1. GPCR/G Protein Neuronal Signaling Immunology/Inflammation
  2. Histamine Receptor
  3. IGN-2098

IGN-2098 is an orally active, competitive histamine H2 receptor antagonist with a pA2 value of 7.32. IGN-2098 inhibits basal and stimulated gastric acid secretion. IGN-2098 accelerates ulcer healing, suppresses ulcer edge elevation, and protects gastric and duodenal mucosa from damage. IGN-2098 can be used in research related to gastric ulcers.

For research use only. We do not sell to patients.

IGN-2098

IGN-2098 Chemical Structure

CAS No. : 126869-04-3

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Description

IGN-2098 is an orally active, competitive histamine H2 receptor antagonist with a pA2 value of 7.32. IGN-2098 inhibits basal and stimulated gastric acid secretion. IGN-2098 accelerates ulcer healing, suppresses ulcer edge elevation, and protects gastric and duodenal mucosa from damage. IGN-2098 can be used in research related to gastric ulcers[1][2].

IC50 & Target[1]

H2 Receptor

7.32 (pA2)

In Vitro

IGN-2098 competitively antagonizes histamine H2 receptors in isolated guinea pig atrial specimens with a pA2 value of 7.32[2].

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

In Vivo

IGN-2098 (10-30 mg/kg; p.o.; twice daily; 14 days) dose-dependently accelerates the healing of acetic acid-induced gastric ulcers in rats, with 10 mg/kg and 30 mg/kg doses achieving 49.6% and 52.7% healing ratios respectively, and significantly reduces ulcer edge prominence compared to controls[1].
IGN-2098 (1-60 mg/kg; p.o., s.c., i.d., i.p.; single dose) potently inhibits basal gastric secretion in pylorus-ligated rats across multiple routes, with subcutaneous administration showing the highest potency (ED50 0.7 mg/kg for acid output inhibition)[2].
IGN-2098 (0.1-30 mg/kg; s.c.; single dose) potently inhibits histamine-stimulated gastric acid secretion in acute fistula rats, with an ED50 of 0.2 mg/kg[2].
IGN-2098 (0.3-30 mg/kg; s.c.; single dose) potently inhibits Carbachol (HY-B1208)-stimulated gastric acid secretion in acute fistula rats, with an ED50 of 0.3 mg/kg[2].
IGN-2098 (1-30 mg/kg; s.c.; single dose) potently inhibits Pentagastrin (HY-A0261)-stimulated gastric acid secretion in acute fistula rats, with an ED50 of 0.1 mg/kg[2].
IGN-2098 (3-60 mg/kg; s.c.; single dose) inhibits 2-deoxy-D-glucose (HY-13966)-stimulated gastric acid secretion in anesthetized rats, with an ED50 of 42.7 mg/kg[2].
IGN-2098 (3-60 mg/kg; p.o., s.c.; single dose) inhibits pylorus ligation-induced gastric ulcers in rats, with an ED50 of 29.7 mg/kg[2].
IGN-2098 (1-60 mg/kg; p.o.; single dose) inhibits water-immersion stress-induced gastric mucosal injury in rats, with an ED50 of 8.4 mg/kg[2].
IGN-2098 (0.3-3 mg/kg; p.o.; single dose) potently inhibits histamine-induced gastric mucosal injury in rats, with an ED50 of 0.9 mg/kg[2].
IGN-2098 (3-30 mg/kg; p.o.; single dose) inhibits Indomethacin (HY-14397)-induced gastric mucosal injury in rats, with an ED50 of 5.4 mg/kg[2].
IGN-2098 (1-30 mg/kg; p.o.; single dose) potently inhibits HCl-Aspirin (HY-14654)-induced gastric mucosal injury in rats, with an ED50 of 1.4 mg/kg, making it 8.1 times more potent than roxatidine[2].
IGN-2098 (3-60 mg/kg; p.o.; single dose) inhibits HCl-ethanol-induced gastric mucosal injury in rats, with an ED50 of 17.0 mg/kg[2].

