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MORPHINE

Product Name
MORPHINE
CAS No.
57-27-2
Chemical Name
MORPHINE
Synonyms
rms;MORPHINA;morph;Morphin;7,8-didehydro-4,5-alpha-epoxy-17-methyl-morphinan-6-alpha-diol;morpho;MORPHINE BASE;PSEUDOMORPHINE;Morphine (CRM);Dehydromorphine
CBNumber
CB0680482
Molecular Formula
C17H19NO3
Formula Weight
285.34
MOL File
57-27-2.mol
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MORPHINE Property

Melting point:
255°C
Boiling point:
427.77°C (rough estimate)
Density 
1.0864 (rough estimate)
refractive index 
1.5400 (estimate)
Flash point:
11 °C
storage temp. 
−20°C
solubility 
Ethanol (Slightly), Methanol (Slightly)
form 
Solid
pka
8.21(at 25℃)
color 
White to Pale Yellow
Water Solubility 
0.4mg/L(25 ºC)
BCS Class
1,3
CAS DataBase Reference
57-27-2
EPA Substance Registry System
Morphinan-3,6-diol, 7,8-didehydro-4,5-epoxy-17-methyl- (5.alpha.,6.alpha.)- (57-27-2)
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Safety

Hazard Codes 
F,T
Risk Statements 
11-23/24/25-39/23/24/25
Safety Statements 
7-16-36/37-45
RIDADR 
UN 1230 3/PG 2
WGK Germany 
2
Hazardous Substances Data
57-27-2(Hazardous Substances Data)
Toxicity
An alkaloid of the opium poppy that makes up between 9% and 14% of good grades of opium. Morphine is usually used clinically as an analgesic in the form of the sulfate or hydrochloride salt. The most important acute toxic effect of large doses of morphine is depression of the respiratory centers in the medulla and pons. Morphine and related drugs also cause somnolence, coma, cold clammy skin, bradycardia, and hypotension. Initial doses of morphine seem to stimulate the chemoreceptor trigger zone to induce emesis, with subsequent doses blocking the vomiting center, hence blocking emesis. Morphine also has profound effects on the gastrointestinal tract, increasing the tone of the intestinal tract, but decreasing the propulsive or spasmodic reflexes, thus resulting in constipation. Morphine stimulates the nucleus of the third cranial nerve to produce miosis, making pinpoint pupil a diagnostic sign both in morphine overdose and morphine addiction. Morphine causes a variety of effects on the CNS and is highly addictive. Many behavioral changes are seen, ranging from euphoria to sedation. These behavioral effects contribute to the problem of abuse with all of the opiates. Tolerance and dependence occur with repeated dosing, with increasingly larger doses being needed to obtain the original effect. Abrupt withdrawal after chronic use can lead to physiological rebound in these same systems. Therapy for acute overdosage involves physiological support (establishment of adequate respiratory exchange), gastric lavage, and use of narcotic antagonists. Morphine and related compounds act by binding to specific high-affinity receptors concentrated in the nervous system, but also located elsewhere in the body. In the nervous system, the endogenous ligands for these morphine receptors are the opioid peptides that include the enkephalins, endorphins, and dynorphins. The multiple and complex actions of morphine are due, in part, to the fact that it acts as an agonist at many of these classes of receptors. Paregoric (camphorated tincture of opium) is used as an antidiarrheal. Paregoric is a schedule III drug under the US Controlled Substances Act and may produce physical dependence.
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Hazard and Precautionary Statements (GHS)

Symbol(GHS)
Signal word
Danger
Hazard statements

H225Highly Flammable liquid and vapour

H370Causes damage to organs

Precautionary statements

P210Keep away from heat/sparks/open flames/hot surfaces. — No smoking.

P280Wear protective gloves/protective clothing/eye protection/face protection.

P370+P378In case of fire: Use … for extinction.

P403+P235Store in a well-ventilated place. Keep cool.

