You are looking at all articles with the topic "Pharmacology". We found 11 matches.

Hint: To view all topics, click here. Too see the most popular topics, click here instead.

Eroom's law is the observation that drug discovery is becoming slower and more expensive over time, despite improvements in technology (such as high-throughput screening, biotechnology, combinatorial chemistry, and computational drug design), a trend first observed in the 1980s. The cost of developing a new drug roughly doubles every nine years (inflation-adjusted). In order to highlight the contrast with the exponential advancements of other forms of technology (such as transistors) over time, the law was deliberately spelled as Moore's law spelled backwards.

The article proposing and naming the law attributes it to four main causes.

• the 'better than the Beatles' problem: the sense that new drugs only have modest incremental benefit over drugs already widely considered as successful, such as Lipitor, and treatment effects on top of already effective treatments are smaller than treatment effects versus placebo. The smaller size of these treatment effects mandates an increase in clinical trial sizes to show the same level of efficacy. This problem was phrased as "better than the Beatles" to highlight the fact that it would be difficult to come up with new successful pop songs if all new songs had to be better than the Beatles.
• the 'cautious regulator' problem: the progressive lowering of risk tolerance seen by drug regulatory agencies that makes R&D both costlier and harder. After older drugs (such as Thalidomide or Vioxx) are removed from the market due to safety reasons, the bar on safety for new drugs is increased.
• the 'throw money at it' tendency: the tendency to add human resources and other resources to R&D, which may lead to project overrun.
• the 'basic research–brute force' bias: the tendency to overestimate the ability of advances in basic research and brute force screening methods to show a molecule as safe and effective in clinical trials. From the 1960s to the 1990s (and later), drug discovery has shifted from whole-animal classical pharmacology testing methods (phenotypic screening) to reverse pharmacology target-approaches that result in the discovery of drugs that may tightly bind with high-affinity to target proteins, but which still often fail in clinical trials due to an under-appreciation of the complexity of the whole organism. Furthermore, drug discovery techniques have shifted from small-molecule and iterative low-throughput search strategies to target-based high-throughput screening (HTS) of large compound libraries. But despite being faster and cheaper, HTS approaches may be less productive.

While some suspect a lack of "low-hanging fruit" as a significant contribution to Eroom's law, this may be less important than the four main causes, as there are still many decades' worth of new potential drug targets relative to the number of targets which already have been exploited, even if the industry exploits 4 to 5 new targets per year. There is also space to explore selectively non-selective drugs (or "dirty drugs") that interact with several molecular targets, and which may be particularly effective as central nervous system (CNS) therapeutics, even though few of them have been introduced in the last few decades.

A caries vaccine is a vaccine to prevent and protect against tooth decay. Streptococcus mutans (S. mutans) has been identified as the major etiological agent of human dental caries. The development of a vaccine for tooth decay has been under investigation since the 1970s. In 1972, a caries vaccine was said to be in animal testing in England, and that it would have begun human testing soon. However, intrinsic difficulties in developing it, coupled with lack of strong economic interests, are the reasons why still no such vaccine is commercially available today. Several types of vaccines are being developed at research centres, with some kind of caries vaccines being considered to diminish or prevent dental caries' impact on young people.

Sofosbuvir, sold under the brand name Sovaldi among others, is a medication used to treat hepatitis C. It is only recommended with some combination of ribavirin, peginterferon-alfa, simeprevir, ledipasvir, daclatasvir, or velpatasvir. Cure rates are 30 to 97% depending on the type of hepatitis C virus involved. Safety during pregnancy is unclear; some of the medications used in combination may result in harm to the baby. It is taken by mouth.

Common side effects include feeling tired, headache, nausea, and trouble sleeping. Side effects are generally more common in interferon-containing regimens. Sofosbuvir may reactivate hepatitis B in those who have been previously infected. In combination with ledipasvir, daclatasvir or simeprevir it is not recommended with amiodarone due to the risk of an abnormally slow heartbeat. Sofosbuvir is in the nucleotide analog family of medication and works by blocking the hepatitis C NS5B protein.

