2. IGN-2098

IGN-2098 是一种口服有效的、竞争性的组胺 H2 受体 (H2 receptor) 拮抗剂，其 pA2 值为 7.32。IGN-2098 可抑制基础及刺激状态下的胃酸分泌。IGN-2098 可加速溃疡愈合、抑制溃疡边缘隆起，并保护胃及十二指肠黏膜免受损伤。IGN-2098 可用于胃溃疡的相关研究。

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IGN-2098

IGN-2098 Chemical Structure

CAS No. : 126869-04-3

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IGN-2098 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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)

体外研究
(In Vitro)

IGN-2098 可竞争性拮抗离体豚鼠心房标本中的组胺 H2 受体，其 pA2 值为 7.32[2]。

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

IGN-2098 相关抗体:
体内研究
(In Vivo)

IGN-2098 (10-30 mg/kg；口服；每日 2 次；连续 14 天) 可剂量依赖性地促进大鼠乙酸诱导胃溃疡的愈合，其中 10 mg/kg 和 30 mg/kg 剂量的愈合率分别达到 49.6%和 52.7%，且与对照组相比能显著降低溃疡边缘隆起程度[1]。
IGN-2098 (1-60 mg/kg；口服、皮下注射、皮内注射、腹腔注射；单次给药) 可通过多种途径强效抑制幽门结扎大鼠的基础胃酸分泌，其中皮下注射的效力最高 (胃酸分泌抑制的 ED50 = 0.7 mg/kg)[2]。
IGN-2098 (0.1-30 mg/kg; 皮下注射; 单次给药) 可强效抑制急性瘘管大鼠中组胺刺激的胃酸分泌，其 ED50 为 0.2 mg/kg[2]。
IGN-2098 (0.3-30 mg/kg；皮下注射；单次给药) 可强效抑制急性瘘管大鼠中 Carbachol (HY-B1208) 刺激的胃酸分泌，其 ED50 为 0.3 mg/kg[2]。
IGN-2098 (1-30 mg/kg；皮下注射；单次给药) 可强效抑制急性瘘管大鼠中 Pentagastrin (HY-A0261) 刺激的胃酸分泌，其 ED50 为 0.1 mg/kg[2]。
IGN-2098 (3-60 mg/kg；皮下注射；单次给药) 可抑制麻醉大鼠中 2-deoxy-D-glucose (HY-13966) 刺激的胃酸分泌，其 ED50 为 42.7 mg/kg[2]。
IGN-2098 (3-60 mg/kg；口服、皮下注射；单次给药) 可抑制大鼠幽门结扎诱导的胃溃疡，其 ED50 为 29.7 mg/kg[2]。
IGN-2098 (1-60 mg/kg；口服；单次给药) 可抑制大鼠水浸应激诱导的胃黏膜损伤，其 ED50 为 8.4 mg/kg[2]。
IGN-2098 (0.3-3 mg/kg；口服；单次给药) 可强效抑制组胺诱导的大鼠胃黏膜损伤，其 ED50 为 0.9 mg/kg[2]。
IGN-2098 (3-30 mg/kg；口服；单次给药) 可抑制 Indomethacin (HY-14397) 诱导的大鼠胃黏膜损伤，其 ED50 为 5.4 mg/kg[2]。
IGN-2098 (1-30 mg/kg；口服；单次给药) 可强效抑制大鼠体内盐酸-Aspirin (HY-14654) 诱导的胃黏膜损伤，其 ED50 为 1.4 mg/kg[2]。
IGN-2098 (3-60 mg/kg；口服；单次给药) 可抑制大鼠由盐酸-乙醇诱导的胃黏膜损伤，其 ED50 为 17.0 mg/kg[2]。

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.
分子量

455.42

Formula

C22H32Cl2N4O2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

IGN-2098 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

IGN-2098126869-04-3IGN2098IGN 2098ratsguinea pig atrial specimensacute fistula ratspylorus-ligated ratsgastric mucosal injuryduodenal mucosagastric ulcergastric acid secretioncarbacholhistamine H2 receptorInhibitorinhibitorinhibit

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