Question:

What is this pill? it is white on one side it has west ward 232 Other side has line down it?

Answer:

Could it be a 292? A white oblong with 292 Westward is Methocarbamol 750 mg. That is a muscle relaxant.

More Info:


MDMEO
1-(1,3-benzodioxol-5-yl)-N-methoxypropan-2-amine CC(NOC)Cc1ccc2OCOc2c1 InChI=1S/C11H15NO3/c1-8(12-13-2)5-9-3-4-10-11(6-9)15-7-14-10/h3-4,6,8,12H,5,7H2,1-2H3Yes 
Key: MTIKJUJMCMDSGM-UHFFFAOYSA-NYes  InChI=1/C11H15NO3/c1-8(12-13-2)5-9-3-4-10-11(6-9)15-7-14-10/h3-4,6,8,12H,5,7H2,1-2H3
Key: MTIKJUJMCMDSGM-UHFFFAOYAV MDMEO, or 3,4-methylenedioxy-N-methoxyamphetamine, is a lesser-known psychedelic drug and a substituted amphetamine. It is also the N-methoxy analogue of MDA. MDMEO was first synthesized by Alexander Shulgin. In his book PiHKAL (Phenethylamines i Have Known And Loved), the minimum dosage is listed as 180 mg. MDMEO may be found as white crystals. It produces few to no effects. Very little data exists about the pharmacological properties, metabolism, and toxicity of MDMEO.

