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Clarithromycin is a macrolide antibiotic. Macrolides are compounds characterized by a macrocyclic lactone ring to which deoxy sugars are attached. Clarithromycin is a semisynthetic derivative of Erythromycin obtained by the addition of methyl group to hydroxyl group at carbon 6. Clarithromycin is effective against gram positive bacteria. Antibiotics require constant drug level in body for therapeutic effect. This is achieved by taking the medication at regular interval of time throughout the day and night as prescribed. Clarithromycin is important to take the drug for the full time period as prescribed. If you discontinue the therapy, it may result in ineffective treatment.

Primary Characteristics

clarithromycin is of Semi Synthetic origin and belongs to Hexopyranosyl. It belongs to Antibacterial (Proetin synthesis inhibitor) pharmacological group on the basis of mechanism of action and also classified in Antibiotics pharmacological group. The Molecular Weight of Clarithromycin is 748.00.



Clarithromycin is primarily indicated in conditions like Chronic bronchitis, Metastatic germ cell cancer, Mycobacterial infection, Otitis media, Pharyngitis, Pneumonia, Respiratory tract infections, Rtis, otitis media, Sinusitis, Skin infections, Soft tissue infections, To counteract the folate-antagonist action of methotrexate, Tonsillitis, and can also be given in adjunctive therapy as an alternative drug of choice in Duodenal ulcer, Endocarditis.


Oral absorption of Clarithromycin is found to be 50% ±50. Volume of distribution is found to be 250 litre and plasma protien binding is 80%. Presystemic metabolism is noted to be 20% ±20 and metabolism is reported via liver. Renal Excretion accounts for 20-30%(unchanged) 10-15%(metabolite) and plasma half life is 2.9-9.2 hr.



Clarithromycin is a macrolide antibiotic whose spectrum of activity includes many gram-positive (Staphylococcus aureus, S. pneumoniae, and S. pyogenes) and gram-negative aerobic bacteria (Haemophilus influenzae, H. parainfluenza, and Moraxella catarrhalis), many anaerobic bacteria, some mycobacteria, and some other organisms including Mycoplasma, Ureaplasma, Chlamydia, Toxoplasma, and Borrelia. Other aerobic bacteria that clarithromycin has activity against include C. pneumoniae and M. pneumoniae. Clarithromycin has an in-vitro activity that is similar or greater than that of erythromycin against erythromycin-susceptible organisms. Clarithromycin is usually bacteriostatic, but may be bactericidal depending on the organism and concentration of drugs.

Mechanism of action

Clarithromycin is first metabolized to 14-OH clarithromycin, which is active and works synergistically with its parent compound. Like other macrolides, it then penetrates bacteria cell wall and reversibly binds to domain V of the 23S ribosomal RNA of the 50S subunit of the bacterial ribosome, blocking translocation of aminoacyl transfer-RNA and polypeptide synthesis. Clarithromycin also inhibits the hepatic microsomal CYP3A4 isoenzyme and P-glycoprotein, an energy-dependent drug efflux pump.


Side Effects

The severe or irreversible adverse effects of Clarithromycin, which give rise to further complications include Renal failure, Interstitial nephritis, Pseudomembranous colitis.

Clarithromycin produces potentially life-threatening effects which include cerebial hemorrhage. which are responsible for the discontinuation of Clarithromycin therapy.

The signs and symptoms that are produced after the acute overdosage of Clarithromycin include Hypoxia, Hypokalemia.

The symptomatic adverse reactions produced by Clarithromycin are more or less tolerable and if they become severe, they can be treated symptomatically, these include Headache, Nausea, Vomiting, Diarrhea, Abdominal pain, Phlebitis, Glossitis, StomatitisX, Elevation of liver enzymes, Taste perversion, Increased intracranial pressure, Hypoglycemia.

Warning / Precautions

Clarithromycin should be used with caution in patients with other illnesses or any allergy, especially allergies to drugs, arrythmias ,liver disease, jaundice (yellowing of the skin or eyes), kidney disease , or a history of colitis or stomach problems. This drug should be used only if clearly needed during pregnancy or lactation.


Storage Conditions

Oral suspension (reconstituted)

Store at room temperature. Refrigeration and Freezing is not recommended. Protect from Sunlight. Use within 14 days if kept at room temperature.


Store in a well closed container, Below 40°C. Protect from Sunlight and Moisture.


Interference in Pathology

Elevations of SGPT and SGOT

Alkaline phosphatase levels are elevated.

Serum creatinine raised.

Interference with serum aspartate amino transferase, urinary catecholamine and 17- hydroxy corticosteroids.




