2. Neuronal Signaling
  3. Amino Acid Decarboxylase
  4. α-FMH

α-FMH (α-Fluoromethylhistidine) is an orally active histidine decarboxylase inhibitor. α-FMH depletes histamine in enterochromaffin-like (ECL) cells, reduces the number and volume density of secretory vesicles in ECL cells, and does not affect histamine storage in mast cells. α-FMH abolishes Omeprazole (HY-B0113)-induced vacuolization of ECL cells and decreases gastrin-induced histamine efflux from ECL cells. α-FMH does not alter the granular characteristics of ECL cells, omeprazole-induced hypertrophy of ECL cells, gastrin-induced pancreastatin-like immunoreactivity efflux, nor does it affect gastric acid secretion induced by histamine or vagal stimulation. α-FMH inhibits basal and gastrin-stimulated gastric acid secretion, reduces acid output induced by gastrin+IBMX (HY-12318), but does not directly affect acid generation in isolated parietal cells.

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α-FMH

α-FMH Chemical Structure

CAS No. : 73804-75-8

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Description

α-FMH (α-Fluoromethylhistidine) is an orally active histidine decarboxylase inhibitor. α-FMH depletes histamine in enterochromaffin-like (ECL) cells, reduces the number and volume density of secretory vesicles in ECL cells, and does not affect histamine storage in mast cells. α-FMH abolishes Omeprazole (HY-B0113)-induced vacuolization of ECL cells and decreases gastrin-induced histamine efflux from ECL cells. α-FMH does not alter the granular characteristics of ECL cells, omeprazole-induced hypertrophy of ECL cells, gastrin-induced pancreastatin-like immunoreactivity efflux, nor does it affect gastric acid secretion induced by histamine or vagal stimulation. α-FMH inhibits basal and gastrin-stimulated gastric acid secretion, reduces acid output induced by gastrin+IBMX (HY-12318), but does not directly affect acid generation in isolated parietal cells[1][2][3][4].

In Vivo

α-FMH (3 mg/kg per h; subcutaneous; continuous infusion; 6 weeks) depletes ECL cell histamine, reduces ECL cell secretory vesicle and microvesicle numbers, and alters secretory vesicle size, but does not affect ECL cell hypertrophy or granule ultrastructure in female Sprague-Dawley rats[1].
α-FMH (3 mg/kg per h; subcutaneous; continuous infusion; 6 weeks) depletes ECL cell histamine, abolishes omeprazole-induced ECL cell vacuole formation, reduces ECL cell secretory vesicle and microvesicle numbers and volume density, but does not affect omeprazole-induced ECL cell hypertrophy or granule ultrastructure in female Sprague-Dawley rats with omeprazole-induced hypergastrinemia[1].
α-FMH (3 mg/kg per h; subcutaneous; 24 h) reduces mouse oxyntic mucosal histamine by ~65%, depletes ECL cell secretory vesicles by ~84%, and increases plasma gastrin levels by 130%[2].
α-FMH (3 mg/kg per h; subcutaneous; 24 h) reduces rat oxyntic mucosal histamine by ~83%, depletes ECL cell secretory vesicles by ~88%, increases plasma gastrin levels by 143%, and does not affect other gastric oxyntic endocrine cell types[2].
α-FMH (3 mg/kg per h; subcutaneous; 24 h) reduces hamster oxyntic mucosal histamine by ~91%, depletes ECL cell secretory vesicles by ~89%, and reduces ECL cell profile size by ~33%, with no effect on plasma gastrin levels[2].
α-FMH (5 mg/kg/h; s.c.; continuous; 24 hours) produces 80% depletion of oxyntic mucosal histamine via irreversible inhibition of HDC, while leaving oxyntic mucosal pancreastatin-LI concentrations unaltered in male Sprague-Dawley rats[3].
α-FMH (3 mg/kg/h, 50 mg/kg; s.c., p.o.; continuous infusion, single dose; 2-6 days, 2 hours before testing) reduces oxyntic mucosal histamine by 80%, inhibits basal gastric acid secretion by over 60%, and almost abolishes gastrin-17-stimulated acid secretion, but does not alter histamine-stimulated or vagally induced (insulin or pylorus ligation) gastric acid secretion in female Sprague-Dawley rats[4].