Muscle relaxant
A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause temporary paralysis. Spasmolytics, also known as "centrally acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only. The earliest known use of muscle relaxant drugs dates back to the 16th century, when European explorers encountered natives of the Amazon Basin in South America using poison-tipped arrows that produced death by skeletal muscle paralysis. This poison, known today as curare, led to some of the earliest scientific studies in pharmacology. Its active ingredient, tubocurarine, as well as many synthetic derivatives, played a significant role in scientific experiments to determine the function of acetylcholine in neuromuscular transmission. By 1943, neuromuscular blocking drugs became established as muscle relaxants in the practice of anesthesia and surgery. The U.S. Food and Drug Administration (FDA) approved the use of carisoprodol in 1959, metaxalone in August, 1962, and cyclobenzaprine in August, 1977. Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the central nervous system, myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function by blocking transmission at the end plate of the neuromuscular junction. Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions, which causes the exocytosis of synaptic vesicles containing acetylcholine. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na+ and Ca2+ ions to enter the cell and K+ ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction. Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase. Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents, such as tubocurarine, block the agonist, acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction. Both of these classes of neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in pancuronium (a nondepolarizing agent). The generation of the neuronal signals in motor neurons that cause muscle contractions are dependent on the balance of synaptic excitation and inhibition the motor neuron receives. Spasmolytic agents generally work by either enhancing the level of inhibition, or reducing the level of excitation. Inhibition is enhanced by mimicking or enhancing the actions of endogenous inhibitory substances, such as GABA. Because they may act at the level of the cortex, brain stem or spinal cord, or all three areas, they have traditionally been referred to as "centrally acting" muscle relaxants. However, it is now known not every agent in this class has CNS activity (e.g. dantrolene), so this name is inaccurate. Most sources still use the term "centrally acting muscle relaxant". According to MeSH, dantrolene is usually classified as a centrally acting muscle relaxant. The World Health Organization, in its ATC, uses the term "centrally acting agents", but adds a distinct category of "directly acting agents", for dantrolene. Use of this terminology dates back to at least 1973. The term "spasmolytic" is also considered a synonym for antispasmodic. Spasmolytics such as carisoprodol, cyclobenzaprine, metaxalone, and methocarbamol are commonly prescribed for low back pain or neck pain, fibromyalgia, tension headaches and myofascial pain syndrome. However, they are not recommended as first-line agents; in acute low back pain, they are not more effective than paracetamol or nonsteroidal anti-inflammatory drugs (NSAIDs), and in fibromyalgia they are not more effective than antidepressants. Nevertheless, some (low-quality) evidence suggests muscle relaxants can add benefit to treatment with NSAIDs. In general, no high-quality evidence supports their use. No drug has been shown to be better than another, and all of them have adverse effects, particularly dizziness and drowsiness. Concerns about possible abuse and interaction with other drugs, especially if increased sedation is a risk, further limit their use. A muscle relaxant is chosen based on its adverse-effect profile, tolerability, and cost. Muscle relaxants (according to one study) were not advised for orthopedic conditions, but rather for neurological conditions such as spasticity in cerebral palsy and multiple sclerosis. Dantrolene, although thought of primarily as a peripherally acting agent, is associated with CNS effects, whereas baclofen activity is strictly associated with the CNS. Muscle relaxants are thought to be useful in painful disorders based on the theory that pain induces spasm and spasm causes pain. However, considerable evidence contradicts this theory. In general, muscle relaxants are not approved by FDA for long-term use. However, rheumatologists often prescribe cyclobenzaprine nightly on a daily basis to increase stage 4 sleep. By increasing this sleep stage, patients feel more refreshed in the morning. Improving sleep is also beneficial for patients who have fibromyalgia. Muscle relaxants such as tizanidine are prescribed in the treatment of tension headaches. Diazepam and carisoprodol are not recommended for older adults, pregnant women, or people who suffer depression or for those with a history of drug or alcohol addiction. Because of the enhancement of inhibition in the CNS, most spasmolytic agents have the side effects of sedation, drowsiness and may cause dependence with long-term use. Several of these agents