Omeprazole is a an oral antiulcer agent. Omeprazole is characterized as a gastric acid pump inhibitor because it blocks the final step of gastric acid production. It has a long duration of action and is very potent, allowing for once-daily administration. Despite its potency, it must be used in combination with antibiotics to be effective against Helicobacter pylori. Due to concern regarding long-term use, it was originally approved by the FDA in September 1989 for acute treatment only. In December 1994, an FDA advisory committee recommended it be approved for maintenance therapy of healed erosive esophagitis. In April 1996, it was approved for the treatment of H. pylori-associated duodenal ulcer. Belongs to a new class of ant secretory agents, the substituted benzimidazoles, which suppress gastric acid secretion by inhibiting the H+/K+ ATPase enzyme system of parietal cells. it, following activation in an acidic pH, binds irreversibly to the H+/K+ ATPase pump on the secretory surface of the parietal cell membrane. Subsequently, the secretion of hydrogen ions into the gastric lumen is inhibited. it inhibits both basal and stimulus-induced acid secretion.

Primary Characteristics

Omeprazole is also known as Proton pump Inhibitor. It is of Synthetic origin and belongs to Benzimidazol. It belongs to H/K At pase proton pump inhibitor pharmacological group on the basis of mechanism of action and also classified in Antacids pharmacological group. The Molecular Weight of Omeprazole is 345.40.

Its pKa is 4.0, 8.7.


Omeprazole is primarily indicated in conditions like Acid reflux disease (long-term management), Benign gastric and duodenal ulceration, Benign gastric and duodenal ulcers, Benign gastric ulcer associated with H.pylori, Duodenal errosions, Duodenal or benign gastric ulcer associated with H.pylori, Duodenal ulcer, Duodenal ulcer associated with h. Pylori, Gastric acid reduction during anaesthesia, Gastric acid reduction during general anesthesia, Gastric ulcer, Gastro-esophageal reflux disease, Gastro-o esophageal reflux disease, Gastro-esophageal reflux disease (refractory to other treatment), Maintenance of recurrent duodenal ulcers, Non-ulcer dyspepsia, NSAID-associated gastric and duodenal ulcers, NSAID-associated gastric and duodenal ulcers (prophylaxis), NSAID-associated gastric and duodenal ulcers and duodenal erosions, NSAID-associated gastric or duodenal ulcers, NSAID-associated gastric or duodenal ulcers (prophylaxis), Prevention of relapse in duodenal ulcer, Prophylaxis for NSAID-associated gastric and duodenal ulcers, Prophylaxis of acid aspiration, Reflux esophagitis, Resistant ulcers, Severe or recurrent duodenal and gastric ulceration, Zollinger-Ellison syndrome, and can also be given in adjunctive therapy as an alternative drug of choice in Acid aspiration syndrome prevention, GI bleeding.



Oral absorption of Omeprazole is found to be 57.5% ±7.5. Volume of distribution is found to be 0.3 – 0.4 l/kg and plasma proteins binding is 95%. Pre systemic metabolism is noted to be 20% and metabolism is reported Hepatic. Renal Excretion accounts for 80% and plasma half life is 1 hr.


Mechanism of action

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump , expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid) .

Omeprazole is a member of a class of anti secretory compounds, the substituted benzimidazoles, that stop gastric acid secretion by selective inhibition of the H+/K+ ATPase enzyme system. Proton-pump inhibitors such as omeprazole bind covalently to cysteine residues via disulfide bridges on the alpha subunit of the H+/K+ ATPase pump, inhibiting gastric acid secretion for up to 36 hours . This anti secretory effect is dose-related and leads to the inhibition of both basal and stimulated acid secretion, regardless of the stimulus .

Mechanism of H. pylori eradication

Peptic ulcer disease (PUD) is frequently associated with Helicobacter pylori bacterial infection (NSAIDs) . The treatment of H. pylori infection may include the addition of omeprazole or other proton pump inhibitors as part of the treatment regimen. H. pylori replicates most effectively at a neutral pH . Acid inhibition in H. pylori eradication therapy, including proton-pump inhibitors such as omeprazole, raises gastric pH, discouraging the growth of Pylori . It is generally believed that proton pump inhibitors inhibit the urease enzyme, which increases the pathogenesis of H. pylori in gastric-acid related conditions .


Side Effects

The severe or irreversible adverse effects of Omeprazole, which give rise to further complications include Interstitial nephritis.

Omeprazole produces potentially life-threatening effects which include Anaphylaxis. which are responsible for the discontinuation of Omeprazole therapy.

The signs and symptoms that are produced after the acute over dosage of Omeprazole include Tachycardia, Drowsiness, Drowsiness, Headache.