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N-Bromosuccinimide Price

Sigma-Aldrich
Product number
M-005
Product name
Morphine solution
Purity
1.0?mg/mL in methanol, ampule of 1?mL, certified reference material, Cerilliant?
Packaging
1mL
Price
$27.7
Updated
2024/03/01
Sigma-Aldrich
Product number
M-030
Product name
Morphine solution
Purity
100?μg/mL in methanol, ampule of 1?mL, certified reference material, Cerilliant?
Packaging
1mL
Price
$21.7
Updated
2022/05/15
Cayman Chemical
Product number
ISO60147
Product name
Morphine (CRM)
Packaging
1mg
Price
$22
Updated
2023/06/20
Cayman Chemical
Product number
15464
Product name
Morphine
Packaging
25mg
Price
$58
Updated
2023/06/20
Cayman Chemical
Product number
15464
Product name
Morphine
Packaging
10mg
Price
$33
Updated
2023/06/20
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MORPHINE Chemical Properties,Usage,Production

Description

Morphine is the principal alkaloid obtained from opium. Opium is the resinous latex that exudes from the seed pod of the opium poppy, Papver somneferum, when it is lacerated. Alkaloids account for approximately 25% of opium, and of this 25% about 60% is morphine.

Chemical Properties

White, crystalline alkaloid. Slightly soluble in water,alcohol, and ether.

Physical properties

Appearance: white or almost white crystalline powder or colorless, silky needles or cubical masses, efflorescent in a dry atmosphere. Solubility: soluble in water, slightly soluble in ethanol, practically insoluble in chloroform or ether. Specific optical rotation: ?110.0° to 115.0°

Originator

Avinza,Aetna Inc.

History

Morphine has a strong analgesic effect, especially for moderate and severe cancer pain. However, morphine has serious side effects, such as addiction, respiratory depression, acute poisoning, and death. Therefore, in regulating the clinical application of morphine at the same time, it is necessary to explore the alternative to morphine with strong analgesic role and minor side effects.
In the 1970s, tramadol was launched and marketed as “Tramal” by the German pharmaceutical company Grünenthal GmbH in West Germany , and 20 years later, it was launched in countries such as the United Kingdom, the United States, and Australia. It is marketed in many brand names worldwide. After R&D of more than 100 years, opioid drugs were increased and have been widely used in clinic as analgesic drugs.

Uses

Once morphine had been determined to be the principal pain-killing ingredient in opium, it was substituted for opium in many treatments. Morphine's analgesic ability is due to its ability to bind and activate opioid receptors in the central nervous system (brain and spinal cord).hen morphine or another opioid analgesic binds to the opioid receptors, it reduces the neurological transfer of pain signals to the brain. Morphine mimics natural pain relievers produced by the body called endorphins. When these natural pain-relieving compounds were discovered in the 1970s, the word endorphin was coined from the words endogenous and morphine.

Uses

Morphine is the most important opium alkaloid,found in the poppy plant (Papaver somniferumL.). It is obtained by extracting thedried latex of poppy. It is also obtained fromopium, which is an air-dried milky exudate ofthe same plant produced by incising unripecapsules. Opium contains about 9–14% ofmorphine. It is used in medicine for its narcoticanalgesic, anesthetic, and pain-reliefactions.

Uses

A degradation product of Morphine. A dimolecular base formed by the gentle oxidation of Morphine in alkaline solution. Name Pseudomorphine is also used for the C17 alkaloid base

Definition

ChEBI: A morphinane alkaloid that is a highly potent opiate analgesic psychoactive drug. Morphine acts directly on the central nervous system (CNS) to relieve pain but has a high potential for addiction, with tolerance and both physical and psychological dependen e developing rapidly. Morphine is the most abundant opiate found in Papaver somniferum (the opium poppy).

Definition

morphine: An opiate that is themain active constituent of opium. Itis used medically in the relief of severepain, and can be acetylated toproduce heroin. Morphine can be detected by the Marquis test.

