CLOFIBRATE Ressources

Application Information

This drug has been submitted to the FDA under the reference 070531/001.

Names and composition

"CLOFIBRATE" is the commercial name of a drug composed of CLOFIBRATE.

Forms

ApplId/ProductId Drug name Active ingredient Form Strenght
070531/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
071603/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
072191/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
072600/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
073396/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG

Similar Active Ingredient

ApplId/ProductId Drug name Active ingredient Form Strenght
016099/002 ATROMID-S CLOFIBRATE CAPSULE/ORAL 500MG
070531/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
071603/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
072191/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
072600/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG
073396/001 CLOFIBRATE CLOFIBRATE CAPSULE/ORAL 500MG

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Answered questions

Why is Chlordiazepoxides, Diazepam, Clofibrate, Barbiturates contraindicated in patients with renal failure?
thanks! Asked by Melodie Jhonston 1 month ago.

Here are the pharmacokinetics of each individual drug: Chlordiazepoxide undergoes oxidative metabolism in the liver, producing several active compounds including demoxepam, desmethylchlordiazepoxide, desmethyldiazepam, and oxazepam. Smoking enhances the hepatic metabolism of some benzodiazepines. Smokers may require increased doses to achieve the desired sedative effect. Chlordiazepoxide has a long half-life (5—30 hours) compared with other benzodiazepines, and the half-lives of its metabolites range from 14—100 hours. The risk of accumulation is high during periods of repeated dosing. Unchanged drug and its active metabolites are excreted in the urine, but the elimination is slower than that of other benzodiazepines because the metabolites can still be present in the blood for several weeks after the initial dosing interval. Clofibrate is absorbed readily and completely from the GI tract and is rapidly hydrolyzed by serum esterases to the active metabolite clofibric acid. Clofibric acid peak plasma concentrations of 80—90 mcg/ml occur 2—6 hours after a single 1 g dose of clofibrate. Plasma concentrations of 160—200 mcg/mL are attained at steady-state in healthy volunteers taking 1 g bid. Clofibric acid is 98% protein-bound and is distributed only into the extracellular space. Serum triglyceride levels decrease within 2—5 days, with maximum clinical effect reached after 21 days. Clofibric acid is excreted in the urine, 20% unchanged and 70% as a glucuronide conjugate. Plasma half-life after a single dose in patients with normal renal and hepatic functions ranges from 12—35 hours. Clofibrate clearance is reduced by about 50% in cirrhosis. Metabolism of diazepam is primarily hepatic and involves demethylation (involving primarily CYP2C19 and CYP3A4) and 3-hydroxylation (involving primarily CYP3A4). Diazepam is extensively metabolized to one major active metabolite desmethyldiazepam and two minor active metabolites temazepam (3-hydroxydiazepam) and oxazepam (3-hydroxy-N-diazepam), with half-lives of 30—100 hours, 9.5—12 hours, and 5—15 hours, respectively. At therapeutic doses, desmethyldiazepam is found in plasma at concentrations equivalent to those of diazepam. Oxazepam and temazepam plasma concentrations are usually undetectable. The half-life of diazepam is 30—60 hours. These metabolites are subsequently glucuronidated and excreted in the urine. Now the reason why all these drugs are contraindicated in renal failure patients is simple because they are not able to be eliminated the drug and their active metabolites from the body via the urine. So with repeated dosing and the inability to eliminate the drug from the body, the drug starts to accumulate in the body to toxic levels. Answered by George Abetrani 1 month ago.

Drugs excreted by the kidney accumulate in renal failure and cause toxicity. That is the reason. Similarly drugs toxic to the kidneys are also to be avoided in renal failure. Answered by Perry Weisberger 1 month ago.

very long story short - cos of the way the body takes them in and gets rid of them. Answered by Bruce Breiter 1 month ago.


Interference with the synthesis of cholesterol is produced by?
Here are the choices: a. clofibrate( Atromid-S) b. niacin (Nicolar) c. cholestyramine(Questran) d dextrothyroxine(Cholixin) I am leaning toward A & C, but I don't quite understand the whole thing. HELP Asked by Riley Mccleary 1 month ago.