Sofosbuvir was discovered in 2007, and approved for medical use in the United States in 2013. It is on the World Health Organization's List of Essential Medicines, the safest and most effective medicines needed in a health system. As of 2016, a 12-week course of treatment costs about US$84,000 in the United States, US$53,000 in the United Kingdom, US$45,000 in Canada, and about US$500 in India. Over 60,000 people were treated with sofosbuvir in its first 30 weeks being sold in the United States.

For over two millennia, texts in Chinese herbology and traditional Chinese medicine have recorded medicinal plants that are also hallucinogens and psychedelics. Some are familiar psychoactive plants in Western herbal medicine (e.g., Chinese: 莨菪; pinyin: làngdàng, i.e. Hyoscyamus niger), but several Chinese plants have not been noted as hallucinogens in modern works (e.g.,Chinese: 雲實; pinyin: yúnshí; lit. 'cloud seed', i.e. Caesalpinia decapetala). Chinese herbals are an important resource for the history of botany, for instance, Zhang Hua's c. 290 Bowuzhi is the earliest record of the psilocybin mushroom xiàojùn 笑菌 (lit. "laughing mushroom", i.e. Gymnopilus junonius).

Modafinil, sold under the brand name Provigil among others, is a medication to treat sleepiness due to narcolepsy, shift work sleep disorder, or obstructive sleep apnea. While it has seen off-label use as a purported cognitive enhancer, the research on its effectiveness for this use is not conclusive. It is taken by mouth.

Common side effects include headache, anxiety, trouble sleeping, and nausea. Serious side effects may include allergic reactions such as anaphylaxis, Stevens–Johnson syndrome, misuse, and hallucinations. It is unclear if use during pregnancy is safe. The amount of medication used may need to be adjusted in those with kidney or liver problems. It is not recommended in those with an arrhythmia, significant hypertension, or left ventricular hypertrophy. How it works is not entirely clear. One possibility is that it may affect the areas of the brain involved with the sleep cycle.

Modafinil was approved for medical use in the United States in 1998. In the United States it is classified as a schedule IV controlled substance. In the United Kingdom it is a prescription only medication. It is available as a generic medication. In the United Kingdom it costs the NHS about £105.21 a month as of 2018. In the United States the wholesale cost per month is about US$34.20 as of 2018. In 2016, it was the 284th most prescribed medication in the United States, with more than a million prescriptions.

Zoopharmacognosy is a behaviour in which non-human animals apparently self-medicate by selecting and ingesting or topically applying plants, soils, insects, and psychoactive drugs to prevent or reduce the harmful effects of pathogens and toxins. The term derives from Greek roots zoo ("animal"), pharmacon ("drug, medicine"), and gnosy ("knowing").

An example of zoopharmacognosy occurs when dogs eat grass to induce vomiting. However, the behaviour is more diverse than this. Animals ingest or apply non-foods such as clay, charcoal and even toxic plants and invertebrates, apparently to prevent parasitic infestation or poisoning.

Whether animals truly self-medicate remains a somewhat controversial subject because early evidence is mostly circumstantial or anecdotal, however, more recent examinations have adopted an experimental, hypothesis-driven approach.

The methods by which animals self-medicate vary, but can be classified according to function as prophylactic (preventative, before infection or poisoning) or therapeutic (after infection, to combat the pathogen or poisoning). The behaviour is believed to have widespread adaptive significance.

Benzodiazepines (BZD, BDZ, BZs), colloquially called "benzos", are a class of depressant drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. They are prescribed to treat conditions such as anxiety disorders, insomnia, and seizures. The first benzodiazepine, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955 and was made available in 1960 by Hoffmann–La Roche, who soon followed with diazepam (Valium) in 1963. By 1977, benzodiazepines were the most prescribed medications globally; the introduction of selective serotonin reuptake inhibitors (SSRIs), among other factors, decreased rates of prescription, but they remain frequently used worldwide.