Production Methods

Morphine is detoxified or biotransformed mainly in the liver by conjugation with glucuronic acid. Morphine is conjugated by a series of reactions involving the formation of uridine diphosphoglucose (UDP-glucose), the oxidation of carbon-6 of glucose to form uridine diphosphoglucuronic acid (UDP-glucuronic acid) and the transfer of glucuronic acid to morphine to form the morphine glucuronide. The following enzymes catalyze the sequential reactions; reaction(1), UDP-glucose pyrophosphorylase; reaction (2), UDP-glucose dehydrogenase; reaction (3), glucuronyl transferase; reaction (4) nucleoside diphosphokinase.

Indications

Morphine is mainly used to treat both acute and chronic severe pain. It is also used for pain caused by myocardial infarction and for labor pains. Morphine relieves pulmonary edema symptoms; anesthesia and preoperative administration can make the patient quiet and drowsy; compound formula of morphine was used for acute and chronic diarrhea.

Manufacturing Process

Morphin was extracted from the plant vegetable (the poppy) by the mixture of water and methanol or the aqueous solution of potassium pyrosulfate. The precipitation of the morphin was carried out by addition to the extract the aqueous solution of sodium carbonate.
Morphin can be obtained from the extract by using the cation exchanger.
Free base of morphin was transformated to the sulfate salt.

brand name

Astramorph (AstraZeneca); Avinza (Ligand); Depodur (Skyepharma); Duramorph (Baxter Healthcare); Infumorph (Baxter Healthcare); Kadian (Alpharma); Ms Contin (Purdue Frederick); Oramorph (Xanodyne).

Therapeutic Function

Narcotic analgesic, Sedative

Acquired resistance

It is important to remember that a minor change in the structure of morphine (or any other opioid) will likely cause a different change in the affinity and intrinsic activity of the new compound at each of the opioid receptor types. Thus, the opioid receptor selectivity profile of the new compound may be different than the structure from which it was made or modeled (i.e., a selective μ agonist may shift to become a selective κ agonist, etc.). In addition, the new compound will have different physicochemical properties than its parent. The different physicochemical properties (e.g., solubility, partition coefficient, and pKa) will result in different pharmacokinetic characteristics for the new drug and can affect its in vivo activity profile. For example, a new drug (Drug A) that is more lipophilic than its parent may distribute better to the brain and appear to be more active, whereas in actuality, it may have lower affinity or intrinsic activity for the receptor. The greater concentration of Drug A reaching the brain is able to overcome its decreased agonist effect at the receptor.

Hazard

Narcotic, habit-forming drug, salerestricted by law in the U.S.

