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Home > Encyclopedia > Cimetidine

Cimetidine

pharmaceutical raw materials
Cimetidine structure

Cimetidine 

structure
  • CAS No:

    51481-61-9

  • Formula:

    C10H16N6S

  • Chemical Name:

    Cimetidine

  • Synonyms:

    Guanidine,N-cyano-N′′-methyl-N′-[2-[[(4-methyl-1H-imidazol-5-yl)methyl]thio]ethyl]-;Guanidine,N-cyano-N′-methyl-N′′-[2-[[(5-methyl-1H-imidazol-4-yl)methyl]thio]ethyl]-;N-Cyano-N′′-methyl-N′-[2-[[(4-methyl-1H-imidazol-5-yl)methyl]thio]ethyl]guanidine;Cimetidine;N-Cyano-N′-methyl-N′′-[2-((4-methyl-5-imidazolyl)-methylthio)ethyl]guanidine;Tagamet;Eureceptor;Histodil;Biomet;Ulcimet;Cimetag;Dyspamet;Acinil;Tametin;Peptol;Ulcofalk;Cimal;Tratul;Ulcerfen;Ulhys;Ulcomedina;Edalene;Cimetum;SKF 92334;Ulcedin;Ulcedine;Gastromet;Ulcomet;Acibilin;NSC 335308;Ulcerex;Tamagret;Fremet;Tagamet HB 200;Tagamet HB;1-Cyano-2-methyl-3-[2-[(5-methyl-1H-imidazol-4-yl)methylsulfanyl]ethyl]guanidine;79347-40-3

  • Categories:

    Active Pharmaceutical Ingredients  >  Digestive System Drugs

Description

White Solid


Cimetidine appears as white crystals with a slight sulfur-mercaptan odor. (NTP, 1992)|Solid


Cimetidine appears as white crystals with a slight sulfur-mercaptan odor. (NTP, 1992)|Cimetidine is a member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach. It has a role as a H2-receptor antagonist, a P450 inhibitor, an anti-ulcer drug, an analgesic and an adjuvant. It is a member of guanidines, a member of imidazoles, an aliphatic sulfide and a nitrile.|A histamine congener, it competitively inhibits histamine binding to histamine H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrins output. It also blocks the activity of cytochrome P-450 which might explain proposals for use in neoadjuvant therapy.|Cimetidine is a Histamine-2 Receptor Antagonist. The mechanism of action of cimetidine is as a Histamine H2 Receptor Antagonist.|Cimetidine is a histamine type 2 receptor antagonist (H2 blocker) which is widely used for treatment of acid-peptic disease and heartburn. Cimetidine has been linked to rare instances of clinically apparent acute liver injury.|Cimetidine is a histamine H(2)-receptor antagonist. Enhancing anti-tumor cell-mediated responses, cimetidine blocks histamine's ability to stimulate suppressor T lymphocyte activity and to inhibit natural killer (NK) cell activity and interleukin-2 production. Cimetidine also may inhibit tumor growth by suppressing histamine's growth-factor activity and blocking histamine-induced stimulation of vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor. (NCI04)|A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.

Cimetidine Basic Attributes

252.34

252.34

257-232-2

80061L1WGD

757428|335308

DTXSID4020329

C374

Crystals

A - Alimentary tract and metabolism

29339900

Characteristics

114

1

Cimetidine appears as white crystals with a slight sulfur-mercaptan odor. (NTP, 1992)

1.2583 (rough estimate)

141-143 °C

488ºC at 760 mmHg

248.9ºC

H2O: 0.5 g/100 mL at 20 ºC

2-8°C

LD50 in mice, rats (mg/kg): 2600, 5000 orally; 150, 106 i.v.; 470, 650 i.p. (Brimblecombe)

Unpleasant odor

Bitter taste

6.8None

6.8|pKa= 6.8

156.5 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|155.7 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Slightly water soluble.