The question means: which of the drugs interfere the synthesis of cholesterol? Actually, synthesis of cholesterol is made by liver. Normally, statins interfere the synthesis. However, it is not in your choices. So, a. clofibrate - (included in the fibrates drugs group) inhibit the absorption of cholesterol in the intestines. b. niacin - interfere the synthesis of blood fats in the liver c. cholestyramine - (is included in the bile-acid sequestrants) utilizes cholesterol to produce bile acids and clear the body from the excessive cholesterol (do not interfere in the synthesis). d. dextrothyroxine - (it is rarely prescribed due to high risks for heart disease; not used anymore in USA and Canada). It also interfere the synthesis of cholesterol and its uptake in the liver. As you see, the correct answers are B and D. Answered by Earle Rendler 1 month ago.

SkepDoc is right, there is no need for me to repeat. Just to reiterate; RedAngel does not actually know whats she's talking about. She goes onto sites like NaturalNews and Mercola and takes anything she reads there at face value, ignoring the fact that these people do not actually have a clue what they are talking about, and cannot interpret data. "Edit: to skepdoc...the evidence is overwhelming that saturated fat are not the bad fats they are made out to be." No, you miss the point; saturated fats are not bad, it's the QUANTITY thats' the problem, along with other factors. "In fact the first heart attack was recorded in Britain in 1878 and it took 42 years for another heart attack to be recorded in 1921.....a long wait indeed...." Er...I'd actually like to see some data to support that comment. I also think you should take into consideration the fact medical technology was not as advanced back then as it is now, many causes of death were not recorded accurately. Also, perhaps it has something to do with the fact everyone is living longer. What you and your ilk fail to understand is that arteriosclerosis (main cause of MIs) is to a certain extent part of the NATURAL ageing process........of course an unhealthy diet and lifestyle will accelerate it. Living longer means managing diseases that occur with age. "but everyone ate saturated fats back then" Yep, they also died back then too and had half the life expectancy. Answered by Holli Dockal 1 month ago.


Can anyone help with this Human Physiology Question?
Your patient is on Coumadin therapy (an anticoagulant) for a blood clot in the leg. Which type of plasma protein would you suspect is low? a. serum b. globulin c. plasma protein d. fibrinogen e. albumin Asked by Kenton Brownley 1 month ago.

Clofibrate is known to potentiate the anticoagulant effect of warfarin during chronic administration. We examined the disposition of racemic warfarin in four healthy volunteers before and during clofibrate coadministration using an intravenous-continuous oral sequence of warfarin administration. An interaction between warfarin and clofibrate, evidenced by longer prothrombin and prothrombin-proconvertin times, was seen in all four subjects. Clofibrate caused a displacement of warfarin from plasma protein binding sites, with a 13% increase in the free drug fraction in plasma. As predicted from theoretical considerations, this displacement resulted in a small (18%) increase in the steady-state volume of distribution, and an increase in total plasma clearance, which, for warfarin, is independent on the free fraction of drug in plasma. The net effect of these changes is that the free concentration of warfarin was not changed during clofibrate coadministration, although total plasma concentrations were lower. This study documents the occurrence in man of a displacement pharmacokinetic interaction between clofibrate and warfarin. However, this pharmacokinetic interaction does not account for the clinical interaction between the two drugs, since free warfarin concentrations are unchanged. Answered by Augustina Ginn 1 month ago.

Human Physiology is not difficult if it is studied with interest.main thing is that we have to understand it deeply. For that definitely Biochemistry will pay a role especially while dealing with metabolism. Answered by Lise Kanatzar 1 month ago.


Does anybody here take the birth control pill Cryselle?
Does it have any interactions with the anti depressant Lexapro? Asked by Neida Bennerman 1 month ago.