Health Hazard

Morphine is a habit-forming substance leadingto strong addiction. It exhibits acutetoxicity of several types and complexity.Morphine simultaneously produces depressingand stimulating actions on the centralnervous system. Depression of the centralnervous system results in drowsinessand sleep. Large doses may produce comaand lowering of heart rate and blood pressure.Initial doses of morphine may producestimulant action, inducing emesis, whichcan cause nausea and vomiting. Subsequentdoses may block emesis. The varietyof effects on the central nervous systemare manifested by behavioral changes rangingfrom euphoria and hallucinations tosedation. Repeated dosing enhances toleranceand dependence, with increasinglylarger doses needed to produce the effectof euphoria. Thus any abrupt terminationto morphine intake after chronic use maylead to physiological rebound (Hodgsonet al. 1988). Haffmans and associates (1987)reported the combating action of phelorphanagainst morphine addiction in chronicmorphine-dependent rats. Administration ofphelorphan (158 mmol/2 mL), an inhibitorof enzymes involved in the biodegradation ofenkephalins, affected the withdrawal symptomsin the addicted animals.
Severe morphine poisoning may result inrespiratory failure after fainting fits, accompaniedby coma and acute miosis. It exertseffects on the gastrointestinal tract, decreasingthe spasmotic reflexes in the intestinaltract, thus resulting in constipation.
LD50 value, oral (mice): 524 mg/kgLD50 value, subcutaneous (mice): 220 mg/kg
A fatal dose in humans may be about0.5–1 g.
Girardot and Holloway (1985) have investigatedthe effect of cold-water immersionon analgesic responsiveness to morphine inmature rats of different ages. This study indicatesthat chronic stress affects the reactivityto morphine in young mature rats but not inold rats.
Studies show that when coadministeredwith morphine, certain substances potentiatedmorphine’s toxicity or mortality in rats.These substances include gentamicin [1403-66-3] (Hurwitz et al. 1988), and doxorubicin(Adriamycin) (Innis et al.1987).
Stroescu and coworkers (1986) havereported the influence of the body’s electrolytecomposition on the toxic effect of morphine.In mice, depletion of body sodiumion increased the toxicity, which was foundto decrease by sodium loading. Glutathionedepletors such as cocaine, when coadministeredwith an opiate such as morphine orheroin, may enhance hepatotoxicity in humans(McCartney 1989). Such a potentiation effecthas been explained by the authors as being aresult of depletion of endogenous glutathione,which conjugates with morphine to preventtoxic interaction with hepatic cells.
Ascorbic acid and sodium ascorbate havebeen reported to prevent toxicity of morphinein mice (Dunlap and Leslie 1985). Sodiumascorbate (1 g/kg) injected intraperitoneally10 minutes before morphine (500 mg/kg)protected the animals against mortality dueto respiratory depression. These investigatorspostulated that ascorbate antagonized thetoxicity of morphine by selectively affectingthe neuronal activity.

Contact allergens

Morphine bitartrate caused contact dermatitis in a worker at a plant producing opium alkaloids. Morphine hydrochloride and morphine bitartrate showed patchtest- positive reactions in another patient with contact dermatitis working in the production of concentrated poppy straw. We observed a concomitant reaction between a morphine base and a codeine base in a patient with drug skin eruption due to codeine.

Pharmacokinetics

Morphine is the prototype opioid. It is selective for μ opioid receptors. The structure of morphine is composed of five fused rings, and the molecule has five chiral centers with absolute stereochemistry 5(R), 6(S), 9(R), 13(S) and 14(R). The naturally occurring isomer of morphine is levo-[(–)] rotatory. (+)-Morphine has been synthesized, and it is devoid of analgesic and other opioid activities.

Pharmacology

Morphine is subject to extensive first-pass metabolism; only 40–50% of the dose reaches the central nervous system when taken orally. Morphine is metabolized primarily in the liver, and approximately 87% of a dose is excreted in the urine after 72?h of administration. Morphine is metabolized primarily into morphine-3-glucuronide and morphine-6-glucuronide via glucuronidation by phase II metabolism enzyme UDP-glucuronosyl transferase-2B7. The half-life is about 2.5–3.5?h .
Morphine, as an agonist of opioid receptor, has many pharmacological effects: 1. Analgesic: morphine can activate the opioid receptor and produce strong analgesic effect by simulating the role of endogenous enkephalin. It is better for persistent dull pain than intermittent sharp pain and visceral cramps. 2. Sedation: in the analgesic at the same time, there is a clear sedative effect, sometimes produce euphoria, which can improve the tension of the patient. 3. Respiratory depression: morphine can inhibit the respiratory center and reduce the sensitivity of the respiratory center to carbon dioxide. The inhibition degree of breathing is parallel to the dose of morphine, and excessive doses can cause respiratory failure or death. 4. Antitussive: morphine can inhibit the cough center, resulting in antitussive effect. 5. Excited smooth muscle: morphine can excite the digestive tract smooth muscle, leading to constipation, and increase tension of bile duct, ureter, and bronchial smooth muscle. 6. The cardiovascular system: morphine can promote the release of endogenous histamine and lead to peripheral vascular dilatation, blood pressure decrease, cerebrovascular expansion, and intracranial pressure increase. 7. Antiemetic and miotic effect: morphine can play antiemetic effect through the central nervous system, and the most important feature with morphine application is the pinhole-like pupil.