also have abuse potential, and their prescription is strictly controlled. The benzodiazepines, such as diazepam, interact with the receptorAGABA in the central nervous system. While it can be used in patients with muscle spasm of almost any origin, it produces sedation in most individuals at the doses required to reduce muscle tone. Baclofen is considered to be at least as effective as diazepam in reducing spasticity, and causes much less sedation. It acts as a GABA agonist at GABAB receptors in the brain and spinal cord, resulting in hyperpolarization of neurons expressing this receptor, most likely due to increased potassium ion conductance. Baclofen also inhibits neural function presynaptically, by reducing calcium ion influx, and thereby reducing the release of excitatory neurotransmitters in both the brain and spinal cord. It may also reduce pain in patients by inhibiting the release of substance P in the spinal cord, as well. Clonidine and other imidazoline compounds have also been shown to reduce muscle spasms by their central nervous system activity. Tizanidine is perhaps the most thoroughly studied clonidine analog, and is an agonist at -adrenergic receptors2α, but reduces spasticity at doses that result in significantly less hypotension than clonidine. Neurophysiologic studies show that it depresses excitatory feedback from muscles that would normally increase muscle tone, therefore minimizing spasticity. Furthermore, several clinical trials indicate that tizanidine has a similar efficacy to other spasmolytic agents, such as diazepam and baclofen, with a different spectrum of adverse effects. The hydantoin derivative dantrolene is a spasmolytic agent with a unique mechanism of action outside of the CNS. It reduces skeletal muscle strength by inhibiting the excitation-contraction coupling in the muscle fiber. In normal muscle contraction, calcium is released from the sarcoplasmic reticulum through the ryanodine receptor channel, which causes the tension-generating interaction of actin and myosin. Dantrolene interferes with the release of calcium by binding to the ryanodine receptor and blocking the endogenous ligand ryanodine by competitive inhibition. Muscle that contracts more rapidly is more sensitive to dantrolene than muscle that contracts slowly, although cardiac muscle and smooth muscle are depressed only slightly, most likely because the release of calcium by their sarcoplasmic reticulum involves a slightly different process. Major adverse effects of dantrolene include general muscle weakness, sedation, and occasionally hepatitis. Other common spasmolytic agents include: methocarbamol, carisoprodol, chlorzoxazone, cyclobenzaprine, gabapentin, metaxalone, and orphenadrine. Muscle relaxants are very powerful drugs which may produce negative effects, including heart failure and paralysis. Patients most commonly report sedation as the main adverse effect of muscle relaxants. Usually, people become less alert when they are under the effects of muscle relaxant drugs. People are normally advised to not drive vehicles or operate heavy machinery while under muscle relaxants' effects. Cyclobenzaprine produces confusion and lethargy, as well as anticholinergic side effects. When taken in excess or in combination with other substances, it may also be toxic. While the body adjusts to this medication, it is possible for patients to experience dry mouth, fatigue, lightheadedness, constipation or blurred vision. Some serious but unlikely side effects may be experienced, including mental or mood changes, possible confusion and hallucinations, and difficulty urinating. In a very few cases, very serious but rare side effects may be experienced: irregular heartbeat, yellowing of eyes or skin, fainting, abdominal pain including stomachache, nausea or vomiting, lack of appetite, seizures, dark urine, or loss of coordination. Patients taking carisoprodol for a prolonged time have reported dependence, withdrawal and abuse, although most of these cases were reported by patients who had had a history of addiction. These effects were also reported by patients who took it in combination with other drugs with abuse potential, and in fewer cases, there were reports of carisoprodol-associated abuse when used without other drugs with abuse potential. Common side effects eventually caused by metaxalone include dizziness, headache, drowsiness, nausea, irritability, nervousness, upset stomach and vomiting. Severe side effects may be experienced when consuming metaxalone, such as severe allergic reactions (rash, hives, itching, difficulty breathing, tightness in the chest, swelling of the mouth, face, lips, or tongue), chills, fever, and sore throat, may require medical attention. Other severe side effects include unusual or severe tiredness or weakness, as well as yellowing of the skin or the eyes. When baclofen is administered intrathecally, it may cause CNS depression accompanied with cardiovascular collapse and respiratory failure. Tizanidine may lower blood pressure. This effect can be controlled by administering a low dose at the beginning and increasing it gradually. M: MUS, DF+DRCT anat (h/n, u, t/d, a/p, l)/phys/devp/hist noco (m, s, c)/cong (d)/tumr, sysi/epon, injr proc, drug (M1A/3)