The symptomatic adverse reactions produced by Omeprazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Flatulence, Dizziness, Headache, Fatigue, Nausea, Diarrhea, Myalgia, Constipation, Insomnia, Abdominal pain, Dry mouth, Urticaria, Pruritus, Photosensitivity, Skin rash, Impotence, Depression, Arthralgia, Myopathy, Gynecomastia, Agitation, Dry mouth, dizziness.



Esomeprazole Magnesium

Esomeprazole is an ulcer-healing drug, that inhibits gastric acid by blocking the proton-pump (Hydrogen-Potassium at pase enzyme system) of the gastric perital cells. Esomeprazole is used for the short-term treatment of gastric and duodenal ulcers and in gastro-oesophageal reflux disease with severe symptoms. Also used in combination with anti bacterial for the eradication of Helicobacter pylori.

Primary Characteristics

Esomeprazole Magnesium trihydrate is the derivative of Esomeprazole. It is of Synthetic origin and belongs to Sulphinyl Benzimidazol. . The Molecular Weight of Esomeprazole is 345.40.


Esomeprazole is indicated for the treatment of acid-reflux disorders including healing and maintenance of erosive esophagitis, and symptomatic gastroesophageal reflux disease (GERD), pepticulcer disease, Hpylorieradication, prevention of gastrointestinal bleeds with NSAID use, and for the long-term treatment of pathological hypersecretory conditions including Zollinger-Ellison Syndrome


Oral absorption of Esomeprazole found to 69.5% ±19.5. Plasma protien binding is 97%. and metabolism is reported Liver. Renal Excretion accounts for Urine and plasma half life is 1.2hour.

Mechanism of action

Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole’s duration of anti secretory effect that persists longer than 24 hours.

Side Effects

The severe or irreversible adverse effects of Esomeprazole, which give rise to further complications include Liver damage.

The signs and symptoms that are produced after the acute over dosage of Esomeprazole include Ataxia, Tremor, Change in respiratory frequency, Intermediate Chronic Convulsion.

The symptomatic adverse reactions produced by Esomeprazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Flatulence, Dizziness, Headache, Fatigue, Diarrhea, Myalgia, Constipation, Abdominal pain, Dry mouth, Blurred vision, Rashes, Pruritus, Malaise, Arthralgia, Nausea and vomiting, Musculoskeletal pain, Dry mouth, dizziness, subacute myopathy, athralgia.

Warning / Precautions

Esomeprazole should be given with caution in patients with renal impairment, liver disease, in pregnancy and in breast-feeding. Proton-pump inhibitors may mask symptoms of gastric cancer, particular care required in those whose symptoms change and in those over 45 years of age the presence of gastric malignancy should excluded before treatment.


Storage Conditions

Store at room temperature, . Protect from Sunlight



Dexlansoprazole (DDR)


Dexlansoprazole is a new generation proton pump inhibitor (PPI) used for the management of symptoms associated with gastroesophageal reflux disease (GERD) and erosive esophagitis. Dexlansoprazole the R-enantiomer of Lansoprazole, which is composed of a racemic mixture of the R- and S-enantiomers. Compared to the older generation of PPIs (which includes Pantoprazole, Omeprazole, and Lansoprazole) , dexlansoprazole MR has a unique pharmacokinetic profile due to its delayed-release and dual-delivery release system. The active ingredient is released in two phases at different pH values and at different time points, resulting in two peak concentrations in the blood; 25% of the dose is released at pH 5.5 in the proximal duodenum, while the remaining 75% is released at pH 6.75 in the distal small intestine . As a result, dexlansoprazole has a peak concentration within 1-2 hours after dosing and another within 4-5 hours . Dexlansoprazole’s unique pharmacokinetics addresses limitations of the older generation PPIs including short plasma half-life, break-through symptoms, and need for meal-associated dosing . These characteristics make dexlansoprazole a good option for people who struggle with adherence and strict dosage timing before meals.

More about Dexlansoprazole

Dexlansoprazole exerts its stomach acid-suppressing effects in the same way as other drugs in the PPI family by inhibiting the final step in gastric acid production. Dexlansoprazole targets the (H+, K+)-ATPase enzyme, which is involved in the secretion of hydrochloric acid through the exchange of H+ ions from the cytoplasm for K+ ions. Normally functioning (H+, K+)-ATPase stimulates hydrochloric acid secretion into the gastric lumen thereby increasing stomach acidity and lowering pH. Once absorbed into circulation, dexlansoprazole covalently binds to the sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells, which leads to inhibition of both basal and stimulated gastric acid secretion. Despite dexlansoprazole’s unique pharmacokinetic profile, efficacy in management of GERD symptoms is considered similar to other medications within the PPI class including Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, and Rabeprazole.

Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as dexlansoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal C. difficile), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life  PPIs such as dexlansoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary .

Dexlansoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as dexlansoprazole may cause a rebound effect and a short term increase in hypersecretion .


Average: 369.36
Monoisotopic: 369.075882366

Chemical Formula



Dexlansoprazole is indicated for healing all grades of erosive esophagitis (EE), maintaining and healing of EE and relief of heartburn, and treating heartburn associated with symptomatic non-erosive gastroesophageal reflux disease (GERD).



Dexlansoprazole is a proton pump inhibitor (PPI) and is included in the drug class of antisecretory compounds. It blocks the final step of gastric acid secretion by specific inhibition of the (H+, K+)-ATPase at the secretory surface of the parietal cells on gastric mucosa.


Mechanism of action

Dexlansoprazole inhibits the H/K ATPase enzyme, which is involved in the secretion of hydrochloric acid, hydrolyzing ATP and exchanging H+ ions from the cytoplasm for K+ ions in the secretory canaliculus, which results in HCl secretion into the gastric lumen. Dexlansoprazole inhibits this effect of H/K ATPase by demonstrating a high degree of activation in the acidic environment. After passing through the liver and reaching the gastric parietal cells activated by a meal, PPIs undergo protonation in the acidic pH environment, followed by conversion to sulphenamide which represents the active form of the drug. Sulphenamide inhibits the activity of the proton pump and hence the transport of hydrogen ions into the gastric lumen via covalent binding to the SH groups of the cysteine residues of H/K ATPase 2. The delivery technology of dexlansoprazole MR is designed to release the drug in two separate pH-dependent phases, the first in the proximal duodenum (25% of total drug dose) and the second (75% of total drug dose) in the more distal small intestine. Dexlansoprazole reduces both basal and stimulated gastric acid secretion.

Route of elimination

Dexlansoprazole is cleared from the body by either fecal excretion (50.7%) or renal excretion (47.6%) following oral ingestion, with no unchanged drug detected in the urine.


Dexlansoprazole is eliminated with a half-life of approximately one to two hours in healthy subjects and in patients with symptomatic GERD.



Apparent clearance (CL/F) in healthy subjects was 11.4 to 11.6 L/hour, respectively, after five days of 30 or 60 mg once daily administration

Adverse Effects

Most commonly reported adverse reactions are diarrhea, abdominal pain, nausea, upper respiratory tract infection, vomiting, and flatulence. There are no reports of significant overdose but serious adverse events of hypertension have been reported in association with twice daily doses of DEXILANT 60 mg. Nonclicnial toxicology of dexlansopraole was assessed using lansoprazole studies. In two 24-month carcinogenicity studies involving rats, lansoprazole induced dose-related gastric ECL cell hyperplasia and ECL cell carcinoids and increased the incidence of intestinal metaplasia of the gastric epithelium in both sexes of rats. Dexlansoprazole is expected to have no effect on fertility and the reproductive system.




Ciprofloxacin is a fluoroquinolone antimicrobial agent with a broad spectrum of activity against both gram-negative and gram-positive bacteria. It relatively non-toxic and well tolerated broad spectrum agent. Excellent bioavailability permits its use for treatment of variety of serious bacterial infections. Require constant drug level in body for therapeutic effect. This is achieved by taking the medication at regular interval of time throughout the day and night as prescribed. For Ciprofloxacin (HCl) it important to take the drug for the full time period as prescribed. If you discontinue the therapy it may result in ineffective treatment.
Ciprofloxacin (HCl) is the monohydrated hydrochloride salt of ciprofloxacin. Ciprofloxacin (HCl) is effective against many gram positive and gram negative bacteria, including some strains resistant to penicillins, cyclosporins and aminoglycosides.

Primary Characteristics

Ciprofloxacin (HCl) is the derivative of Ciprofloxacin. It is of Semi Synthetic origin and belongs to Quinoline Carboxylic Acid. It belongs to DNA Gyrase inhibitor pharmacological group on the basis of mechanism of action and also classified in Antibiotics pharmacological group. The Molecular Weight of Ciprofloxacin is 346.00. Its pKa is 6-8.8.