Although Lexapro is not mentioned by name all medicine for mental depression might interact: What drug(s) may interact with ethinyl estradiol; norgestrel? (Cryselle etc). •anastrozole •antibiotics or medicines for infections, especially rifampin, rifabutin, rifapentine, and griseofulvin •aprepitant, a medicine used for chemotherapy-induced nausea and vomiting •barbiturate medicines for producing sleep or treating seizures (convulsions) •bosentan •carbamazepine •caffeine •clofibrate •cyclosporine •dantrolene •doxercalciferol •exemestane •grapefruit juice •hydrocortisone •letrozole •medicines for anxiety or sleeping problems, such as diazepam or temazepam •medicines for mental depression •medicines for diabetes, including troglitazone and pioglitazone •mineral oil •modafinil •mycophenolate •nefazodone •oxcarbazepine •phenytoin •prednisolone •ritonavir or other medicines for the treatment of the HIV virus or AIDS •selegiline •soy isoflavones supplements •St. John's wort •tamoxifen or raloxifene •testolactone •theophylline •topiramate •warfarin Tell your prescriber or health care professional about all other medicines you are taking, including non-prescription medicines, nutritional supplements, or herbal products. Also tell your prescriber or health care professional if you are a frequent user of drinks with caffeine or alcohol, if you smoke, or if you use illegal drugs. These may affect the way your medicine works. Check before stopping or starting any of your medicines. What side effects may I notice from taking ethinyl estradiol; norgestrel? (Back to top) Severe side effects are relatively rare in women who are healthy and do not smoke while they are taking oral contraceptives. On average, more women have problems due to complications from getting pregnant than have problems with oral contraceptives. Many of the minor side effects may go away as your body adjusts to the medicine. However, the potential for severe side effects does exist and you may want to discuss these with your health care provider. The following symptoms or side effects may be related to blood clots and require immediate medical or emergency help: •chest pain •coughing up blood •dizziness or fainting spells •leg, arm or groin pain •severe or sudden headaches •stomach pain (severe) •sudden shortness of breath •sudden loss of coordination, especially on one side of the body •swelling of the hands, feet or ankles, or rapid weight gain •vision or speech problems •weakness or numbness in the arms or legs, especially on one side of the body Answered by Roman Huddleson 1 month ago.

why would you want fake birth control pills?? do not say you are trying to trick a guy into getting you pregnant... Answered by Elfreda Kryston 1 month ago.


Low Cholesterol but High Triglyceride ?
Philippa states ...."It is endogenous (diet plays a small part in it but your body depends highly on fatty acids for energy and stores these in adipose tissue. We all differ in our capacity to mobilise fatty acids for metabolism)." So if if its not due to diet what might be the causes ? Could... Asked by Kirstie Biffer 1 month ago.

My Cholesterol is 3.8 nmol/l HDL 2.1 nmol/l LDL 0.8 nmol/l Cholesterol / HDL ratio 1.81 Perfect readings ? So why is my Triglyceride up at 1.9 nmol/l ? Where is it coming from ? Is it likely to undo the beneficial effects of my good cholesterol profile and lead to arteriosclerosis ? And why doesn't LDL + HDL add up to Total Cholesterol ? Answered by Dorotha Matyi 1 month ago.

Philippa states ...."It is endogenous (diet plays a small part in it but your body depends highly on fatty acids for energy and stores these in adipose tissue. We all differ in our capacity to mobilise fatty acids for metabolism)." So if if its not due to diet what might be the causes ? Could fasting, or dieting elevate the breakdown and release of adipose fats into the bloodstream, rather like in ketosis ? Answered by Denice Skubis 1 month ago.

Triglycerides are chemically distinct from the sterols (i.e. derivatives of cholesterol such as sex hormones, glucocorticoids and mineralocorticoids). They are formed by a glycerol molecule bound by fatty acid chains (drawn schematically, they look more like tadpoles compared to the ring-like structure of sterols). Hence, triglycerides may be elevated primarily without any abnormality of cholesterol. The treatment is with drugs known as fibrates (such as clofibrate), to reduce synthesis of triglycerides. This is a different family of drugs to those used to treat cholesterol (the HMG-CoA reductase inhibitors, such as simvastatin). It is endogenous (diet plays a small part in it but your body depends highly on fatty acids for energy and stores these in adipose tissue. We all differ in our capacity to mobilise fatty acids for metabolism). Hypertriglyceridaemia needs treating because it does increase risks of arterial disease except it is athersclerosis NOT arteriosclerosis which these lipids increase the risk of (including cholesterol in the definition of lipid). Hypertriglyceridaemia can also cause pancreatitis, eruptive xanthomata and xanthelasma, pseudohyponatraemia and other health problems but it is treatable (see above). LDL + HDL do not add up to Total Cholesterol as they are not the only forms of cholesterol transport in the blood. The terms HDL and LDL stand for High Density and Low Density Lipoproteins respectively. These are protein and lipid complexes which emulsify cholesterol (itself lipophilic and hence insoluble in water) and transport it around the body in blood. The LDL represents likely excess cholesterol and is crudely understood as delivery vectors of cholesterol TO body tissues from liver, hence it is labelled the bad cholesterol. HDL on the other hand seems to transport cholesterol back to the liver from peripheral tissue for either recycling or excretion (in bile, the human body cannot itself destroy the sterol ring although it can convert fatty acids into sterols if need be). The missing story: chylomicrons and some other lipoproteins also exist, they help transport lipids in the diet from gut to lymphatics and hence through the circulation and eventually to the liver for processing and distribution elsewhere via LDL. Hope this helps. Answered by Leandra Emlin 1 month ago.


