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

IGN-2098 (10-30 mg/kg; oral; twice daily; 14 days) accelerated the healing of acetic acid-induced gastric ulcers in rats in a dose-dependent manner, with healing rates of 49.6% and 52.7% at doses of 10 mg/kg and 30 mg/kg, respectively, and significantly reduced the protrusion of ulcer edges compared with the control group [1]. IGN-2098 (1-60 mg/kg; oral, subcutaneous, oral, intraperitoneal; single dose) effectively inhibited basal gastric acid secretion in rats with pyloric ligation through multiple routes, with subcutaneous administration showing the highest efficacy (ED50 for inhibiting gastric acid secretion was 0.7 mg/kg) [2]. IGN-2098 (0.1-30 mg/kg; subcutaneous injection; single dose) effectively inhibited histamine-stimulated gastric acid secretion in rats with acute fistulas, with an ED50 of 0.2 mg/kg [2]. IGN-2098 (0.3-30 mg/kg; subcutaneous injection; single dose) effectively inhibited carbacholine-stimulated gastric acid secretion in rats with acute fistulas, with an ED50 of 0.3 mg/kg[2]. IGN-2098 (1-30 mg/kg; subcutaneous injection; single dose) effectively inhibited pentagastrin-stimulated gastric acid secretion in rats with acute fistulas, with an ED50 of 0.1 mg/kg[2]. IGN-2098 (3-60 mg/kg; subcutaneous injection; single dose) inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion in anesthetized rats, with an ED50 of 42.7 mg/kg[2]. IGN-2098 (3-60 mg/kg; oral, subcutaneous injection; single dose) inhibited pyloric ligation-induced gastric ulcers in rats, with an ED50 of 29.7 mg/kg[2]. IGN-2098 (1-60 mg/kg; orally; single dose) inhibited water immersion stress-induced gastric mucosal damage in rats, with an ED50 of 8.4 mg/kg[2]. IGN-2098 (0.3-3 mg/kg; orally; single dose) effectively inhibited histamine-induced gastric mucosal damage in rats, with an ED50 of 0.9 mg/kg[2]. IGN-2098 (3-30 mg/kg; orally; single dose) inhibited indomethacin-induced gastric mucosal damage in rats, with an ED50 of 5.4 mg/kg[2]. IGN-2098 (1-30 mg/kg; orally; single dose) effectively inhibited aspirin hydrochloride-induced gastric mucosal damage in rats, with an ED50 of 1.4 mg/kg, which is 8.1 times more potent than roxatidine[2]. IGN-2098 (3-60 mg/kg; orally; single dose) inhibited HCl-ethanol-induced gastric mucosal damage in rats, with an ED50 of 17.0 mg/kg[2].

Animal/Disease Models:Sprague-Dawley mice (male, 7 weeks old, gastric ulcer induced by 20% acetic acid injection)[1]
Doses: 10 mg/kg; 30 mg/kg
Route of Administration: Oral; twice daily; 14 days
Experimental Results: The average ulcer area in the 10 mg/kg dose group decreased to 6.4 mm², and the healing rate reached 49.6%, which was significantly different from the control group. The average ulcer area in the 30 mg/kg dose group decreased to 6.0 mm², and the healing rate reached 52.7%, which was significantly different from the control group. Both the 10 mg/kg and 30 mg/kg dose groups significantly reduced the protrusion of the ulcer edge.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 1-60 mg/kg (oral); 0.3-30 mg/kg (subcutaneous); 1-30 mg/kg (intradermal); 1-30 mg/kg (intraperitoneal)
Route of Administration: Oral; single dose (0.5, 3 or 9 hours before pyloric ligation); subcutaneous; single dose (0.5 hours before pyloric ligation); intradermal; single dose (immediately after pyloric ligation); intraperitoneal; single dose (0.5 hours before pyloric ligation)
Experimental Results: Oral administration of 10 mg/kg 0.5 hours before ligation reduced gastric fluid volume by 53.1%, gastric acid secretion by 78.5%, and the ED50 for inhibiting gastric acid secretion was 4.3 mg/kg. Oral administration of 10 mg/kg 3 hours before ligation reduced gastric acid secretion by 71.7%; oral administration of 30 mg/kg 3 hours before ligation reduced gastric acid secretion by 88.0%, with an ED50 of 5.0 mg/kg. Oral administration of 30 mg/kg 9 hours before ligation reduced gastric acid secretion by 66.5%; oral administration of 60 mg/kg 9 hours before ligation reduced gastric acid secretion by 78.8%, with an ED50 of 16.9 mg/kg. Subcutaneous injection of 1 mg/kg reduced acid secretion by 71.2%, with an ED50 of 0.7 mg/kg. Intraperitoneal injection of 3 mg/kg reduced acid secretion by 65.0%, with an ED50 of 1.1 mg/kg. Intraperitoneal injection of 10 mg/kg reduced acid secretion by 64.5%, with an ED50 of 3.6 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 0.1-30 mg/kg
Route of Administration: Subcutaneous injection; single dose (0.5 hours before the first administration of histamine)
Experimental Results: Histamine-stimulated gastric acid secretion decreased 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. The ED50 for inhibiting gastric acid secretion was 0.2 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 0.3-30 mg/kg
Route of Administration: Subcutaneous injection; single dose (0.5 hours before carbachol infusion)
Experimental Results: Carbachol-stimulated gastric acid secretion decreased 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. The ED50 for inhibiting gastric acid secretion was 0.3 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 1-30 mg/kg
Route of Administration: Subcutaneous injection; single administration (0.5 hours before pentagastrin infusion)
Experimental Results: Pentagastrin-stimulated gastric acid secretion decreased 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. The ED50 for inhibiting gastric acid secretion was 0.1 mg/kg.