Amines, Phosphines, and Pyridines

Safety Information

3

60-42/43-36/37/38-20/22

53-26-36/37/39-45-36-22

MF0035500

T,Xn

P201, P202, P280, P281, P305+P351+P338, P308+P313, P310, P405, P501

H318

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

Dixon JS, Page MC; Interactions Between Non-steroidal Anti-inflammatory Drugs and H2-Receptor Antagonists or Prostaglandin Analogues; Rheumatol Int 11 (1): 13-8 (1991). Published pharmacokinetic studies investigating possible interaction between H2-receptor antagonists (n = 22) or prostaglandin analogues (n = 6) and nonsteroidal anti-inflammatory drugs have been reviewed.|Cimetidine, an H2-receptor antagonist, has been shown to enhance a variety of immunologic functions both in vivo and in vitro because of its inhibitory effects on suppressor-cell function.[Kumar A; Cimetidine: An Immunomodulator; DICP 24 (3): 289-95 (1990)]|Feldman M, Burton ME; Histamine2-Receptor Antagonists: Standard Therapy for Acid-Peptic Diseases. Part 2; N Engl J Med 323 (Dec 20): 1749-44 (1990). A review of 4 histamine H2 receptor blockers, cimetidine, famotidine, ranitidine and nizatidine, is presented, including a discussion of the results of multiple studies of therapeutic efficacy of H2 blockers for duodenal ulcer, gastric ulcer, Zollinger-Ellison syndrome, gastroesophageal reflux disease, and acute stress ulcers and erosions.|Lee RM, McDowall RD; Recent Advances in Pharmaceutical Chemistry. Review 2. Histamine H2-Receptor Antagonists; J Clin Hosp Pharm 11 (Dec): 389-408 (1986). The concept of histamine receptors and the pharmacological actions, structure-activity relationships and pharmacokinetics of H2-antagonists including cimetidine, ranitidine, oxmetidine, lupitidine and loxtidine are reviewed|For more Special Reports (Complete) data for CIMETIDINE (7 total), please visit the HSDB record page.

Flash point data for this compound are not available. It is probably combustible. (NTP, 1992)

|Danger|H318 (39.42%): Causes serious eye damage [Danger Serious eye damage/eye irritation]|P201, P202, P260, P280, P281, P305+P351+P338, P308+P313, P310, P314, P405, and P501|Aggregated GHS information provided by 138 companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. You should then dampen the solid spill material with 60-70% methanol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with methanol to pick up any remaining material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent-wash contaminated surfaces with 60-70% methanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material under ambient conditions. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

Toxicity

Symptoms of overdose include nausea, vomiting, diarrhea, increased saliva production, difficulty breathing, and a fast heartbeat.

Chronic therapy with cimetidine has been associated with minor elevations in serum aminotransferase levels in 1% to 4% of patients, but similar rates were reported in placebo recipients. The ALT elevations were usually asymptomatic and transient and usually resolved even without dose modification. Several instances of clinically apparent liver injury have been reported in patients receiving cimetidine, but the time to onset and pattern of injury has varied greatly. Onset can be as short as a few days to as long as 7 months, and the serum enzyme pattern varies from hepatocellular to cholestatic, most cases having a “mixed” hepatocellular-cholestatic pattern of injury (Cases 1 and 2). The injury is rarely severe and resolves within 4 to 12 weeks of stopping cimetidine. Liver biopsy histology often shows prominent centrolobular necrosis. Immunoallergic features (rash, fever, eosinophilia) are uncommon, as is autoantibody formation.