Slightly raised ggt levels?
My ggt levels were slightly raised after a liver function test, how do i lower it? Asked by Michele Mulkern 1 month ago.

ggt or Gamma-glutamyl transpeptidase can be decreased by drugs such as clofibrate and oral contraceptives Answered by Roberto Mahnke 1 month ago.


How i reduce Blood TG (2700) & Cl 260 how i reduce TG? plz help?
Please help me my Blood TG is 2717 and calestrole is 260 how i reduce my TG my age is 32 and weight is 70kg . hight is 5.8 Asked by Helga Rasely 1 month ago.

Hi Afzal, your TG is extremely high. But fortunately your cholesterol isn't off the charts. I assume your doctor has already put you on a fibrate (gemfibrozil, clofibrate...) plus niacin combo. If you haven't seen a doctor or if you aren't on meds, you should definitely be on this combo. Other than that do the following: 1. Exercise 2. Eat less saturated and trans fats. 3. cook food in canola, olive or peanut oils 4. increase your fiber intake (whole grain, oatmeal, fruits) 5. limit sugar intake 6. drink 1 glass of wine a day (no more, no less. and not beer) 7. increase Omega-3 intake (salmon, fish-oil) The above are mainly to decrease your TG. But it will help with your LDL and increase your HDL too. Hope that helps, and best of luck to you. Answered by Eura Vulich 1 month ago.

You may reduce your cholesterol by diet (reduce carbohydrate & sugar), exercise and statin drug. High triglyceride blood levels may cause pancreatitis. Omega-3 fatty acid may reduce high triglycerides. Eat a low-cholesterol, low-fat diet, which includes cottage cheese, fat-free milk, fish, vegetables, poultry, and egg whites. Use monounsaturated oils such as olive, peanut, and canola oils or polyunsaturated oils such as corn, safflower, soy, sunflower, cottonseed, and soybean oils. Avoid foods with excess fat in them such as meat (especially liver and fatty meat), egg yolks, whole milk, cream, butter, shortening, pastries, cakes, cookies, gravy, peanut butter, chocolate, olives, potato chips, coconut, cheese (other than cottage cheese), coconut oil, palm oil, and fried foods. Normal level: Cholesterol- < 200 mg/dL; Triglycerides- < 150 mg/dL. Answered by Chrystal Rhymes 1 month ago.

thank u all Answered by Lydia Anchondo 1 month ago.


Can a CK level of 60000 damage any organs?
My husband had an episode that has caused his CK enzymes to sky rocket to 60000. He is in renal failure and now they are looking at his heart. I want to know if this enzyme can cause damage to other organs if it is this high. Asked by Thomas Demarinis 1 month ago.

Possible causes of an elevated CK Cardiac muscle Infarction Myopathy Myocarditis Skeletal muscle Injury/Trauma Crush, Surgery, IM injections, Ischaemia Alcohol Acute/Chronic alcohol excess Drugs Statins, Amphotericin B, Azathioprine, Chloroquine, Clofibrate, Colchicine, Cyclosporin, Opioids, Steroids, Vincristine, Verapamil, Proton Pump Inhibitors Infections Influenza, Coxsackie A and B, Clostridia, Streptococcus pyogenes, Parasitic infestations Endocrine Hypothyroidism, Hyperthyroidism, Steroid myopathy Metabolic Hypokalaemia, Vitamin D deficiency, Carnitine deficiency, Carnitine Palmitoyl-tranferase deficiency, Hypoparathyroidism, Myophosphorylase deficiency, Mitochondrial disorders Autoimmune Polymyositis, Dermatomyositis Exercise Severe exertion, Marathon run, Convulsions, Paroxysmal myoglobinuria Heat stroke Malignant hyperpyrexia Muscular dystrophy Miscellaneous Macro-CK (request CK electrophoresis) Malignancy Cerebrovascular disease Diabetic ketoacidosis Useful further tests Troponin Serum LD and AST CK-Isoenzymes, CK electrophoresis Urinary myoglobin Autoimmune immunology DNA tests for muscular dystrophy COPYRIGHT © SULLIVAN NICOLAIDES PATHOLOGY 2011 IP111 MARCH 2011 Answered by Lorie Yambao 1 month ago.


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