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Morphine is a highly potent opiate analgesic psychoactive drug and the principal alkaloid obtained from opium. It is derived from the opium poppy, Papaver somniferum, and is a white or almost white crystalline powder or colorless, silky needles or cubical masses. 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 dependence developing rapidly.


Used in Medical Applications:
Morphine is used as a potent analgesic for the relief of severe pain. It is effective due to its ability to bind and activate opioid receptors in the central nervous system (brain and spinal cord), reducing the neurological transfer of pain signals to the brain. Morphine mimics natural pain relievers produced by the body called endorphins.
Used in Pharmaceutical Industry:
Morphine is the most important opium alkaloid and is used in the production of various pharmaceutical products. Some brand names include Astramorph (AstraZeneca), Avinza (Ligand), Depodur (Skyepharma), Duramorph (Baxter Healthcare), Infumorph (Baxter Healthcare), Kadian (Alpharma), MS Contin (Purdue Frederick), and Oramorph (Xanodyne).
Chemical Properties:
Morphine is a white, crystalline alkaloid that is slightly soluble in water, alcohol, and ether. It has a specific optical rotation ranging from -110.0° to -115.0°.
Physical Properties:
Morphine appears as a white or almost white crystalline powder or colorless, silky needles or cubical masses, and is efflorescent in a dry atmosphere. It is soluble in water, slightly soluble in ethanol, and practically insoluble in chloroform or ether.
Additional Information:
Morphine can be detected by the Marquis test and can be acetylated to produce heroin. It is also a degradation product of morphine and a dimolecular base formed by the gentle oxidation of morphine in an alkaline solution. The name Pseudomorphine is also used for the C17 alkaloid base.


Avinza,Aetna Inc.


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.

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.


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.

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.


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/kgA 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.


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.


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.


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.

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.


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.]


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)

Check Digit Verification of cas no

The CAS Registry Mumber 57-27-2 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 5 and 7 respectively; the second part has 2 digits, 2 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 57-27:
52 % 10 = 2
So 57-27-2 is a valid CAS Registry Number.



According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 17, 2017

Revision Date: Aug 17, 2017


1.1 GHS Product identifier

Product name morphine

1.2 Other means of identification

Product number -
Other names sec-Butyl-dihydrogenphosphat

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:57-27-2 SDS

57-27-2Relevant articles and documents

Site- and species-specific hydrolysis rates of heroin

Sz?cs, Levente,Orgován, Gábor,Tóth, Gergo,Kraszni, Márta,Gergó, Lajos,Hosztafi, Sándor,Noszál, Béla

, p. 105 - 114 (2016)

The hydroxide-catalyzed non-enzymatic, simultaneous and consecutive hydrolyses of diacetylmorphine (DAM, heroin) are quantified in terms of 10 site- and species-specific rate constants in connection with also 10 site- and species-specific acid-base equilibrium constants, comprising all the 12 coexisting species in solution. This characterization involves the major and minor decomposition pathways via 6-acetylmorphine and 3-acetylmorphine, respectively, and morphine, the final product. Hydrolysis has been found to be 18-120 times faster at site 3 than at site 6, depending on the status of the amino group and the rest of the molecule. Nitrogen protonation accelerates the hydrolysis 5-6 times at site 3 and slightly less at site 6. Hydrolysis rate constants are interpreted in terms of intramolecular inductive effects and the concomitant local electron densities. Hydrolysis fraction, a new physico-chemical parameter is introduced and determined to quantify the contribution of the individual microspecies to the overall hydrolysis. Hydrolysis fractions are depicted as a function of pH.

A rapid, high yield conversion of codeine to morphine


, p. 164 - 165 (1977)

Brief treatment of codeine (1) in chloroform with boron tribromide has consistently given morphine (2) in 90-91% yield after a simple isolation procedure. The yield and simplicity of operation in this method are vastly superior to those previously reported for this transformation.



, (1952)


Preparation of morphine 3H by microwave discharge activation of tritium gas


, p. 563 - 565 (1973)



Morrison et al.

, p. 4055 (1967)


New approach in the synthesis of M6G

Trécant, Claire,Dlubala, Alain,Ripoche, Isabelle,Troin, Yves

, p. 4753 - 4755 (2011)

Morphine-6-glucuronide (M6G) is the primarily active metabolite of morphine, produced endogenously by the UGT enzyme, which displays analgesic activity. For this reason, M6G is a promising drug candidate for the treatment of severe pain. We described herein a new, efficient and scalable synthesis of M6G using dimorphinic derivatives. This preparation of M6G could be performed on multigram scale with good yield and high purity.

Method for catalyzing asymmetric synthesis of codeine and morphine


Paragraph 0066; 0110-0112, (2019/05/02)

The invention discloses a method for synthesizing codeine and morphine. The method comprises the following steps: (I) taking 3-butyne-1-alcohol as a starting raw material to synthesize a compound 6: (shown in the description) (II) compound 6 firstly has intramolecular Michael addition reaction under the catalysis of a spirocyclic amine catalyst, and then acid is added to perform the dehydration cyclization reaction to obtain a chiral compound 7 with a hydrogenated dibenzofuran structure: (shown in the description) (III) the compound 7 has allylation, ozone oxidation, Foucault reaction, epoxidation, Wharton oxygen transfer reaction, debenzylation, Mitsunobu reaction, DMP oxidation, and the conversion by virtue of the reduction of sodium borohydride and Birch reduction to obtain the codeine(shown in the description). Under the action of boron tribromide, the methyl protecting group is removed from the codeine to obtain morphine. Compared with the existing synthesis method, the total synthesis method of the invention is simpler, and the catalytic asymmetric reaction has the advantages of high enantioselectivity, high yield and the like.

Kinetic characterization of cholinesterases and a therapeutically valuable cocaine hydrolase for their catalytic activities against heroin and its metabolite 6-monoacetylmorphine

Kim, Kyungbo,Yao, Jianzhuang,Jin, Zhenyu,Zheng, Fang,Zhan, Chang-Guo

, p. 107 - 114 (2018/08/21)

As the most popularly abused one of opioids, heroin is actually a prodrug. In the body, heroin is hydrolyzed/activated to 6-monoacetylmorphine (6-MAM) first and then to morphine to produce its toxic and physiological effects. It has been known that heroin hydrolysis to 6-MAM and morphine is accelerated by cholinesterases, including acetylcholinesterase (AChE) and/or butyrylcholinesterase (BChE). However, there has been controversy over the specific catalytic activities and functional significance of the cholinesterases, which requires for the more careful kinetic characterization under the same experimental conditions. Here we report the kinetic characterization of AChE, BChE, and a therapeutically promising cocaine hydrolase (CocH1) for heroin and 6-MAM hydrolyses under the same experimental conditions. It has been demonstrated that AChE and BChE have similar kcat values (2100 and 1840 min?1, respectively) against heroin, but with a large difference in KM (2170 and 120 μM, respectively). Both AChE and BChE can catalyze 6-MAM hydrolysis to morphine, with relatively lower catalytic efficiency compared to the heroin hydrolysis. CocH1 can also catalyze hydrolysis of heroin (kcat = 2150 min?1 and KM = 245 μM) and 6-MAM (kcat = 0.223 min?1 and KM = 292 μM), with relatively larger KM values and lower catalytic efficiency compared to BChE. Notably, the KM values of CocH1 against both heroin and 6-MAM are all much larger than previously reported maximum serum heroin and 6-MAM concentrations observed in heroin users, implying that the heroin use along with cocaine will not drastically affect the catalytic activity of CocH1 against cocaine in the CocH1-based enzyme therapy for cocaine abuse.