Mycophenolate mofetil

433.49

433.49

9242ECW6R0

758905|724229

DTXSID3023340

C1468

White to off-white crystalline powder

L04AA06

94.5

3.2

white to beige

1.2±0.1 g/cm3

95-96°C

637.6ºC at 760 mmHg

339.4±31.5 °C

1.557

H2O: Slightly soluble (43 mg/mL at pH 7.4);DMSO: ≥15mg/mL

Store at RT

1.9X10-13 mm Hg at 25 deg C (est)

Henry's Law constant = 5.5X10-15 atm-cu m/mol at 25 °C (est)

5.6 for the morpholino group and 8.5 for the phenolic group|pKa1 = 5.6 (tertiary amine); pKa2 = 8.5 (phenol)

197.3 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Hydroxyl radical reaction rate constant = 4.5X10-10 cu cm/molecule sec at 25 °C (est)

UN 3077 9 / PGIII

22

22-24/25

MP7746700

Xn

P273

H302-H400

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl mycophenolate mofetil, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.|The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl mycophenolate mofetil hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Mycophenolate mofetil hydrochloride/

|Danger|H302 (98.08%): Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P264, P270, P273, P281, P301+P312, P308+P313, P314, P330, P391, P405, and P501|Aggregated GHS information provided by 52 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

LD50 The LD50 of oral mycophenolate mofetil in rats is 250 mg/kg and >4000 mg/kg in mice. **Overdose information** Possible signs and symptoms of acute overdose may consist of hematological abnormalities including leukopenia and neutropenia, and gastrointestinal symptoms.

Serum enzyme elevations occur in a small proportion of patients on mycophenolate mofetil, but the abnormalities are usually mild, asymptomatic and resolve spontaneously or with dose reduction. A small number of cases of clinically apparent liver injury have been reported in patients on mycophenolate. The onset of injury is usually during the first month of therapy and the pattern of serum enzyme elevations is hepatocellular or mixed. The liver injury is usually mild and self-limiting. Autoimmune and immunoallergic features are uncommon.

In the presence of renal impairment, acyclovir or ganciclovir may compete with mycophenolic acid glucuronide (MPAG) for tubular secretion, thus further increasing plasma concentrations of each.|Potential pharmacokinetic interaction (decreased plasma concentrations of levonorgestrel). Oral contraceptives should be administered with caution in patients receiving mycophenolate mofetil and additional methods of birth control methods should be considered.|Concurrent administration /with magnesium or aluminum hydroxide containing antacids/ may result in decreased absorption of mycophenolate; simultaneous administration is not recommended.|Plasma concentrations of mycophenolic acid (MPA) may be decreased as a result of interruption of enterohepatic recirculation of mycophenolic acid glucuronide (MPAG) possibly caused by intestinal binding with cholestyramine /when mycophenolate and cholestyramine are used concurrently/.|For more Interactions (Complete) data for MYCOPHENOLATE MOFETIL (7 total), please visit the HSDB record page.

Because mycophenolate mofetil inhibits inosine monophosphate dehydrogenase, the drug should be avoided, on theoretical grounds, in patients with rare hereditary deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT), including Kelley-Seegmiller or Lesch-Nyhan syndrome.|CellCept Oral Suspension contains aspartame, a source of phenylalanine (0.56 mg phenylalanine/mL suspension). Therefore, care should be taken if CellCept Oral Suspension is administered to patients with phenylketonuria.

The protein binding of mycophenolic acid, the metabolite of mycophenolate mofetil, is 97% and it is mainly bound to albumin. MPAG, the inactive metabolite, is 82% bound to plasma albumin at normal therapeutic concentrations. At elevated MPAG concentrations due to various reasons, including renal impairment, the binding of MPA may be decreased due to competition for binding.