OUTPUT OF INTRINSIC FACTOR OF CASTLE IN RESPONSE TO BETAZOLE IS INHIBITED BY CIMETIDINE, BUT BASAL SECRETION OF THE PROTEIN IS ONLY SLIGHTLY AFFECTED AND NO EVIDENCE OF DEFICIENT ABSORPTION OF VITAMIN B12 HAS BEEN NOTED, EVEN DURING LONG-TERM TREATMENT.|Antacids reduce the oral bioavailability of concomitantly administered cimetidine or ranitidine. ... These drugs probably should be given one hour apart.|REDUCED HEPATIC BLOOD FLOW /AFTER ADMIN OF CIMETIDINE/ HAS BEEN REPORTED TO PROLONG THE CLEARANCE AND, THEREFORE, EXAGGERATE THE EFFECTS OF MORPHINE ... AND LIDOCAINE.|SIX OUT OF 8 PATIENTS TREATED WITH CARMUSTINE, 80 MG/SQ M/DAY FOR 3 DAYS, CIMETIDINE, 300 MG 6 HOURLY, AND STEROIDS DEMONSTRATED MARKED LEUCOPENIA AND THROMBOCYTOPENIA ... AFTER FIRST ADMIN. IN COMPARISON ONLY 6 OUT OF 40 PATIENTS WHO WERE SIMILARLY TREATED, BUT WITHOUT CIMETIDINE, SHOWED COMPARABLE WHITE CELL AND PLATELET DEPRESSION.|For more Interactions (Complete) data for CIMETIDINE (37 total), please visit the HSDB record page.

15-20%

Cimetidine's production and use as an anti-ulcerative(1) (an antagonist to Histamine H2 receptors especially in the treatment of duodenal and gastric ulcers(2)), may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated Koc value of 39(SRC), determined from an experimental log Kow(2) and a recommended regression-derived equation(3), indicates that cimetidine should have very high mobility in soil(SRC). However, cimetidine will exist in both the undissociated and cation form under environmental conditions (pH 5-9), (pKa of 6.8)(6); no experimental data are available to indicate whether the cation will adsorb to soil more strongly than its estimated Koc value for the undissociated form indicates(SRC). Volatilization of cimetidine should not be important from moist soil surfaces(SRC) given an estimated Henry's Law constant of 9.5X10-16 atm-cu m/mole(SRC), using a recommended regression equation(4) or from dry soil surfaces(SRC) based on an estimated vapor pressure of 5.5X10-9 mm Hg(SRC), using a fragment constant method(5). Insufficient data are available to determine the rate or importance of biodegradation of cimetidine in soil(SRC).|AQUATIC FATE: Based on a recommended classification scheme(1), an estimated Koc value of 39(SRC), determined from an experimental log Kow(2) and a recommended regression-derived equation(1), indicates that cimetidine would not adsorb to suspended solids and sediment(SRC) in the water. However, cimetidine will exist in both the undissociated and cation form under environmental conditions (pH 5-9), (pKa of 6.8)(5);no experimental data are available to indicate whether the cation will adsorb to soil more strongly than its estimated Koc value for the undissociated form indicates(SRC). Cimetidine will be essentially non-volatile from water surfaces based on an estimated Henry's Law constant of 9.5X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(3). An estimated BCF value of 1.2(1,SRC), from an experimental log Kow(2), suggests that cimetidine will not bioconcentrate in aquatic organisms(SRC), according to a recommended classification scheme(4). Insufficient data are available to determine the rate or importance of biodegradation of cimetidine in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), cimetidine, which has an estimated vapor pressure of 5.5X10-9 mm Hg at 25 °C(2,SRC), will exist primarily in the particulate phase in the ambient atmosphere. Vapor-phase cimetidine is degraded in the atmosphere by reaction with photochemically produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be about 1.8 hours(3,SRC). Particulate-phase cimetidine may be physically removed from the air by wet deposition(SRC).

The rate constant for the vapor-phase reaction of cimetidine with photochemically produced hydroxyl radicals has been estimated as 2.1X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1,SRC). This corresponds to an atmospheric half-life of about 1.8 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1,SRC).