Ciprofloxacin primarily indicated in conditions like Acromegaly (short-term treatment before pituitary surgery), Chronic prostatitis, GI infections, Gonorrhoea, Iron-deficiency anaemia prophylaxis or for mild iron deficiency, Iron-deficiency anaemia with chronic renal failure, Most other infections, Muscle relaxation (long duration) for surgery and intubation, , Osteomyelitis, Pseudomonal lower+RTI in cystic fibrosis, Respiratory tract infections, Sexually transmitted disease, Sexually transmitted infections, Skin infections, Skin structure infections, Status epilepticus (unlicensed use), Surgical prophylaxis, Urinary tract infection.



Oral absorption of Ciprofloxacin is found to be 67% ±17. Volume of distribution is found to be 177-217 litre and plasma protien binding 30%. and metabolism reported 5% via liver. Renal Excretion accounts for 70% unchanged, 10% metabolites of IV dose and plasma half life is 3-4 hr.


 Mechanism of action

Ciprofloxacin acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Ciprofloxacin’s targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication.


Ciprofloxacin is primarily metabolized by CYP1A2. The primary metabolites oxociprofloxacin and sulociprofloxacin make up 3-8% of the total dose each. Converted to the minor metabolites desethylene ciprofloxacin and formylciprofloxacin. These 4 metabolites account for 15% of a total oral dose.

There a lack of available data on the enzymes and types of reactions involved in forming these metabolites.


Ciprofloxacin is contraindicated in conditions like Epilepsy, and Hypersensitivity.

Side Effects

The severe or irreversible adverse effects, which give rise to further complications include Hearing loss, Seizures and Pseudomembranous colitis.

Produces potentially life-threatening effects which include Anaphylactoid reactions, Stevens Johnson syndrome, Acute Renal Failure, Epidermal necrolysis, Fluminant hepatic failure. which are responsible for the discontinuation of Ciprofloxacin therapy.

The symptomatic adverse reactions produced by Ciprofloxacin are more or less tolerable and if they become severe, they can treated symptomatically, these include Dizziness, Headache, Nausea, Vomiting, Diarrhoea, Tachycardia, Nervousness, Tremors, Rashes, Urticaria, Pruritus, Photosensitivity, Elevation of liver enzymes, Thrombocytopenia, Eosinophilia, Increased intracranial pressure, nervousness, joint symptoms, agranulocytosis.

Warning / Precautions

Ciprofloxacin used with caution in patients with known or suspected central nervous system (CNS) disorders, renal impairment or hepatic disease, with a history of GI disease especially colitis or who dehydration. Do not exceed the recommended dose. Take appropriate measures if secondary infections occur.


Storage Conditions

Eye Solution/ Eye ointment

Store at room temperature, Below 30°C or in refrigerator. Do not Freeze. Protect from Sunlight.

Injection (reconstituted solutions)

Store at room temperature, Below 25°C or in refrigerator. Do not Freeze. Protect from Sunlight. Use within 2 weeks if kept at room temperature.

Store .


Interference in Pathology

Elevations of SGPT and SGOT

Serum creatinine raised

Elevation in ALT or AST

blood urea raised.


Cyclobenzaprine HCL


Cyclobenzaprine hydrochloride is a tricyclic amine salt with the empirical formula C20H21N•HCl. Cyclobenzaprine is a central nervous system (CNS) muscle relaxant intended for short-term use in the treatment of pain, tenderness, and limitation of motion caused by muscle spasms. It is thought to act within the CNS at the brain stem rather than spinal cord levels, although action at the spinal cord level may contribute to some of its skeletal muscle relaxant action.

Primary Characteristics

. It belongs to Muscle Relaxants pharmacological group on the basis of mechanism of action. The Molecular Weight of cyclobenzaprine hydrochloride is 311.90. Its pKa is 8.47.


Cyclobenzaprine is indicated as a short-term (2-3 weeks) adjunct therapy, along with rest and physical therapy, for relief of muscle spasm associated with acute, painful musculoskeletal conditions. It not been found effective in the treatment of spasticity originating from cerebral or spinal cord disease, or spasticity in children with cerebral palsy. Cyclobenzaprine is also occasionally used off-label for reducing pain and sleep disturbances in patients with fibromyalgia.


Oral absorption of cyclobenzaprine hydrochloride is found to be 44% ±11. Plasma protein binding is high. and metabolism is reported P-450 3A4, 1A2, and, to a lesser extent, 2D6. Renal Excretion accounts for as glucuronides and plasma half life is 18 Hours.



Cyclobenzaprine hydrochloride is contraindicated in conditions like Hyperthyroidism, Congestive heart failure, Hypersensitivity to any component of product.


