(+)-Igmesine (1 nM-10 μM; 52 hours) hydrochloride effectively inhibited the proliferation of rat lymphocytes stimulated by phytohemagglutinin-P, concanavalin A and pokeweed mitogen, and reduced the uptake of tritium-labeled thymidine [4]. (+)-Igmesine (1 nM-10 μM; 40 minutes-52 hours) hydrochloride dose-dependently inhibited rat neutrophil phagocytosis and mitogen-stimulated rat lymphocyte proliferation [4].

(+)-Igmexin (1-10 mg/kg; oral; single dose) hydrochloride effectively protects rats from cysteine-induced duodenal ulcers, with an ED50 of 4.14 mg/kg (oral) and a 71% reduction in ulcer index at a dose of 10 mg/kg (oral) [1]. (+)-Igmexin (oral; single dose) hydrochloride has a weak protective effect against various gastric mucosal injury models, with ED50 values ranging from 25.2 to 55.4 mg/kg (oral) [1]. (+)-Igmexin (1-30 mg/kg; intradermal injection; single dose) hydrochloride did not show gastric acid secretion inhibitory activity in rats with pyloric ligation [1]. (+)-Igmexin (0.25-2 mg/kg; intravenous injection; single bolus) hydrochloride stimulates duodenal bicarbonate secretion in anesthetized rats in a dose-dependent manner [1]. (+)-Igmexin (25-100 mg/kg; orally; 1, 24 and 48 hours post-surgery) hydrochloride has a statistically significant neuroprotective effect against ischemia-induced neuronal death in the CA1 region of the hippocampus in gerbils [2]. (+)-Igmexin (100 mg/kg; intraperitoneally; 30 minutes, 6, 24 and 48 hours post-surgery) hydrochloride significantly reduced ischemia-induced hyperactivity in the hippocampus and brainstem and elevated NO synthase activity in gerbils [2].

Animal/Disease Models:Sprague-Dawley (male, 180-220 g, cysteamine-induced duodenal ulcers) [1]
Doses: 1 mg/kg; 3 mg/kg; 10 mg/kg
Route of Administration: Oral; Single dose
Experimental Results: Dose-dependent decrease in ulcer index was observed, with an oral ED50 of 4.14 mg/kg. At 10 mg/kg, the mean ulcer index decreased from 33.2 mm2 to 9.7 mm2, a decrease of 71%. The protective effect was lost after prior treatment with haloperidol (1 or 3 mg/kg subcutaneously), BMY 14,802 (10 mg/kg orally), or devarperidine (30 mg/kg orally).

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Animal/Disease Models:Sprague-Dawley (male, 250-400 g, pylorus-ligated Shay rat model) [1]
Doses: 1 mg/kg; 3 mg/kg; 10 mg/kg; 30 mg/kg
Route of Administration: id; single dose
Experimental Results: Compared with the control group rats, no significant changes were observed in free or total gastric acid concentration or secretion at any of the tested doses.

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Animal/Disease Models:Sprague-Dawley (male, 250-400 g, anesthetized orthotopic duodenal perfusion model) [1]
Doses: 0.25 mg/kg; 0.5 mg/kg; 1 mg/kg; 2 mg/kg
Route of Administration: Intravenous injection; single bolus injection
Experimental Results: The induction of duodenal bicarbonate excretion increased in a dose-dependent manner, with a threshold dose of 0.25 mg/kg (intravenous injection) and a maximum response dose of 1 mg/kg (intravenous injection). The plateau period of bicarbonate excretion lasted for 2 hours at 14.8 μEq·cm-1·h-1 when the baseline level of 7.60 μEq·cm-1·h-1 was increased to 1 mg/kg (intravenous injection) (P < 0.001). After doubling the dose to 2 mg/kg (intravenous injection), the secretion did not increase further. The stimulating effect disappeared after prior administration of haloperidol (0.50 mg/kg, intravenous), BMY 14,802 (5 mg/kg, intravenous), hexamethylammonium (1 mg/kg, intravenous), tetrodotoxin (5 μg/kg, intravenous), divalperidine (0.50 mg/kg, intravenous), or bilateral injection. Trunk vagotomy was performed. No significant changes in stimulating effect were observed after administration of atropine (0.25 mg/kg, intravenous), SCH 23,390 (0.50 mg/kg, intravenous), sulpiride (1 mg/kg, intravenous), prazosin (0.50 mg/kg, intravenous), yohimbine (2 mg/kg, intravenous), naloxone (0.20 mg/kg, intravenous), indomethacin (0.25 mg/kg, intravenous), or intraventricular injection of divalperidine (17 μg/rat).

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Animal/Disease Models:Male Mongolian gerbils (at least 3 months old, weighing >60 g, 5-minute bilateral carotid artery occlusion surgery) [2]
Doses: 25 mg/kg; 50 mg/kg; 75 mg/kg; 100 mg/kg
Route of Administration: Oral; 1, 24 and 48 hours post-surgery
Experimental Results: The 25 mg/kg dose had a partial neuroprotective effect against ischemia-induced CA1 neuronal death. The 50 mg/kg dose had a significant neuroprotective effect against ischemia-induced CA1 neuronal death (P < 0.03). The 75 mg/kg dose had a significant neuroprotective effect against ischemia-induced CA1 neuronal death (P < 0.01). The 100 mg/kg dose had a significant neuroprotective effect against ischemia-induced CA1 neuronal death (P < 0.005).

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Animal/Disease Models:Male Mongolian gerbils (at least 3 months old, weighing >60 g, 5-minute bilateral carotid artery occlusion surgery) [2]
Doses: 100 mg/kg
Route of Administration: Intraperitoneal injection; 30 minutes, 6 hours, 24 hours and 48 hours postoperatively
Experimental Results: A decrease in ischemia-induced hyperactivity was observed 2–7 hours after occlusion (statistically significant, P < 0.0018 to 0.02). The increase in NO synthase activity induced by ischemia was decreased in multiple brain regions, with statistically significant decreases in the hippocampus (P < 0.03) and brainstem (P < 0.05).

[1]. Effects of a new sigma ligand, JO 1784, on cysteamine ulcers and duodenal alkaline secretion in rats. Gastroenterology. 1993;104(2):427-434.

[2]. The sigma receptor ligand JO 1784 (igmesine hydrochloride) is neuroprotective in the gerbil model of global cerebral ischaemia. Eur J Pharmacol. 1995;283(1-3):217-225.

[3]. Central action of sigma receptor ligand, JO 1784, to suppress CRF-induced inhibition of gastric function in conscious rats. Eur J Pharmacol. 1992;223(2-3):197-199.

[4]. Comparison between the effects of sigma receptor ligand JO 1784 and neuropeptide Y on immune functions. Eur J Pharmacol. 1998;345(1):79-87.

C23H30CLN

355.94

Igmesine hydrochloride

White to off-white solid

[H]Cl.CN(CC1CC1)[C@@](C/C=C/C2=CC=CC=C2)(CC)C3=CC=CC=C3

JO1784

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). 本产品在运输和储存过程中需避光（避免光照）。  (2). 请将本产品存放在密封且受保护的环境中（例如氮气下），避免暴露在潮湿环境中。

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

DMSO : ~17.79 mg/mL (~49.98 mM; with sonication and warming)

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.)