An estimated BCF value of 1.2 was calculated for cimetidine(SRC), using an experimental log Kow of 0.40(1) and a recommended regression-derived equation(2). According to a recommended classification scheme(3), this BCF value suggests that bioconcentration in aquatic organisms will not be an important fate process(SRC).

The Koc of cimetidine is estimated as approximately 39(SRC), using an experimental log Kow of 0.40(1) and a regression-derived equation(2,SRC). According to a recommended classification scheme(3), this estimated Koc value suggests that cimetidine should have very high mobility in soil(SRC). However, cimetidine will exist in both the undissociated and cation form under environmental conditions (pH 5-9), (pKa of 6.8)(4), and no experimental data are available to indicate whether the cation will adsorb to soil more strongly than its estimated Koc value for the undissociated form indicates(SRC).

The Henry's Law constant for cimetidine is estimated as 9.5X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This value indicates that cimetidine will be essentially nonvolatile from water surfaces(2,SRC). Cimetidine's vapor pressure, 5.5X10-9 mm Hg(3,SRC) and Henry's Law constant(1,SRC) indicate that volatilization from dry and moist soil surfaces should not occur(SRC).

Drug concentrated in human milk. /from Table 6/

Cimetidine is an antagonist to Histamine H2 receptors especially in the treatment of duodenal and gastric ulcers(1); therefore, many in the general population will be consuming cimetidine by ingestion. In occupational settings, workers may be exposed to cimetidine through inhalation of dust and through eye and skin contact(SRC).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 11,101 workers (9,114 of these are female) are potentially exposed to cimetidine in the USA(1).

Dialysis fluid from human subjects injected with 300 mg cimetidine, contained 1.1-4.3% of the original dose after 24 hours(1). Urine samples from human subjects fed 400 mg cimetidine contained an average of 157.6 mg after 48 hours(1).

Drug Information

For the treatment and the management of acid-reflux disorders (GERD), peptic ulcer disease, heartburn, and acid indigestion.|FDA Label

Cimetidine is a histamine type 2 receptor antagonist (H2 blocker) which is widely used for treatment of acid-peptic disease and heartburn. Cimetidine has been linked to rare instances of clinically apparent acute liver injury.

Antiulcer Agents

Adjuvants, Immunologic; Analgesics, Non-Narcotic; Anti-Ulcer Agents; Enzyme Inhibitors; Histamine H2 Antagonists|IN MAN, A SINGLE DOSE (300 MG) WILL INHIBIT BASAL (FASTING) SECRETION AND ALSO SECRETION INDUCED BY SOLID, LIQ, OR PEPTONE MEALS, SHAM FEEDING, FUNDIC DISTENTION, PENTAGASTRIN, BETHANECHOL, INSULIN, AND CAFFEINE, AS WELL AS THE PHYSIOLOGICAL STIMULUS PROVIDED BY EATING. ... THIS SPECTRUM INCL THE CEPHALIC OR VAGAL PHASE.|CIMETIDINE IS THE PREFERRED ALTERNATIVE FOR MANY PATIENTS WHO CANNOT OR WILL NOT TOLERATE AN INTENSIVE, PROLONGED ANTACID REGIMEN.|Cimetidine is a useful alternative to antacids in preventing aspiration pneumonitis during childbirth and elective surgical procedures. It is less useful than antacids during emergency surgery because of its slow onset of action. This drug had been given to prevent alkalosis in patients subjected to prolonged nasogastric aspiration, especially those secreting large amounts of acid, and to decrease ileostomy/jejunostomy output in the short bowel syndrome.|For more Therapeutic Uses (Complete) data for CIMETIDINE (21 total), please visit the HSDB record page.