Cyclobenzaprine is a skeletal muscle relaxant that works on areas of the brainstem to reduce skeletal muscle spasm, though its exact pharmacodynamic behavior is currently unclear. Despite its long half-life, it is relatively short-acting with a typical duration of action of 4-6 hours. Cyclobenzaprine has been reported to contribute to the development of serotonin syndrome when used in combination with other serotonergic medications. Symptoms of serotonin syndrome may include autonomic instability, changes to mental status, neuromuscular abnormalities, or gastrointestinal symptoms. treatment with cyclobenzaprine should be discontinued immediately if any of these reactions occur during therapy.

Mechanism of Action

The exact mechanism of action of cyclobenzaprine has not been fully elucidated in humans, and much of the information available regarding its mechanism has been ascertained from early animal studies. There is some evidence that cyclobenzaprine exerts its effects at the supraspinal level, specifically within the locus coeruleus of the brainstem, with little-to-no action at neuromuscular junctions or directly on skeletal musculature. Action on the brainstem is thought to result in diminished activity of efferent alpha and gamma motor neurons, likely mediated by inhibition of coeruleus-spinal or reticulospinal pathways, and ultimately depressed spinal cord interneuron activity.

More recently it has been suggested that inhibition of descending serotonergic pathways in the spinal cord via action on 5-HT2 receptors may contribute to cyclobenzaprine’s observed effects.


Cyclobenzaprine is extensively metabolized in the liver via both oxidative and conjugative pathways. Oxidative metabolism, mainly N-demethylation, is catalyzed primarily by CYP3A4 and CYP1A2 (with CYP2D6 implicated to a lesser extent) and is responsible for the major metabolite dimethyl cyclobenzaprine. Cyclobenzaprine also undergoes N-glucuronidation in the liver catalyzed by UGT1A4 and UGT2B1, and has been shown to undergo enterohepatic circulation


The effective half-life of cyclobenzaprine in young healthy subjects is approximately 18 hours. These values are extended in the elderly and those with hepatic insufficiency, with a mean effective half-life of 33.4 hours and 46.2 hours in these groups, respectively

Side Effects

The severe or irreversible adverse effects of cyclobenzaprine hydrochloride, which give rise to further complications include Irregular heart beat.

cyclobenzaprine hydrochloride produces potentially life-threatening effects which include Hypersensitivity reactions. which are responsible for the discontinuation of cyclobenzaprine hydrochloride therapy.

The signs and symptoms that are produced after the acute over dosage of cyclobenzaprine hydrochloride include Nausea, Tachycardia, Hallucinations, Drowsiness, Changes in ECG, Slurred speech, Dizziness, Coma, Severe hypotension, Seizures, Cardiac dysrhythmias, Confusion, Tremor, Vomiting, Ataxia, Agitation, Hypertension.

The symptomatic adverse reactions produced by cyclobenzaprine hydrochloride are more or less tolerable and if they become severe. They can be treated symptomatically, these include Headache, Drowsiness, Fatigue, Nausea, Diarrhea, Constipation, Abdominal pain, Dry mouth, Acid regurgitation.

Warning / Precautions

Use of Cyclobenzaprine Hydrochloride for periods longer than two or three weeks is not recommended. Less frequent dosing should be considered for hepatically impaired or elderly patients. It is contraindicated in acute recovery phase of myocardial infarction, and patients with arrhythmias, heart block or conduction disturbances, or congestive heart failure. Used with caution in elderly patients with reduced doses. It should be used with caution in patients with a history of urinary retention. Angle closure glaucoma, increased intraocular pressure, and in patients taking anticholinergic medication. Used with caution in subjects with mild hepatic impairment starting with a 5 mg dose and titrating slowly upward. In subjects with moderate to severe impairment is not recommended. Safety and effectiveness of cyclobenzaprine hydrochloride in pediatric patients below 15 years of age have not been established.


Storage Conditions

Store Between 15°C-30°C.



Vision Pharmaceutical’s powders for injections are sterile, pyrogen-free powder substances including our lyophilized material packed in glass container. When sterile water for injection (provided in the packaging) added into this powder. it rapidly form a clear solution that can injected intravenously or intramuscularly.

Parenteral preparations may require the use of excipients such as solvents, substances to enhance solubility, suspending agents, buffering agents, substances to make the preparation isotonic with blood, stabilizers or antimicrobial preservatives. Vision Pharmaceutical ensures that these addition of excipients kept to a minimum. Our R&D department thoroughly investigate and then recommends specific excipients so that they do not adversely affect the stability, bioavailability, safety or efficacy of the active ingredient. It ensured that all the components of the dry powder ampules perfectly compatible with each other.


Vision Pharmaceutical strives to make sure that our manufacturing process meet the standard of cGMP. The following main general guidelines followed at every step of production to meet the requirements.