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

Animal Model: Sprague-Dawley (male, 7 weeks old, gastric ulcer induced by 20% acetic acid injection)[1]
Dosage: 10 mg/kg; 30 mg/kg
Administration: p.o.; twice daily; 14 days
Result: Reduced mean ulcer index to 6.4 mm2 and achieved a 49.6% healing ratio at 10 mg/kg, with a significant difference versus control.
Reduced mean ulcer index to 6.0 mm2 and achieved a 52.7% healing ratio at 30 mg/kg, with a significant difference versus control.
Significantly reduced prominent ulcer edges versus control at both 10 mg/kg and 30 mg/kg.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 1-60 mg/kg (p.o.); 0.3-30 mg/kg (s.c.); 1-30 mg/kg (i.d.); 1-30 mg/kg (i.p.)
Administration: p.o.; single dose (0.5, 3, or 9 hours before pylorus ligation); s.c.; single dose (0.5 hours before pylorus ligation); i.d.; single dose (immediately after pylorus ligation); i.p.; single dose (0.5 hours before pylorus ligation)
Result: Reduced gastric juice volume by 53.1% and acid output by 78.5% at 10 mg/kg p.o.
0.5 hours before ligation, with an ED50 of 4.3 mg/kg for acid output inhibition.
Reduced acid output by 71.7% at 10 mg/kg p.o.
3 hours before ligation, and by 88.0% at 30 mg/kg p.o.
3 hours before ligation, with an ED50 of 5.0 mg/kg.
Reduced acid output by 66.5% at 30 mg/kg p.o.
9 hours before ligation, and by 78.8% at 60 mg/kg p.o.
9 hours before ligation, with an ED50 of 16.9 mg/kg.
Reduced acid output by 71.2% at 1 mg/kg s.c., with an ED50 of 0.7 mg/kg.
Reduced acid output by 65.0% at 3 mg/kg i.d., with an ED50 of 1.1 mg/kg.
Reduced acid output by 64.5% at 10 mg/kg i.p., with an ED50 of 3.6 mg/kg.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 0.1-30 mg/kg
Administration: s.c.; single dose (0.5 hours before first histamine administration)
Result: Reduced histamine-stimulated acid output by 30.3% at 0.1 mg/kg, 69.3% at 0.3 mg/kg, 73.5% at 1 mg/kg, 89.4% at 3 mg/kg, 92.0% at 10 mg/kg, and 97.5% at 30 mg/kg.
Achieved an ED50 of 0.2 mg/kg for acid output inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 0.3-30 mg/kg
Administration: s.c.; single dose (0.5 hours before carbachol infusion)
Result: Reduced carbachol-stimulated acid output by 42.9% at 0.3 mg/kg, 65.5% at 1 mg/kg, 78.1% at 3 mg/kg, 85.6% at 10 mg/kg, and 80.8% at 30 mg/kg.
Achieved an ED50 of 0.3 mg/kg for acid output inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 1-30 mg/kg
Administration: s.c.; single dose (0.5 hours before pentagastrin infusion)
Result: Reduced pentagastrin-stimulated acid output by 79.5% at 1 mg/kg, 52.7% at 3 mg/kg, 84.9% at 10 mg/kg, and 98.3% at 30 mg/kg.
Achieved an ED50 of 0.1 mg/kg for acid output inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 3-60 mg/kg
Administration: s.c.; single dose (0.5 hours after stimulated secretion stabilized)
Result: Reduced 2-deoxy-D-glucose-stimulated acid output by 65.9% at 60 mg/kg.
Achieved an ED50 of 42.7 mg/kg for acid output inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 3-60 mg/kg
Administration: p.o.; single dose (30 minutes before ligation); s.c.; single dose (7 hours after ligation)
Result: Reduced ulcer coefficients by 55.9% at 30 mg/kg, and 61.8% at 60 mg/kg.
Achieved an ED50 of 29.7 mg/kg for ulcer inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 1-60 mg/kg
Administration: p.o.; single dose (30 minutes before stress exposure)
Result: Reduced lesion length by 43.1% at 3 mg/kg, 59.1% at 10 mg/kg, 55.8% at 30 mg/kg, and 84.0% at 60 mg/kg.
Achieved an ED50 of 8.4 mg/kg for lesion inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 0.3-3 mg/kg
Administration: p.o.; single dose (30 minutes before histamine administration)
Result: Reduced lesion area by 86.7% at 3 mg/kg.
Achieved an ED50 of 0.9 mg/kg for lesion inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 3-30 mg/kg
Administration: p.o.; single dose (30 minutes before indomethacin administration)
Result: Reduced lesion length by 52.2% at 10 mg/kg, and 91.8% at 30 mg/kg.
Achieved an ED50 of 5.4 mg/kg for lesion inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 1-30 mg/kg
Administration: p.o.; single dose (30 minutes before HCl-aspirin administration)
Result: Reduced lesion length by 78.1% at 3 mg/kg, 90.9% at 10 mg/kg, and 95.0% at 30 mg/kg.
Achieved an ED50 of 1.4 mg/kg for lesion inhibition.
Animal Model: Sprague-Dawley (male, SPF, 220-270g)[2]
Dosage: 3-60 mg/kg
Administration: p.o.; single dose (30 minutes before HCl-ethanol administration)
Result: Reduced lesion length by 62.0% at 20 mg/kg, 77.3% at 30 mg/kg, and 94.1% at 60 mg/kg.
Achieved an ED50 of 17.0 mg/kg for lesion inhibition.
Molecular Weight

455.42

Formula

C22H32Cl2N4O2

CAS No.
SMILES

O=C1N=C(NC/C=C/COC2=CC=CC(CN3CCCCC3)=C2)NC(C)=C1C.Cl.Cl

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Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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IGN-2098
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