Mycophenolate mofetil's production and use as an immunosuppressive agent(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 470(SRC), determined from a log Kow of 2.4(2) and a regression-derived equation(3), indicates that mycophenolate mofetil is expected to have moderate mobility in soil(SRC). Measured pKa values for mycophenolate mofetil are 5.6 (tertiary amine) and 8.5 (phenol)(4), indicating that this compound will exist partially in the anion form under basic conditions and partially in the cation form under acidic conditions in the environment. Volatilization of mycophenolate mofetil from moist soil surfaces is not expected to be an important fate process(SRC) because ionic compounds do not volatilize and based on an estimated Henry's Law constant of 5.5X10-15 atm-cu m/mole for the neutral species(SRC), calculated using a fragment constant estimation method(5). Mycophenolate mofetil is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-13 mm Hg(SRC), determined from a fragment constant method(6). Biodegradation data were not available(SRC, 2006).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 470(SRC), determined from a log Kow of 2.4(2) and a regression-derived equation(3), indicates that mycophenolate mofetil is expected to adsorb very little to suspended solids and sediment(SRC). Measured pKa values for mycophenolate mofetil are 5.6 (tertiary amine) and 8.5 (phenol)(4), indicating that this compound will exist partially in the anion form under basic conditions and partially in the cation form under acidic conditions in the environment. Volatilization from water surfaces is not expected(3) becuase ionic compounds do not volatilize and based upon an estimated Henry's Law constant of 5.5X10-15 atm-cu m/mole for the neutral species(SRC), developed using a fragment constant estimation method(5). According to a classification scheme(6), an estimated BCF of 38(SRC), from a log Kow of 2.4(2), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). A base-catalyzed second-order hydrolysis rate constant of 0.14 L/mole-sec(SRC) was estimated using a structure estimation method(7); this corresponds to half-lives of 1.6 years and 59 days at pH values of 7 and 8, respectively. Biodegradation data were not available(SRC, 2006).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), mycophenolate mofetil, which has an estimated vapor pressure of 1.9X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase mycophenolate mofetil may be removed from the air by wet or dry deposition(SRC). Mycophenolate mofetil does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

A base-catalyzed second-order hydrolysis rate constant of 0.14 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 1.6 years and 59 days at pH values of 7 and 8, respectively(1). Mycophenolate mofetil does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 38 was calculated for mycophenolate mofetil(SRC), using a measured log Kow of 2.4(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC).

The Koc of mycophenolate mofetil is estimated as 470(SRC), using a log Kow of 2.4(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that mycophenolate mofetil is expected to have moderate mobility in soil. Measured pKa values for mycophenolate mofetil are 5.6 (tertiary amine) and 8.5 (phenol)(4), indicating that this compound will exist partially in the anion form under basic conditions and partially in the cation form under acidic conditions in the environment.

The Henry's Law constant for mycophenolate mofetil is estimated as 5.5X10-15 atm-cu m/mole(SRC) using a fragment constant estimation method(1). Measured pKa values for mycophenolate mofetil are 5.6 (tertiary amine) and 8.5 (phenol)(2), indicating that this compound will exist partially in the anion form under basic conditions and partially in the cation form under acidic conditions in the environment. Based on this Henry's Law constant and the fact that ionic compounds do not volatilize, mycophenolate mofetil is expected to be essentially nonvolatile from moist soil or water surfaces(3). Mycophenolate mofetil is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-13 mm Hg(SRC), determined from a fragment constant method(4).

While data specific to mycophenolate mofetil were not located(SRC, 2006), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

It is not known whether mycophenolate is distributed into breast milk in humans. However, studies in rats treated with mycophenolate have shown mycophenolic acid (MPA) to be distributed into milk.

Occupational exposure to mycophenolate mofetil may occur through inhalation and dermal contact with this compound at workplaces where mycophenolate mofetil is produced or used. Exposure to mycophenolate mofetil among the general population may be limited to those administered this substance as a drug. (SRC)

Mycophenolate mofetil is indicated for the prophylaxis of organ rejection in patients undergoing allogeneic renal, hepatic, or cardiac transplants. It should be used with cyclosporine and corticosteroids. Mycophenolate mofetil may also be used off-label as a second-line treatment for autoimmune hepatitis that has not responded adequately to first-line therapy. Other off-label uses of this drug include lupus-associated nephritis and dermatitis in children.|FDA Label|Myfenax is indicated in combination with ciclosporin and corticosteroids for the prophylaxis of acute transplant rejection in patients receiving allogeneic renal, cardiac or hepatic transplants.|Mycophenolate mofetil Teva is indicated in combination with ciclosporin and corticosteroids for the prophylaxis of acute transplant rejection in patients receiving allogeneic renal, cardiac or hepatic transplants.|CellCept is indicated in combination with ciclosporin and corticosteroids for the prophylaxis of acute transplant rejection in patients receiving allogeneic renal, cardiac or hepatic transplants.|Myclausen is indicated in combination with ciclosporin and corticosteroids for the prophylaxis of acute transplant rejection in patients receiving allogeneic renal, cardiac or hepatic transplants.