DESPITE POOR PENETRATION TO THE CNS, NEURAL DYSFUNCTION HAS BEEN ENCOUNTERED, PARTICULARLY WITH HIGH DOSES IN ELDERLY PATIENTS AND IN ASSOCIATION WITH IMPAIRED RENAL EXCRETION. THE EFFECTS INCL CONFUSION, SLURRED SPEECH, DELIRIUM, HALLUCINATIONS, AND COMA.|IN SOME INSTANCES, WITHDRAWAL OF CIMETIDINE AFTER A PERIOD OF TREATMENT HAS BEEN FOLLOWED BY RELAPSES IN THE SYMPTOMS OF ULCER AND EVEN BY PERFORATION OF DUODENAL, ESOPHAGEAL, OR GASTRIC ULCERS.|... CIMETIDINE IS INEFFECTIVE IN ACUTE OR ALCOHOLIC PANCREATITIS AND IT MAY ACTUALLY INCR AND PROLONG HYPERAMYLASEMIA.|... CLIN EXPERIENCE IN CHILDREN IS EXTREMELY LIMITED, AND THE BENEFIT/RISK RATIO SHOULD BE CONSIDERED CAREFULLY.|For more Drug Warnings (Complete) data for CIMETIDINE (15 total), please visit the HSDB record page.

GRADUALLY DECR RESPONSIVENESS AFTER PROLONGED USE HAS BEEN REPORTED OCCASIONALLY.

Cimetidine is a histamine H2-receptor antagonist. It reduces basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin. It is used to treat gastrointestinal disorders such as gastric or duodenal ulcer, gastroesophageal reflux disease, and pathological hypersecretory conditions. Cimetidine inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Cimetidine include an increase in gastric bacterial flora such as nitrate-reducing organisms.

Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief. (See all compounds classified as Anti-Ulcer Agents.)|Drugs and compounds which inhibit or antagonize the biosynthesis or actions of CYTOCHROME P-450 CYP1A2. (See all compounds classified as Cytochrome P-450 CYP1A2 Inhibitors.)|Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood. (See all compounds classified as Histamine H2 Antagonists.)

Rapid 60-70%|The principal route of excretion of cimetidine is the urine.|About 15% of cimetidine is metabolized in the liver. Seventy percent is excreted unchanged in the urine, with fecal losses accounting for approximately 10%.|Given orally, cimetidine and ranitidine are almost completely absorbed. Because of first-pass metabolism in the liver, the bioavailability is 50-60%. Both drugs are little bound to plasma proteins (10-20%).|Both drugs are mainly excreted in urine - cimetidine up to 90% within 24 hr (50-75% unchanged) and ranitidine up to 60% within 24 hr (about 40% unchanged). The apparent volume of distribution is quite large, in the range of 1.5 l/kg bw, demonstrating that nearly all drug exists outside the intravascular space.|Cimetidine is widely distributed throughout the body and is 15-20% bound to plasma proteins. Animal studies indicate that the drug crosses the placenta. Cimetidine is distributed into milk.|For more Absorption, Distribution and Excretion (Complete) data for CIMETIDINE (14 total), please visit the HSDB record page.

Hepatic|About 50% to 80% of an intravenous dose is excreted as unchanged drug; 40% of an oral dose is excreted unchanged in the urine in patients with peptic ulcer disease. Most of the remainder of the drug appears in the urine as 5-hydroxymethyl or sulfoxide metabolites.|Cimetidine is metabolized in the liver to sulfoxide and 5-hydroxymethyl derivatives, and possibly guanylurea, although this latter compound may result from in vitro degradation.

2 hours|ELEVEN PATIENTS WITH ASCITIC CIRRHOSIS & ELEVEN PATIENTS WITHOUT LIVER DISEASE RECEIVED 200 MG OF CIMETIDINE ORALLY AND IV. NO DIFFERENCES WERE OBSERVED IN CIMETIDINE T/2 BETWEEN THE 2 GROUPS. CIMETIDINE CLEARANCE WAS DIMINISHED IN CIRRHOTIC PATIENTS (0.426 + OR - 0.138 VERSUS 0.649 + OR - 0.163 L/HR/KG).|The elimination half-life in man is 1.9 to 2.2 hours.|The plasma elimination half-life is about 2 hours.|The half-time for elimination of cimetidine ... is 2 to 3 hours ... .