Benzodiazepines are depressants that enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABA_A receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties. High doses of many shorter-acting benzodiazepines may also cause anterograde amnesia and dissociation. These properties make benzodiazepines useful in treating anxiety, panic disorder, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal and as a premedication for medical or dental procedures. Benzodiazepines are categorized as short, intermediate, or long-acting. Short- and intermediate-acting benzodiazepines are preferred for the treatment of insomnia; longer-acting benzodiazepines are recommended for the treatment of anxiety.

Benzodiazepines are generally viewed as safe and effective for short-term use—about two to four weeks—although cognitive impairment and paradoxical effects such as aggression or behavioral disinhibition can occur. A minority of people have paradoxical reactions after taking benzodiazepines such as worsened agitation or panic. Benzodiazepines are associated with an increased risk of suicide due to aggression, impulsivity, and negative withdrawal effects. Long-term use is controversial because of concerns about decreasing effectiveness, physical dependence, benzodiazepine withdrawal syndrome, and an increased risk of dementia and cancer. The elderly are at an increased risk of both short- and long-term adverse effects, and as a result, all benzodiazepines are listed in the Beers List of inappropriate medications for older adults. There is controversy concerning the safety of benzodiazepines in pregnancy. While they are not major teratogens, uncertainty remains as to whether they cause cleft palate in a small number of babies and whether neurobehavioural effects occur as a result of prenatal exposure; they are known to cause withdrawal symptoms in the newborn.

Taken in overdose, benzodiazepines can cause dangerous deep unconsciousness, but they are less toxic than their predecessors, the barbiturates, and death rarely results when a benzodiazepine is the only drug taken. Combined with other central nervous system (CNS) depressants such as alcohol and opioids, the potential for toxicity and fatal overdose increases significantly. Benzodiazepines are commonly used recreationally and also often taken in combination with other addictive substances, and are controlled in most countries.

Some fruit juices and fruits can interact with numerous drugs, in many cases causing adverse effects. The effect was first discovered accidentally, when a test of drug interactions with alcohol used grapefruit juice to hide the taste of the ethanol.

The effect is most studied with grapefruit and grapefruit juice, but similar effects have been observed with certain other citrus fruits. One medical review advises patients to avoid all citrus juices until further research clarifies the risks. Effects have been observed with apple juice, but their clinical significance is not yet known.

One whole grapefruit, or a small glass (200 mL (6.8 US fl oz)) of grapefruit juice, can cause drug overdose toxicity. Fruit consumed three days before the medicine can still have an effect. The relative risks of different types of citrus fruit have not been systematically studied. Affected drugs typically have an auxiliary label saying “Do not take with grapefruit” on the container, and the interaction is elaborated upon in the package insert. People are also advised to ask their physician or pharmacist about drug interactions.

The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids). These chemicals inhibit key drug metabolizing enzymes, such as cytochrome P450 3A4 (CYP3A4). CYP3A4 is a metabolizing enzyme for almost 50% of drugs, and is found in the liver and small intestinal epithelial cells. As a result, many drugs are affected. Inhibition of enzymes can have two different effects, depending on whether the drug is either

1. metabolized by the enzyme to an inactive metabolite, or
2. activated by the enzyme to an active metabolite.

In the first instance, inhibition of drug-metabolizing enzymes results in elevated concentrations of an active drug in the body, which may cause adverse effects. Conversely, if the medication is a prodrug, it needs to be metabolised to be converted to the active drug. Compromising its metabolism lowers concentrations of the active drug, reducing its therapeutic effect, and risking therapeutic failure.

Low drug concentrations can also be caused when the fruit suppresses drug absorption from the intestine.

Human anti-mouse antibody or human anti-murine antibody (HAMA) is an antibody found in humans which reacts to immunoglobins found in mice.

Miraculin is a taste modifier, a glycoprotein extracted from the fruit of Synsepalum dulcificum. The berry, also known as the miracle fruit, was documented by explorer Chevalier des Marchais, who searched for many different fruits during a 1725 excursion to its native West Africa.

Miraculin itself does not taste sweet. When taste buds are exposed to miraculin, the protein binds to the sweetness receptors. This causes normally sour-tasting acidic foods, such as citrus, to be perceived as sweet. The effect can last for one or two hours.