New York State Route 292
NYS Route 292 marker New York State Route 292 (NY 292) is a short state highway in the Hudson Valley of New York in the United States, bridging Putnam and Dutchess counties. The southern terminus of the route is at an intersection with NY 311 in the town of Patterson, and the northern terminus is at a junction with NY 55 in the town of Pawling. NY 292 traverses mostly rural areas as it heads northwestward through Patterson and Pawling. Along the way, NY 292 passes along the southern and western edges of Whaley Lake. The portion of NY 292 between West Patterson and Whaley Lake originated as a dirt road named the Patterson–Dutchess County Line Road. This road was reconstructed in 1919 and became part of NY 39, a highway extending from Poughkeepsie to Patterson by way of West Pawling, in the 1920s. In the 1930 renumbering of state highways in New York, the segment of NY 39 from East Fishkill to West Patterson was incorporated into the new NY 52. By the end of the 1930s, the portion of NY 52 from Stormville to West Patterson was renumbered to NY 216. In 1970, NY 216 was truncated to its current length and NY 216's former alignment from West Pawling to Patterson was renumbered to NY 292. Route 292 begins at NY 311 near the hamlet of Patterson. It heads west initially, paralleling the Putnam–Dutchess county line as it passes south of the Patterson Veteran Memorial Park and intersects County Route 63 (CR 63). It crosses a minor stream and briefly turns towards the southwest. After passing through the hamlet of West Patterson, NY 292 turns northwest, crosses the stream once again, and enters Dutchess County. Just north of the county line in the Pawling hamlet of Holmes, the route intersects with CR 30. Near Holmes, the highway heads due north and passes between two small ponds. The route continues onward, traveling north through a rural, wooded area of Pawling with little development before curving west to pass along the southern edge of Whaley Lake. At the southwestern tip of the lake, NY 292 turns north, paralleling the western and northern shores of the lake as it heads toward the hamlet of West Pawling. North of the lake in West Pawling, Route 292 turns east onto a former routing of NY 55 for a short distance before ending at modern NY 55 in the northwest corner of Pawling. Part of the highway was once part of the Patterson–Dutchess County Line Road, a 1.61-mile (2.59 km) dirt road that extended from Banks Corner to Whaley Lake. Plans were finalized in 1919 to rebuild the previously inadequate road; the project cost an estimated $43,500 ($517,298 2007 USD), including $15,225 ($181,054 2007 USD) of Putnam County's portion of the construction. In May 1919, the Danbury News reported, "On the road between Sodom and Pawling turn left and run through Patterson and continue to West Patterson. From West Patterson a new road about one and one-half miles in length is under construction which connects with a good macadam road passing Whaley Pond and running to Stonehouse, thence continuing ... to Newburgh." The new road was completed in November of that year. Route 292 was originally part of NY 39 in the 1920s, which ran from Patterson to Poughkeepsie via West Patterson and East Fishkill. In the 1930 renumbering, the portion of NY 39 between East Fishkill and the western fringe of Patterson was redesignated as part of the new NY 52. Between Patterson and NY 22, old NY 39 was renumbered to NY 311. NY 52 was realigned c. to follow its current alignment between Stormville and Lake Carmel. The former routing of NY 52 between Stormville and Patterson became part of NY 216. The route remained unchanged until January 1, 1970, when NY 216 was truncated to its current eastern terminus in Poughquag. As part of the truncation, its former alignment from West Pawling to Patterson was renumbered to NY 292.

