52-28-8COc1ccc2c3c1O[C@H]1[C@@H](O)C=C[C@H]4[C@@H](C2)N(C)CC[C@@]341.O=P(O)(O)OWUXLCJZUUHIXFY-FFHNEAJVSA-NCodeine Phosphate can cause developmental toxicity according to state or federal government labeling requirements.
FDA approved drugs -> Active ingredient
FDA approved drugs -> Active ingredient
Sicherheitsangaben dienen nur zur Orientierung und ersetzen weder das Sicherheitsdatenblatt (SDB) des Lieferanten noch geltende Vorschriften oder eine fachliche Bewertung.
Danger
H301 (95.6%): Toxic if swallowed [Danger Acute toxicity, oral]
P203, P233, P260, P261, P264, P270, P271, P272, P280, P284, P301+P316, P302+P352, P304+P340, P318, P321, P330, P333+P317, P342+P316, P362+P364, P403, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 45 reports by companies from 15 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Hazard Traits - Developmental Toxicity
Codeine phosphate: Does not have an individual approval but may be used under an appropriate group standard
SYMPTOMS: Symptoms of exposure to this compound include dryness of the mouth, nose and throat, urticaria, drug rash, anaphylactic shock, photosensitivity, excessive perspiration, chills, hypotension, headache, palpitations, tachycardia, extrasystoles, hemolytic anemia, thrombocytopenia, agranulocytosis, sedation, sleepiness, dizziness, disturbed coordination, fatigue, confusion, restlessness, tremor, irritability, excitation, anxiety, nervousness, insomnia euphoria, paresthesias, blurred vision, diplopia, acute labyrinthitis, tinnitus, hysteria, neuritis, convulsions, central nervous system depression, hallucinations, epigastric distress, anorexia, nausea, vomiting, diarrhea, constipation, change in urinary frequency, difficult urination, urinary retention, early menses, thickening of bronchial secretions, tightness of chest, wheezing, nasal stuffiness, respiratory depression, psychic dependence and physical dependence.
Hepatic. Codeine is a prodrug, itself inactive, but demethylated to the active morphine by the liver enzyme CYP2D6 to morphine. 70-80% of the dose undergoes glucuronidation to form codeine-6-glucuronide. This process is mediated by UDP-glucuronosyltransferase UGT2B7 and UGT2B4. 5-10% of the dose undergoes O-demethylation to morphine and 10% undergoes N-demethylation to form norcodeine. CYP2D6 mediates the biotransformation to morphine. CYP3A4 is the enzymes that mediates the conversion to norcodiene. Morphine and norcodeine are further metabolized and undergo glucuronidation. The glucuronide metabolites of morphine are morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G). Both morphine and morphine-6-glucuronide are active and have analgesic activity. Norcodiene and M3G do not have any analgesic properties. Route of Elimination: 90% of the total dose of codeine is excreted through the kidneys, of which 10% is unchanged codeine. Half Life: Plasma half-lives of codeine and its metabolites have been reported to be approximately 3 hours.
Compounds with activity like OPIATE ALKALOIDS, acting at OPIOID RECEPTORS. Properties include induction of ANALGESIA or NARCOSIS.
Agents that suppress cough. They act centrally on the medullary cough center. EXPECTORANTS, also used in the treatment of cough, act locally.
Agents that induce NARCOSIS. Narcotics include agents that cause somnolence or induced sleep (STUPOR); natural or synthetic derivatives of OPIUM or MORPHINE or any substance that has such effects. They are potent inducers of ANALGESIA and OPIOID-RELATED DISORDERS.
VerwendenPresent in opium from 0.7% to 2.5%, depending on the source. Weak narcotic analgesic, perhaps due to conversion to morphine, with minimal hypnotic properties; potent antitussive. Controlled substance (opiate)
Keine Reaktionsaufzeichnungen unter den aktuellen Filterkriterien.
Wird geladen…
52-28-8DTXSID0024844CHEMBL6067642CODEINE PHOSPHATE is sensitive to exposure to light. (NTP, 1992). Materials that are acidic salts are generally soluble in water. The resulting solutions contain moderate concentrations of hydrogen ions and have pH's of less than 7.0. They react as acids to neutralize bases. These neutralizations generate heat, but less or far less than is generated by neutralization of inorganic acids, inorganic oxoacids, and carboxylic acid. They usually do not react as either oxidizing agents or reducing agents but such behavior is not impossible.
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)
Naloxone antagonizes most effects of codeine. Protect the airway as Naloxone may induce vomiting. Naloxone has a shorter duration of action than codeine; repeated doses may be needed. Protect the patient's airway and support ventilation and perfusion. Meticulously monitor and maintain, within acceptable limits, the patient's vital signs, blood gases, serum electrolytes, etc. Absorption of drugs from the gastrointestinal tract may be decreased by giving activated charcoal, which in many cases, is more effective than emesis or lavage; consider charcoal instead of or in addition to gastric emptying. Repeated doses of charcoal over time may hasten elimination of some drugs that have been absorbed. Safeguard the patient's airway when employing gastric emptying or charcoal. (L1712)
Oral, Intramuscular. Well absorbed following oral administration with a bioavailability of approximately 90%. Maximum plasma concentration occurs 60 minutes post-administration. Food does not effect the rate or extent of absorption of codeine.
Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Codeine's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.