Pharmacology

Morphine is a relatively hydrophilic phenanthrene derivative. It may be given orally (immediate or modified release), rectally, topically, parenterally and via the neuraxial route. The standard parenteral dose for adults is 10mg, although many factors affect this and the dose should be titrated to effect. I ts oral bioavailability is dependent on first-pass hepatic metabolism and may be unpredictable (35%–75%). S ingle-dose studies of morphine bioavailability indicate that the relative potency of oral to intramuscular morphine is 1:6, although with repeated regular administration, this ratio becomes approximately 1:3. The dose of short-acting morphine for breakthrough pain should be approximately one-sixth of the total daily dose. Morphine has a plasma half-life of approximately 3 h and duration of analgesia of 4–6 h. Morphine is metabolised, at least in part, by microsomal UDP glucuronyl transferases (UDPGT) in the liver, kidney and intestines. Several of these metabolites may have clinically significant effects. Although morphine conjugation occurs in the liver, extrahepatic sites may also be important, such as the kidney and GI tract. The site of conjugation on the molecule also varies, leading to a variety of metabolites. After glucuronidation, metabolites are excreted in urine or bile, dependent on molecular weight and polarity; more than 90% of morphine metabolites are excreted in the urine. The main metabolite in humans is morphine-3- glucuronide (60%–80%), and this may have an excitatory effect via CNS actions not related to opioid receptor activation. Morphine-6-glucuronide (M- 6-G) is active at the MOP receptor, producing analgesia and other MOP related effects. I t is significantly more potent than morphine. Therefore M-6- G produces significant clinical effects despite only 10% of morphine being metabolised in this way. A s it is excreted via the kidneys, it may accumulate in patients with impaired renal function, causing respiratory depression. A ccumulation of morphine metabolites, especially M-6-G, may become significant when creatinine clearance declines to 50 ml min–1 or less.

Clinical Use

Morphine remains the standard by which other analgesic drugs are compared. The predominant effects of morphine are at the μ-opioid receptor, although it interacts with other opioid receptors as well. Morphine is indicated for the treatment of moderate to severe and chronic pain. It is useful preoperatively for sedation,anxiolytic effects, and to reduce the dose of anesthetics.
Morphine is the drug of choice for the treatment of myocardial infarction because of its bradycardiac and vasodilatory effects. In addition, morphine is the most commonly used drug for the treatment of dyspneaassociated pulmonary edema. It is thought that morphine reduces the anxiety associated with shortness of breath in these patients along with the cardiac preload and afterload.
The use of morphine via the oral route has drawbacks because of its first-pass effect; however, oral morphine has been recommended for use in cancer patients for its ease of administration. In particular, the longacting preparations of morphine, such as MS-Contin and Ora-Morph, are described as the cornerstone of pain treatment in cancer patients, either alone or in combination with nonopioids.
Morphine is the most commonly used analgesic drug administered via the epidural route because it is potent, efficacious, and hydrophilic. The more hydrophilic the drug, the slower the onset and the longer the duration of action following epidural administration. Single-dose or continuous infusion of morphine is used to provide pain relief in thoracic and abdominal surgical patients and in cancer patients at high risk for developing side effects associated with systemic opioids. Since morphine does not produce anesthesia via the epidural route, the patient is able to move about normally; motor function is preserved.The drawback to epidural use of morphine is that certain types of pain are relatively unresponsive, such as that associated with visceral stimuli, as in pancreatitis, and neuropathic pain from nerve deafferentation. In addition, patients can develop respiratory depression and nausea from the rostral flow of the drug to medullary centers, although the effects are much less severe than those observed following the systemic administration of the drug, and can be alleviated by elevation of the head of the patient at a 30-degree angle. Patients may also itch because of histamine release.
Patient-controlled analgesia (PCA) is an alternative method of administration of morphine.The use of an indwelling catheter allows the patient to administer the drug at frequent intervals for pain relief. PCA systems allow patients the freedom to assess the need for their own analgesia and to titrate a dose tailored to their needs. Dependence is rarely observed in patients using PCA for acute pain management.