Cimetidine binds to an H2-receptor located on the basolateral membrane of the gastric parietal cell, blocking histamine effects. This competitive inhibition results in reduced gastric acid secretion and a reduction in gastric volume and acidity.|H2 antagonists inhibit gastric acid secretion elicited by histamine & other H2 agonists in a dose-dependent, competitive manner; the degree of inhibition parallels the concentration of the drug in plasma over a wide range. The H2 antagonists also inhibit acid secretion elicited by gastrin &, to a lesser extent, by muscarinic agonists. Importantly, these drugs inhibit basal (fasting) & nocturnal acid secretion & that stimulated by food, sham feeding, fundic distention, & various pharmacological agents; this property reflects the vital role of histamine in mediating the effects of diverse stimuli. The H2 antagonists reduce both the volume of gastric juice secreted & its H+ concentration. The output of pepsin, which is secreted by the chief cells of gastric glands (mainly under cholinergic control), generally falls in parallel with the reduction in volume of gastric juice. /H2 antagonists/|Cimetidine blocks H2-receptors, which in part are responsible for the inflammatory response, in the cutaneous blood vessels of humans.|The effects of cimetidine, omeprazole and atropine sulfate on the healing of acetic acid-induced gastric ulcers in rats with limited food intake time (9:00-10:00 am and 5:00-6:00 pm) were evaluated 15 days after the acid injection. Oral repeated admin of cimetidine (25-100 mg/kg twice daily) or omeprazole (10-50 mg/kg once daily) dose dependently accelerated ulcer healing. ... A single oral admin of omeprazole (50 mg/kg) or cimetidine (100 mg/kg) resulted in potent and long-lasting anti-acid secretory and gastrin-releasing actions. The degree and duration of anti-acid secretion by atropine sulfate were equal to those of cimetidine, but the elevation of gastrin release by atropine sulfate was weak and temporary. These results indicate that the gastric ulcers of rats with a limited food intake time are useful for evaluating the healing effects of cimetidine and omeprazole on gastric ulcers. In addition, the effects of both drugs may be related to the incr gastrin release rather than to the reduced acid secretion.|Both KB-5492, a new anti-ulcer agent, and cimetidine, admin po at 25-200 mg/kg, dose-dependently prevented cysteamine (400 mg/kg, sc)-induced duodenal ulcers in rats with ED50 values of 63 and 40 mg/kg, respectively. Anti-ulcer doses of cimetidine, but not KB-5492, inhibited gastric acid hypersecretion induced by cysteamine (400 mg/kg, sc). In contrast, anti-ulcer doses of KB-5492, but not cimetidine, incr duodenal HC03- secretion in normal anesthetized rats. These findings suggest that KB-5492 prevents cysteamine-induced duodenal ulcers by stimulating duodenal HC03- secretion, whereas cimetidine does so by inhibiting cysteamine-induced gastric acid hypersecretion.

SYMPTOMS: Symptoms of exposure to this compound can include, dermatitis, hair growth, rash, pruritus, erythema annulare centrifugum; anorexia, gastritis, gastrointestinal changes, diarrhea, constipation, nausea, ulcer perforation upon withdrawal; hepatitis, jaundice, increases in serum creatinine and liver enzymes, changes in kidney tubules, interstitial nephritis and possible renal failure; hypotension, increased body temperature, sweating; muscle weakness and/or pain; endocrine changes, gynecomastia; leukopenia, agranulocytosis, thrombocytopenia; transient psychosis, confusion, disorientation, agitation, hallucinations, dizziness, somnolence, headache, fatigue, malaise; loss of libido and impotence. ACUTE/CHRONIC HAZARDS: When heated to decomposition this compound emits very toxic fumes of NOx and SOx. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