The quality and grade of raw material, manufacturing machinery, maintenance of the equipment and the method of powder production. maintained at highest standard to ensure the stability of the active substance and of the final product and that the final product sterile and free of pyrogens and particulate matter.

If any antimicrobial agent added, the quantity kept minimum and according to guidelines provided by regulatory authority. Sterilisation performed prior to production and maintained throughout the procedure. For glass container sterilisation autoclave the preferred method because it ensures rapid and complete sterilisation.

Vision Pharmaceutical extra cautious in filling of oxidation sensitive formulas and filling of such powder done in the atmosphere of suitable sterile inert gas, such as nitrogen, whereby the air in the container replaced by this gas.

Suitable and controlled particle size in maintained, dependent upon the intended use of the dry powder formulation.

Vision Pharmaceutical monitors manufacturing process by validation and carrying out appropriate in-process controls. These chalked out in a way to guarantee effectiveness of each stage of production. Monitoring of environmental conditions (especially with respect to particulate and microbial contamination), bacterial endotoxins, pH and clarity of solution. Freedom from particulate matter and integrity of the container-closure system (absence of leakage, etc.) utmost importance in this regard. We ensure that production procedure of powders for injections must include uniformity of mass, moisture content and the ease of reconstitution.

Our quality control department validate every production phase and inspect final product for particulate matter, discoloration. Precipitation of solid matter and other sign of chemical or physical instability. Vision Pharmaceutical guarantees that all our parenteral preparations comply with Test for sterility. Test for bacterial endotoxins, or, where applicable with Test for pyrogens. In single active ingredient formula it ensured that the Sterile Powder for Injection must  uniform mass and particle size.


Drug Pellet formation may appear as semicircular granules to an unaided eye. But is it the same plain, old, bitter tastings medicinal stuff, nay! It indeed a marvelous of modern pharmaceutical research. We at Vision Pharmaceutical put literally our heart and soul with critical Thinking brains and expert hands into making drug palletization a reality and its wider availablity to local as well as international consumers.

Vision Pharmaceutical with its focused and result oriented R&D makes the formation of nearly spherical particles into final, pellitized product possible undergoing the process of fine particulating ,tumble drying, addition of binders and additives in various pellitization equipment.

Our unique pellitization techniques make us not only on par with any standardized international pellet manufacturers but give us un upper hand in economically competitive market as well. Drug Pellets manufacturing an art in itself and undergoes stages of production under uber scientific principles. What factors work deep down in these processing and how complicated it  ,let us have a look.

At first moist content of dried particles is reduced to form an effective air water interface. Make a granulation of particles possible with the help of both physical and applied forces. Physical forces impart tensile strength and liquid bridging among particles, changing capillary and surface tension of granules.

At Vision Pharmaceutical purpose built fully automated manufacturing unit makes tumbling motion of the particles possible and applied forces.   That arise as a result bring individual wetted particles close to each other and uniform distribution of active ingredients. This mechanism makes it possible to initiate pellitization process and subsequent growth of individual pellets under the following factors.

  1. Nucleation

Nucleation the Formation of nuclei and the process of particles formation from the continuos phase via interaction within the physical environment. In this stage liquid bridges created making formation of three dimensional water-air-liquid bonding possible, this give particles specific physical appearance and properties. Vision Pharmaceuticals makes sure that particles size must kept smaller for better bonding strength.

  1. Coalescence:

The second stage is coalescence, its a transition stage. This region affected by growth factors of coalescence and drug layering. Very important indeed so it needs to be closely supervised and Our R&D strives to make the process up to date. Coalescence brings discreet changes to size and no of particles but not to their mass.

  1. Layering

Layering is a third and final factor in manufacturing process of pellet formation. It is a continuous phase where both size and properties of particulate matter changes with drug layering. Vision Pharmaceutical advanced, fully automated production facility. Makes its possible to layer single or multiple active drugs on a single granule. Masking of bitter tastings drugs with addition of layers of Tasteless additives also ensured in this process.

All these Physical and Chemical processes work simultaneously in delicate ways to make scientifically quantified, tasteless, single/multi ingredient active drug pellets a reality and Vision as a pioneer in the science of pellitization.


Vision Pharmaceutical has one of a kind, state of art production machinery. That unique in its own way and utilise every modern pellitization Techniques, a quality unmatched in local market as well as neighbouring India. A Vision Pharmaceutical fully automated plant, R&D and Quality control department work in synchronisation to produce products with unmatched quality, economy, efficacy and Heartfelt satisfaction from our end consumers.

Vision Pharmaceutical utilises every modern standardised technique and pharmaceutical manufacturing procedures to produce drug pellets of unmatched quality.