Side effects

The opioids generally have a high level of safety when used in therapeutic dosages. However, there are several notable exceptions. Morphine and other opioids are contraindicated in patients with hypersensitivity reactions to the opioids. In addition, morphine should not be used in patients with acute bronchial asthma and should not be given as the drug of first choice in patients with pulmonary disease, because it has antitussive effects that prevent the patient from clearing any buildup of mucus in the lungs. Opioids with less antitussive effects, such as meperidine, are better for such situations.
When used via the epidural route, the site for injection must be free of infection. In addition, the use of corticosteroids by the patient should be halted for at least 2 weeks prior to the insertion of the catheter to prevent infection, since morphine increases the immunosuppressive effects of the steroids.
Opioids are contraindicated in head trauma because of the risk of a rise in intracranial pressure from vasodilation and increased cerebrospinal fluid volume. In addition, in such patients the onset of miosis following opioid administration can mask the pupillary responses used diagnostically for determination of concussion. The clearance of morphine and its active metabolite, morphine-6-glucuronide depends on adequate renal function. The elderly are particularly susceptible to accumulation of the drugs, hence respiratory depression and sedation. Morphine, like all opioids, passes through the placenta rapidly and has been associated with prolongation of labor in pregnant women and respiratory depression in the newborn.
Morphine and other opioids exhibit intense sedative effects and increased respiratory depression when combined with other sedatives, such as alcohol or barbiturates. Increased sedation and toxicity are observed when morphine is administered in combination with the psychotropic drugs, such as chlorpromazine and monoamine oxidase inhibitors, or the anxiolytics, such as diazepam.
Respiratory depression, miosis, hypotension, and coma are signs of morphine overdose.While the IV administration of naloxone reverses the toxic effects of morphine, naloxone has a short duration of action and must be administered repeatedly at 30- to 45minute intervals until morphine is cleared from the body.

Safety Profile

Poison experimentally by ingestion, intracerebral, intraperitoneal, subcutaneous, and intravenous routes. Human reproductive effects by an unspecified route: effects on newborn, including drug dependence. Experimental reproductive effects. Mutation data reported.
Morphine is the constituent of opium most responsible for its toxic effects. When taken orally, the effects of morphine poisoning begin to appear in 20-40 minutes; if taken hypodermically, the symptoms appear much earlier and narcotism is more likely to follow the early symptoms. Abuse leads to habituation or adlction. Inlvidual susceptibility varies greatly and children are more susceptible than adults. When heated to decomposition it emits toxic fumes of NOx.

Drug interactions

Potentially hazardous interactions with other drugs
Analgesics: possible opioid withdrawal with buprenorphine and pentazocine.
Antibacterials: metabolism increased by rifampicin.
Antidepressants: possible CNS excitation or depression with MAOIs - avoid concomitant use, and for 2 weeks after stopping MAOI; possible CNS excitation or depression with moclobemide; increased sedative effects with tricyclics.
Antiepileptics: increases bioavailability of gabapentin.
Antihistamines: increased sedative effects with sedating antihistamines.
Antipsychotics: enhanced hypotensive and sedative effects.
Antivirals: concentration possibly reduced by ritonavir.
Dopaminergics: avoid with selegiline.
Nalmefene: avoid concomitant use.
Sodium oxybate: enhanced effect of sodium oxybate - avoid.

Metabolism

Extensive first-pass metabolism in the liver and gut. The majority of a dose of morphine is conjugated with glucuronic acid in the liver and gut to produce morphine 3-glucuronide and morphine-6-glucuronide (active). Other active metabolites include normorphine, codeine, and morphine ethereal sulphate. After an oral dose, about 60% is excreted in the urine in 24 hours, with about 3% excreted as free morphine in 48 hours. After a parental dose, about 90% is excreted in 24 hours, with about 10% as free morphine, 65-70% as conjugated morphine, 1% as normorphine and 3% as normorphine glucuronide. Up to 10% of a dose may be excreted in the bile.