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

Animal Model: Ross 308 (5 days old, food-deprived for 3 hours prior to injection)[1]
Dosage: 250 nmol (alone); 250 nmol (co-injected with 10 μg oxytocin)
Administration: i.c.v.; single injection
Result: Had no significant effect on cumulative food intake compared to the control group at 30, 60, or 120 minutes post-injection.
Significantly attenuated the hypophagic effect of oxytocin at 30, 60, and 120 minutes post-injection.
Animal Model: C57BL/6 wild-type (male, 22 to 25 g weight, ischemic stroke model via 30 min middle cerebral artery occlusion followed by 24 h reperfusion, preceded by 3 h normobaric hypoxic preconditioning with 8% O2)[2]
Dosage: 25 mg/kg
Administration: i.p.; single injection; 3 hours before hypoxic preconditioning
Result: Reversed the neuroprotective effects of hypoxic preconditioning, eliminating the reduction in infarct volume and improvement in neurologic deficit scores seen in untreated preconditioned wild-type mice.
Aggravated the reduction in peripheral cerebral blood flow during ischemia.
Prevented the hypoxia-induced increase in VEGF protein expression in the cerebral cortex.
Had no effect on infarct volume when administered alone.
Animal Model: Sprague-Dawley (female, 200-225 g at study start)[3]
Dosage: 3 mg/kg per h
Administration: subcutaneous; continuous infusion; 6 weeks
Result: Depleted ECL-cell histamine content and exerted no effects on ECL cell profile, cytoplasm area, granule number, or volume density.
Reduced secretory vesicle number and volume density with a decreased median diameter to 165 nm, and lowered microvesicle number without altering its volume density.
Eliminated ECL cell vacuoles, reduced the secretory vesicle-to-granule ratio to 2.8, and induced large, diffuse, weakly electron-dense cores in vesicles and granules.
Animal Model: Sprague-Dawley (6 months to 1 year-old male, healthy, free of pulmonary infection)[4]
Dosage: 0.2 mg/100 g; 0.5 mg/100 g; 1.0 mg/100 g
Administration: i.v.; single dose
Result: Determined the 50% inhibitory dose (ED50) for inhibition of mast cell histidine decarboxylation activity as 0.07 mg/100 g.
Reduced histamine formation to ~18,000 cpm (×103 cpm/105 mast cells) at 0.2 mg/100 g dose.
Reduced histamine formation to ~8,000 cpm (×103 cpm/105 mast cells) at 0.5 mg/100 g dose.
Reduced histamine formation to ~1,000 cpm (×103 cpm/105 mast cells) at 1.0 mg/100 g dose.
Animal Model: Sprague-Dawley (6 months to 1 year-old male, healthy, free of pulmonary infection)[4]
Dosage: 0.5 mg/100 g (i.v.); 2.0 mg/100 g (s.c.)
Administration: i.v.; single dose; s.c.; single dose
Result: Caused near-complete inhibition of histidine decarboxylation at 2 hours, with recovery to ~50% of baseline activity by 6 hours and full recovery.
Caused near-complete inhibition at 2 hours, with recovery to only ~20,000 cpm (×103 cpm/105 mast cells).
Animal Model: Sprague-Dawley (6 to 7-week-old male, healthy, free of pulmonary infection)[4]
Dosage: 1.07 mg/100 g per day
Administration: s.c.; continuous infusion; up to 6 days
Result: Reduced histamine formation to ~15,000 cpm (×103 cpm/105 mast cells) by day 1.
Reduced histamine formation to ~3,000 cpm (×103 cpm/105 mast cells) by day 2.
Maintained histamine formation at ~3,000 cpm (×103 cpm/105 mast cells) through day 6, sustaining inhibition below 10% of normal activity.
Animal Model: Sprague-Dawley (6 to 7-week-old male, healthy, free of pulmonary infection)[4]
Dosage: 2 mg/100 g (priming); 0.9 mg/100 g per day (infusion); 2 mg/100 g (priming); 1.8 mg/100 g per day (infusion)
Administration: i.v.; single priming dose; s.c.; continuous infusion; 14 days
Result: Reduced peritoneal histamine‑forming activity in a dose‑dependent manner after 14‑day administration.
Stabilized peritoneal cell histamine content at near‑baseline levels at both doses and blocked the marked histamine elevation observed in untreated controls.
Produced body weight gains comparable to untreated controls.
Animal Model: Sprague-Dawley (6 to 7-week-old male, healthy, free of pulmonary infection, mast cell histamine depletion induced by Polymyxin B (HY-149179))[4]
Dosage: 2 mg/100 g (priming); 0.9 mg/100 g per day (infusion); 2 mg/100 g (priming); 1.8 mg/100 g per day (infusion)
Administration: i.v.; single priming dose; s.c.; continuous infusion; 14 days
Result: Maintained peritoneal cell histamine content at 4.6 μg at 0.9 mg/100 g per day dose after 14 days.
Maintained peritoneal cell histamine content at 2.4 μg at 1.8 mg/100 g per day dose after 14 days.
Animal Model: ddy mice (male, 8 weeks old, 22 g)[5]
Dosage: 1 mg/kg; 5 mg/kg; 10 mg/kg; 25 mg/kg; 50 mg/kg; 100 mg/kg
Administration: i.p.; single dose
Result: Reduced brain, fundic stomach, and skin HDC activity to 10% of control at 5, 10, and 50 mg/kg within 4 h, respectively.
Dose-dependently decreased brain and stomach histamine to 40-50% of control, without affecting skin histamine.
Rapidly suppressed HDC activity in all three tissues within 1 h at 25 mg/kg.
Sustained brain HDC inhibition for 12 h (full recovery by 96 h); stomach HDC recovered by 48 h; skin HDC remained low for 48 h.
Lowered brain histamine to 50% for ≥ 48 h and stomach histamine to 40% within 8 h, while skin histamine was unchanged for 48 h.
Molecular Weight

187.17

Formula

C7H10FN3O2
CAS No.
SMILES

OC([C@@](CF)(N)CC1=CN=CN1)=O
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Keywords:

α-FMH73804-75-8α-FluoromethylhistidineAmino Acid Decarboxylasehistaminehistidine decarboxylaseECL cellHIF-1αC57BL/6 miceVEGFrat hypothalamus homogenateischemic strokesecretory vesicleSprague-Dawley ratsInhibitorinhibitorinhibit

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