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Animal/Disease Models:Sprague-Dawley chickens (male, SPF, 220-270g)[2]
Doses: 3-60 mg/kg
Route of Administration: Subcutaneous injection; single dose (0.5 hours after stimulation of secretion stabilization)
Experimental Results: At a dose of 60 mg/kg, 2-deoxy-D-glucose-stimulated gastric acid secretion was reduced by 65.9%. The ED50 for inhibiting gastric acid secretion was 42.7 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 3-60 mg/kg
Route of Administration: Oral; single dose (30 minutes before ligation); subcutaneous injection; single dose (7 hours after ligation)
Experimental Results: The ulcer coefficient was reduced by 55.9% at a dose of 30 mg/kg and by 61.8% at a dose of 60 mg/kg. The ED50 for ulcer inhibition was 29.7 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 1-60 mg/kg
Route of Administration: Oral; single dose (30 minutes before stress exposure)
Experimental Results: Lesion length was reduced 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. The ED50 for lesion inhibition was 8.4 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 0.3-3 mg/kg
Route of Administration: Oral; single dose (30 minutes before histamine administration)
Experimental Results: The lesion area was reduced by 86.7% at a dose of 3 mg/kg. The ED50 for lesion inhibition was 0.9 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 3-30 mg/kg
Route of Administration: Oral; single dose (30 minutes before indomethacin administration)
Experimental Results: Lesion length was reduced by 52.2% at 10 mg/kg and by 91.8% at 30 mg/kg. The ED50 for lesion inhibition was 5.4 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 1-30 mg/kg
Route of Administration: Oral; single dose (30 minutes before aspirin hydrochloride administration)
Experimental Results: Lesion length was reduced by 78.1% at 3 mg/kg, 90.9% at 10 mg/kg, and 95.0% at 30 mg/kg. The ED50 for lesion inhibition was 1.4 mg/kg.

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Animal/Disease Models:Sprague-Dawley mice (male, SPF, 220-270g)[2]
Doses: 3-60 mg/kg
Route of Administration: Oral; single dose (30 minutes before hydrochloric acid-ethanol administration)
Experimental Results: Lesion length was reduced by 62.0% at 20 mg/kg, 77.3% at 30 mg/kg, and 94.1% at 60 mg/kg. The ED50 for lesion inhibition was 17.0 mg/kg.

[1]. [Therapeutic effect of IGN-2098, a new antiulcer drug (H2-antagonist), in the ulcer diminishing period against acetic acid-induced gastric ulcer in rats]. Nihon Yakurigaku Zasshi. 1995 Mar;105(3):153-9. Japanese.

[2]. [Effects of IGN-2098, a new histamine H2-receptor antagonist, on gastric secretion and gastric and duodenal lesions induced in rats. Comparison with roxatidine]. Nihon Yakurigaku Zasshi. 1992 Mar;99(3):167-80. Japanese.

C22H32CL2N4O2

455.42

126869-04-3

Typically exists as solids at room temperature

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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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