We herby Discuss Vision Pharma’s pellitization Techniques in detail.

Extrusion Spheronization:

This technique widely used in modern pellitization worldwide. Vision Pharmaceutical utilises it as a major pellitization procedure in its operations. Our unique extrusions Spheronization takes place in three steps.

. Feed preparation

. Pellets production

. Pellets curing

Feed preparation, the first step and it initiated by mixing of drug-excipients with desired additives such as solution of binding agents. Then the second and most important step follows, and the process of agglomeration, where desired size of pellets are formed in pellitizater. The final step curing of wet pellets by thermal drying. Vision Pharmaceutical also utilises technique of simple stockpiling for some drug pellets.

The pellitization begins with the dispensing of powder feed material with binding solutions to the granulator to form a plasticized wet mass. This mass allowed to the screening chamber of extruder. Here pressure blades provide enough Compression to wet mass against the exterior of the screen. The extruder material discharged into discharge unit through scrapper blade and then finally into Spheronizer. Pellitizer disk  rolls the extruded with high speed in the direction of the roller and a rolling movement of helical like structure takes place. This makes the extrudes smooth in short amount of time. Due to intense rolling action and finally uniformed and spherical pellets discharged at the discharge unit.

More about Pellitization Technique

Pellitization Technique needs careful evaluation and continuous monitoring.  Vision Pharmaceutical’s production and quality control departments keep a keen eye. Monitors and document the whole process according to strict guidelines at every step of production. We ensure that every step thoroughly followed and not even a slight mistake is tolerated. We at Vision ensure that.

. In order to produce pellets of uniform size and shape the whole procedure of spheronization properly optimized.

. Extrudate should be in proper wet condition before entering spheronizer. So that it can be spheronized smoothly and no further breakdown occur.

. Different types of extruders are used for different formulations in order to achieve uniform pellitization.

. Amount of binders strictly controlled to avoid hardness and irregular shapes of pellets.

. Formation of big lumps of pellets  avoided at every cost.

. This type of pellitization process  more labor intensive but result in very ideal uniform shaped also spherical pellets.


Drug Pellets must have specific Pharmaceutical Properties to be considered as better alternative to conventional dosage forms. Vision Pharmaceutical ensures the highest possible standard of these requisites, both qualitatively and quantitatively and our formulated pellets best example of ,what benefits do this scientific novice and far better dosage form carries. Vision Pharmaceutical ensures that every standardised procedure and SOPs are thoroughly followed to impart unique qualities to our Drug Pellets.

At every phase of Pellets production Vision Pharmaceutical ensures that our end products comply all international standards and posses quality that second to none. Our highest qualified workforce and Fully Automated Plant ensures that no stone left unturned to achieve the goal of Ideal pellitization equipped with best Pharmaceutical properties.

In contrast to Semi Automated Production plant ,our Fully Automated Production Unit omits any chance or possibility of human error. Vision Pharmaceutical takes pride in drug pellitization, where every individual pellet carry unmatched Pharmaceutical qualities.


Pellets as drug delivery carries must have uniform size, almost spherical shape and free flowing properties. Vision Pharmaceutical drug Pellets have unifrom size and flow properties that guarantee best subsequent encapsulation and compression.

Shape and Tensile strength:

We at Vision Pharmaceutical make sure that our formulated pellets have a specific comparatively better tensile strength. The single most important Pharmaceutical property of our pellets that provide our end product with targeted drug delivery module.

Our oral contral release medication posses  qualities of dispersion all along the Gastrointestinal tract and exhibits prolong GI transit time. The tensile strength of our pellets impart it with sufficient mechanical strength to withstand abrasion during handling and further processing.

Shape and size play important role in dissolution and disintegration of drug pellets. Shape and size determing factors in devising dose strenght as pellets’ particles may form cluster and may remain there for long time within stomach even when food expelled out of stomach long before.

Smaller pellets of less then 2.4 mm diameter not affected by digestive functioning and closing down of pyloric sphincter. For multi unit drug pellets the ideal diameter 1.5 mm. Vision Pharmaceutical ensures that particle size standards strictly maintend.

Vision Pharmaceutical pellets production unit follows strict guidelines in maintaining the Ideal tensile strength of pellet granules. Our Pellets posses strength enough to withstand handling, transportation, storage, and further processing. We at Vision focus on strength of both wet and dry pellets.

Vision Pharmaceutical use a combination of additives and production techniques to ensure that our pellets posses ideal qualities. Quantity and nature of Adhesive , moisture content, salts and binders used in order to increase the strength of pellets.

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