ACUTE RENAL FAILURE DEVELOPED IN A PATIENT AFTER SHE RECEIVED CIMETIDINE THERAPY. A RENAL BIOPSY SPECIMEN SHOWED ACUTE INTERSTITIAL NEPHRITIS. WITHDRAWAL OF CIMETIDINE THERAPY LED TO IMPROVEMENT OF RENAL FUNCTION.|THREE EPISODES, IN WHICH PATIENTS SUFFERED A CARDIAC ARREST IN CLOSE ASSOC WITH RECEIVING A BOLUS IV INJECTION OF CIMETIDINE, ARE REPORTED.|THREE PATIENTS ARE PRESENTED WHO EXPERIENCED AGITATION, DISORIENTATION, AND HALLUCINATIONS WHILE BEING TREATED WITH CIMETIDINE.|A HEALTHY YOUNG WOMAN DEVELOPED MARKED DEPRESSION AND LOSS OF LIBIDO WHILE TAKING CIMETIDINE. HER SYMPTOMS PROMPTLY RESOLVED AFTER DISCONTINUATION OF CIMETIDINE SUGGESTING THAT HER SYMPTOMS REPRESENT AN ADVERSE DRUG REACTION.|For more Human Toxicity Excerpts (Complete) data for CIMETIDINE (14 total), please visit the HSDB record page.

Altramet

Cimetidine Use and Manufacturing

Methods of Manufacturing

The intermediate (I) and 2-aminoethanethiol hydrochloride are reacted in the presence of hydrogen bromide, and then neutralized with potassium carbonate to obtain compound (II). Then it reacts with the corresponding thiourea to obtain cimetidine.

Uses

Competitive histamine H2-receptor antagonist which inhibits gastric acid secretion and reduces pepsin output

Sales approximated $100 x 10+6/year as of mid-year 1977.

BIOMAG, BRUMETIDINA, CIMET, NOTUL. /CIMETIDINE HYDROCHLORIDE/

The liquid chromatograph is equipped with a 220 nm detector and 4.6 mm X 25 cm column that contains packing L1. The flow rate is about 2 ml/min. Sample volume is 50 ul. The relative standard deviation of the response for replicate injections is not more than 2.0%.|Dissolve 2110 mg of Cimetidine, accurately weighed, in 75 ml of glacial acetic acid, and titrate with 0.1N perchloric acid VS, determining the end point potentiometrically.

A MICRO PROCEDURE FOR THE HIGH PRESSURE LIQUID CHROMATOGRAPHIC ANALYSIS OF CIMETIDINE IN SERUM OR PLASMA IS DESCRIBED. IT HAS BEEN USED IN STUDIES TO DETERMINE THE SERUM CONCN IN PATIENT RECEIVING THE DRUG BY BOTH THE ORAL & IV ROUTE.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients

Computed Properties

Molecular Weight:252.34
XLogP3:0.4
Hydrogen Bond Donor Count:3
Hydrogen Bond Acceptor Count:4
Rotatable Bond Count:7
Exact Mass:252.11571571
Monoisotopic Mass:252.11571571
Topological Polar Surface Area:114
Heavy Atom Count:17
Complexity:296
Covalently-Bonded Unit Count:1
Compound Is Canonicalized:Yes

Drug Function and Efficacy

It can significantly inhibit the basal gastric acid secretion during the day and night, and can also inhibit the gastric acid secretion induced by food, histamine, pentagastrin, caffeine and insulin.

This ingredient has been used in drugs with the following functions (note: it does not mean that the ingredient itself has the following health functions)

Related Drugs

Registered Holders

  • Wuxi Kaili Pharmaceutical Co., Ltd.

    China China
    Active
  • UNION QUIMICO FARMACEUTICA SA (UQUIFA SA)

    United States United States
    Active
  • LIANYUNGANG LONGZHU CHEMICAL CO., LTD.

    Japan Japan
    Active

Recommended Suppliers of Cimetidine

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