0.05 mg/kg p.o.; produced 52% inhibition inside and 41% inhibition outside NA neurons at 0.1 mg/kg p.o.
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Animal Model:Sprague-Dawley rats (male, 200-300 g)[3]
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Dosage:0.5 mg/kg; 0.1 mg/kg
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Administration:i.p.; single injection
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Result:Oral pretreatment with leucine (1 g/kg p.o.) attenuated the MAO inhibitory effect in brain but not in peripheral tissues.
Carbidopa attenuated the effect of FMMT in the heart, liver, and duodenum.
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Animal Model:Fisher 344N rat (male, 2 months old, 200 g)[4]
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Dosage:0.5 mg/kg
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Administration:i.p.; single dose
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Result:Elevated pineal melatonin to 1.49 ng/pineal compared to 0.19 ng/pineal in saline controls.
Elevated pineal 5-HT to 52.96 ng/pineal compared to 38.13 ng/pineal in saline controls.
Elevated pineal NAS to 1.4 ng/pineal compared to 0.15 ng/pineal in saline controls.
Decreased pineal 5-HIAA to 2.15 ng/pineal compared to 4.18 ng/pineal in saline controls.
Chemical Information
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CAS No. 99630-95-2
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Molecular Weight 211.19
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Formula C10H10FNO3
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Synonyms
FMMT
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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.
Protocols
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Human pluripotent stem cell midbrain dopaminergic neuron differentiation
Human pluripotent stem cells are directed toward midbrain dopaminergic neurons by first inducing a neural floor-plate-like progenitor state, then patterning cells with ventralizing SHH signaling and midbrain/WNT-FGF cues, and finally maturing progenitors into neurons expressing dopaminergic markers such as TH, NURR1/NR4A2, PITX3, DAT/SLC6A3, VMAT2/SLC18A2, GIRK2/KCNJ6, FOXA2, LMX1A, and EN1. The main readouts are loss of pluripotency, acquisition of FOXA2+/LMX1A+ midbrain floor-plate progenitors, emergence of βIII-tubulin+/MAP2+ neurons, and production of TH+ dopaminergic neurons with molecular, dopamine-release, and electrophysiological features of midbrain dopaminergic identity.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- MDL 72394
- 99630-95-2
- FMMT
- MDL72394
- MDL-72394
- Drug Intermediate
- 5-HT Receptor
- Monoamine Oxidase
- serotonergic neurons
- bioprecursor amino acid
- MAO-B
- MAO-A
- (E)-β-fluoromethylene-m-tyramine
- L neutral amino acid transport system
- noradrenergic and dopaminergic neurons
- noradrenaline transporter
- brain-selective monoamine oxidase (MAO) inhibitor
- AADC-mediated decarboxylation
- Inhibitor
- inhibitor
- inhibit