Georgia State Route 292
State Route 292 marker Georgia State Routes
Former State Route 292 (SR 292) is a west-east state highway located in the east-central part of the U.S. state of Georgia. It runs from Higgston to just east of Bellville. SR 292 begins in Montgomery County at an intersection with SR 15/SR 29 in Higgston, where the roadway continues as Saw Mill Road. The route heads east and enters Toombs County, just before entering Vidalia along North Street. In downtown Vidalia, SR 292 intersects SR 130/SR 297 (McIntosh Street), where SR 130 and SR 292 share a four-block concurrency. The highway heads to the southeast, into Lyons, It parallels US 280/SR 30 along the way. In Lyons, SR 292 has intersections with US 1/SR 4 and SR 152. East of Lyons is an intersection with SR 86. Just past SR 86, the route crosses the Ohoopee River, where it enters Tattnall County. Farther to the southeast, in the city of Collins, is an intersection with SR 23/SR 57/SR 121. The route continues east through Manassas and enters the city of Bellville. There, it intersects SR 169. Just east of Bellville, SR 292 meets its eastern terminus, an intersection with US 280/SR 30. Media related to Georgia State Route 292 at Wikimedia Commons

Carisoprodol
InChI=1S/C12H24N2O4/c1-5-6-12(4,7-17-10(13)15)8-18-11(16)14-9(2)3/h9H,5-8H2,1-4H3,(H2,13,15)(H,14,16)Yes 
Key:OFZCIYFFPZCNJE-UHFFFAOYSA-NYes  Carisoprodol is a centrally acting skeletal muscle relaxant. It is slightly soluble in water and freely soluble in alcohol, chloroform and acetone. The drug's solubility is practically independent of pH. Carisoprodol is manufactured and marketed in the United States by Meda Pharmaceuticals under the brand name Soma, and in the United Kingdom and other countries under the brand names Sanoma and Carisoma. The drug is available by itself or mixed with aspirin, and in one preparation with codeine and caffeine, as well. On June 1, 1959 several American pharmacologists convened at Wayne State University in Detroit, Michigan to discuss a new drug. The drug, originally thought to have antiseptic properties, was found to have central muscle-relaxing properties. It had been developed by Frank M. Berger at Wallace Laboratories and was named carisoprodol. Carisoprodol was a modification of meprobamate, intended to have better muscle relaxing properties, less potential for abuse, and less risk of overdose. The substitution of one hydrogen atom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a molecule with new pharmacological properties. Reports from Norway have shown carisoprodol has abuse potential as a prodrug of meprobamate and/or potentiator of hydrocodone, dihydrocodeine, codeine and similar drugs. It continues to be prescribed in North America, alongside orphenadrine and cyclobenzaprine (Flexeril). In Europe, doctors favor the safer cyclobenzaprine. In the United Kingdom, benzodiazepines are preferred, instead. All of the above, plus chlorzoxazone and tizanidine, are used in Canada. As of November 2007, carisoprodol (Somadril, Somadril comp.) has been taken off the market in Sweden due to problems with dependence and side effects. The agency overseeing pharmaceuticals considered other drugs used with the same indications as carisoprodol to have the same or better effects without the risks of the drug. In May 2008 it was taken off the market in Norway as well. In the EU, the European Medicines Agency issued a release recommending member states suspend marketing authorization for this product in the treatment of acute (not chronic) back pain. On December 12, 2011, the Administrator of the Drug Enforcement Administration (DEA) issued the final ruling placing the substance carisoprodol into Schedule IV of the Controlled Substances Act (CSA). This is effective January 11, 2012. Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and anxiolytic effects. Also, because of its potentiating effects on narcotics, it is often abused in conjunction with many opioid drugs. Also it is not detected on standard drug testing screens. On March 26, 2010 the DEA issued a Notice of Hearing on proposed rule making in respect to the placement of carisoprodol in schedule IV of the Controlled Substances Act. Carisoprodol is sometimes mixed with date rape drugs. The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence, and mild to significant euphoria or dysphoria, but the euphoria is generally short lived. The medication is well tolerated and without adverse effects in the majority of patients for whom it is indicated. In some patients, however, and/or early in therapy, carisoprodol can have the full spectrum of sedative side effects and can impair the patient's ability to operate a firearm, motorcycle, and other machinery of various types, especially when taken with medications containing alcohol, in which case an alternative medication would be considered. The intensity of the side effects of carisoprodol tends to lessen as therapy continues, as is the case with many other drugs. The interaction of carisoprodol with essentially all opioids, and other centrally acting analgesics, but especially those of the codeine-derived subgroup of the semisynthetic class (codeine, ethylmorphine, dihydrocodeine, hydrocodone, oxycodone, nicocodeine, benzylmorphine, the various acetylated codeine derivatives including acetyldihydrocodeine, dihydroisocodeine, nicodicodeine and others) which allows the use of a smaller dose of the opioid to have a given effect, is useful in general and especially where injury and/or muscle spasm is a large part of the problem. The potentiation effect is also useful in other pain situations and is also especially useful with opioids of the open-chain class, such as methadone, levomethadone, ketobemidone, phenadoxone and others. In recreational drug users, deaths have resulted from carelessly combining overdoses of hydrocodone and carisoprodol. Another danger of misuse of carisoprodol and opiates is the potential to aspirate while unconscious, which usually requires quick intervention and long hospital stays, if death can even be avoided. Meprobamate and other muscle-relaxing drugs often were subjects of misuse in the 1950s and 1960s. Overdose cases were reported as early as 1957, and have been reported on several occasions since then. Carisoprodol, meprobamate, and related drugs such as tybamate, have the potential to produce physical dependence with prolonged use. Withdrawal of the drug after extensive use may require hospitalization in medically compromised patients. Because of potential for more severe side effects, this drug is on the list to avoid in the elderly. Carisoprodol has a rapid, 30-minute onset of action, with the aforementioned effects lasting about two to six hours. It is metabolized in the liver via the cytochrome P450 oxidase isozyme CYP2C19, excreted by the kidneys and has about an eight-hour half-life. A considerable proportion of carisoprodol is metabolized to meprobamate, which is a known drug of abuse and dependence; this could account for the abuse potential of carisoprodol. Carisoprodol is a carbamic acid ester. It is a racemic mixture of two stereoisomers. Carisoprodol is synthesized by reacting 2-methyl-2-propylpropane-1,3-diol with 1 molar equivalent of phosgene, forming the chloroformate, from which carbamate is formed by reacting it with isopropylamine. Reacting this with either urethane or sodium cyanate gives carisoprodol. Carisoprodol synthesis.png Note: See the receptor PAMsAGABA navbox for a full list of GABAA positive allosteric modulators. M: MUS, DF+DRCT anat (h/n, u, t/d, a/p, l)/phys/devp/hist noco (m, s, c)/cong (d)/tumr, sysi/epon, injr proc, drug (M1A/3)