Purification Methods

Crystallise the narcotic from MeOH or anisole. It dehydrates at 130o. Its solubility in H2O is 0.2g/L at 20o and 0.9g/L at 100o, and in EtOH it is 5g/L at 20o and 10g/L on boiling. The styphnate has m 189o (from aqueous EtOH). [Beilstein 27 II 118, 27 III/IV 2223.]

References

Derosne., Ann. Chirn., 45, 257 (1803)
Laurent., Ann. Chirn. Phys., 19, iii, 359 (1847)
Muller., Apoth. Zeit., 18, 257 (1903)
Mannich., Chern. Zentr., II, 820 (1916)
Emde., Helv. Chirn. Acta, 13, 1035 (1930)
Gates, Tschudi., 1. Arner. Chern. Soc., 78, 1380 (1956)
Crystal structure: MacKay, Hodgkin., 1. Chern. Soc., 3261 (1955)
Synthesis: Gates, TschudL,J. Arner. Chern. Soc., 74, 1109 (1952)
Elad, Ginsburg., ibid, 76,312 (1954)
Elad, Ginsburg., J. Chern. Soc., 3052 (1954)
Morrison, Waite, Shavel., Tetrahedron Lett., 4055 (1967)
NMR and mass spectra: Rull., Bull. Soc. Chim. Fr., 586 (1963)
Okuda et al., Chern. Pharrn. Bull. (Tokyo), 11, 1465 (1963)
Wheeler, Kinstle, Rinehart., J. Arner. Chern. Soc., 89,4494 (1967)
Biosynthesis: Barton et aI., J. Chern. Soc., 2423 (1965)
Pharmacology: Vahlen., Arch. expo Path. Pharrn., 47, 368 (1902)
Small et al., Public Health Reports, Suppl. 138, Washington (1938)
Krueger, Eddy, Sumwalt., ibid, No. 165, Washington (1943)

MORPHINE Preparation Products And Raw materials

Raw materials

Preparation Products

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MORPHINE Suppliers

57-27-2, MORPHINERelated Search:


  • PSEUDOMORPHINE
  • MORPHINA
  • MORPHINE
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  • EXTRACT OF OPIUM
  • CODEINE IMP B
  • (5alpha,6alpha)-Didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol
  • 7,8-didehydro-4,5-alpha-epoxy-17-methyl-morphinan-6-alpha-diol
  • Morphine (CRM)
  • Morphinan-3,6a-diol, 7,8-didehydro-4,5a-epoxy-17-methyl- (8CI)
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  • Morphine (base and/or unspecified salts)
  • (5a,6a)-(5'a,6'a-7,7',8,8'-Tetradehydro-4,5:4',5'-diepoxy-17,17'-dimethyl-[2,2'-bimorphinan]-3,3',6,6'-tetrol
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  • 7,8-didehydro-4,5-epoxy-17-methyl-morphinan-3,6-diol
  • 9H-9,9c-Iminoethanophenanthro(4,5-bcd)furan-3,5-diol, 4a,5,7a,8-tetrahydro-12-methyl-
  • 9h-9,9c-iminoethanophenanthro(4,5-bcd)furan-3,5-diol,4a,5,7a,8-tetrahydro-12
  • 9h-9,9c-iminoethanophenanthro(4,5-bcd)furan-3,5-diol,4a,5,7a,8-tetrahydro-12-m
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  • D-(-)-Morphine
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  • Morphinan-3,6alpha-diol, 7,8-didehydro-4,5alpha-epoxy-17-methyl-
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  • Morphinism
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  • (5S,9α,13α,14α)-7,8-Didehydro-4,5β-epoxy-17-methylmorphinan-3,6β-diol
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