Methocarbamol
InChI=1S/C11H15NO5/c1-15-9-4-2-3-5-10(9)16-6-8(13)7-17-11(12)14/h2-5,8,13H,6-7H2,1H3,(H2,12,14)Yes 
Key:GNXFOGHNGIVQEH-UHFFFAOYSA-NYes  Methocarbamol (trade name Robaxin, which is marketed by Actient Pharmaceuticals in the United States and Pfizer in Canada) is a central muscle relaxant used to treat skeletal muscle spasms. Methocarbamol is the carbamate of guaifenesin, but does not produce guaifenesin as a metabolite, since the carbamate bond is not hydrolyzed metabolically; metabolism is by Phase I ring hydroxylation and O-demethylation, followed by Phase II conjugation. All the major metabolites are unhydrolyzed carbamates. Methocarbamol is marketed under different names when presented in combination with other active ingredients. In combination with acetaminophen (Paracetamol), under trade names Robaxacet and Tylenol Body Pain Night, whereas Robax Platinum is the trade name for a formulation of methocarbamol and ibuprofen. A combination of methocarbamol and aspirin is marketed as Robaxisal, however in Spain Robaxisal is used for the Paracetamol combination instead of Robaxacet. Unlike other carbamates such as meprobamate and its prodrug carisoprodol, methocarbamol has greatly reduced abuse potential. Studies comparing it to lorazepam (Ativan) and diphenhydramine (Benadryl), along with placebo, find that methocarbamol produces increased "liking" responses and some sedative-like effects, however, at higher doses dysphoria is reported. It is considered to have an abuse profile similar to, but weaker than, lorazepam. Potential side-effects include: drowsiness, dizziness, upset stomach, flushing, blurred vision, and fever. Serious side-effects include the development of a severe skin rash or itching, slow heart rate, fainting, jaundice, persistent nausea/vomiting, stomach/abdominal pain, mental/mood changes, clumsiness, trouble urinating, signs of infection. If taken in large amounts at once or more than directed or as prescribed, dysphoria or suicidal thoughts may occur. In addition, methocarbamol may cause urine to turn black, blue, or green. However, this effect is harmless. Because of potential for side-effects, this drug is considered to be a high-risk medication for the elderly. Methocarbamol can be synthesized from guaifenesin by successive reaction with phosgene and then ammonia. M: MUS, DF+DRCT anat (h/n, u, t/d, a/p, l)/phys/devp/hist noco (m, s, c)/cong (d)/tumr, sysi/epon, injr proc, drug (M1A/3)

C11H15NO3
The molecular formula C11H15NO3 (molar mass: 241.24 g/mol, exact mass : 241.095023) may refer to:
Methocarbamol Carbamates
Organic chemistry

Organic chemistry is a chemistry subdiscipline involving the scientific study of the structure, properties, and reactions of organic compounds and organic materials, i.e., matter in its various forms that contain carbon atoms. Study of structure includes using spectroscopy and other physical and chemical methods to determine the chemical composition and constitution of organic compounds and materials. Study of properties includes both physical properties and chemical properties, and uses similar methods as well as methods to evaluate chemical reactivity, with the aim to understand the behavior of the organic matter in its pure form (when possible), but also in solutions, mixtures, and fabricated forms. The study of organic reactions includes both their preparation—by synthesis or by other means—as well as their subsequent reactivities, both in the laboratory and via theoretical (in silico) study.

The range of chemicals studied in organic chemistry include hydrocarbons, compounds containing only carbon and hydrogen, as well as compositions based on carbon but containing other elements. Organic chemistry overlaps with many areas including medicinal chemistry, biochemistry, organometallic chemistry, and polymer chemistry, as well as many aspects of materials science.

Methocarbamol
Muscle relaxants

A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause temporary paralysis. Spasmolytics, also known as "centrally acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only.

The earliest known use of muscle relaxant drugs dates back to the 16th century, when European explorers encountered natives of the Amazon Basin in South America using poison-tipped arrows that produced death by skeletal muscle paralysis. This poison, known today as curare, led to some of the earliest scientific studies in pharmacology. Its active ingredient, tubocurarine, as well as many synthetic derivatives, played a significant role in scientific experiments to determine the function of acetylcholine in neuromuscular transmission. By 1943, neuromuscular blocking drugs became established as muscle relaxants in the practice of anesthesia and surgery.

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