Mycophenolate mofetil is an antimetabolite and potent immunosuppressive agent used as adjunctive therapy in prevention of allograft rejection and in the treatment of serious autoimmune diseases. Mycophenolate therapy can be associated with mild serum enzyme elevations and it has been linked to rare instances of clinically apparent liver injury.

Transplant Agents

Anti-Inflammatory Agents, Non-Steroidal, Antineoplastic Agents, Dermatologic Agents, Enzyme Inhibitors, Immunosuppressive Agents|MEDICATION: Immunosuppressant|Mycophenolate is indicated, in combination with cyclosporine and corticosteroids, for prevention of rejection of allogeneic cardiac, hepatic and renal transplants. /Included in US product labeling/|Mycophenolate is indicated for the treatment of lupus nephritis. /NOT included in US product labeling/

Severe GI bleeding (requiring hospitalization) has occurred in 3, 1.7, or 5.4% of renal, cardiac, or hepatic transplant recipients, respectively, receiving 3-g daily dosages of mycophenolate mofetil in clinical studies. Because mycophenolate mofetil has been associated rarely with an increased incidence of adverse GI effects (e.g., ulceration, hemorrhage, perforation), the drug should be administered with caution in patients with active serious GI disease.|FDA Pregnancy Risk Category: C /RISK CANNOT BE RULED OUT. Adequate, well controlled human studies are lacking, and animal studies have shown risk to the fetus or are lacking as well. There is a chance of fetal harm if the drug is given during pregnancy; but the potential benefits may outweigh the potential risk./|Severe neutropenia (i.e., absolute neutrophil counts (ANC) of less than 500/cu mm) has been reported in up to 2, 2.8, or 3.6% of renal, cardiac, or hepatic allograft recipients, respectively, receiving 3-g daily dosages of mycophenolate mofetil. Neutropenia has been observed most frequently between 31-180 days post-transplant in patients receiving immunosuppressive therapy for the prevention of rejection of kidney, heart, or liver allograft. Neutropenia may be related to mycophenolate mofetil, concomitant therapies, viral infection, or a combination of these causes.|Potential for the development of lymphoma and other malignancies, particularly of the skin, which may result from immunosuppression. Because of the increased risk for skin cancer, patients should be advised to limit their exposure to sunlight or other UV light by wearing protective clothing and using sunscreen with a high protection factor. Lymphoproliferative disease or lymphoma occurred in 0.4-1% of allograft recipients receiving mycophenolate mofetil in conjunction with other immunosuppressive agents in clinical studies. Non-melanoma skin carcinoma was reported in 1.6-4.2% of patients while other types of malignancy were reported in 0.7-2.1% of patients.|For more Drug Warnings (Complete) data for MYCOPHENOLATE MOFETIL (15 total), please visit the HSDB record page.

Mycophenolate mofetil is a prodrug of mycophenolic acid (MPA). The active form of mycophenolate, MPA, prevents the proliferation of immune cells and the formation of antibodies that cause transplant rejection. The above effects lead to higher rates of successful transplantation, avoiding the devastating effects of graft rejection.

Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms. (See all compounds classified as Antibiotics, Antineoplastic.)|Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)|Substances obtained from various species of microorganisms that are, alone or in combination with other agents, of use in treating various forms of tuberculosis; most of these agents are merely bacteriostatic, induce resistance in the organisms, and may be toxic. (See all compounds classified as Antibiotics, Antitubercular.)

Mycophenolate mofetil is rapidly absorbed in the small intestine. The maximum concentration of its active metabolite, MPA, is attained 60 to 90 minutes following an oral dose. The average bioavailability of orally administered mycophenolate mofetil in a pharmacokinetic study of 12 healthy patients was 94%. In healthy volunteers, the Cmax of mycophenolate mofetil was 24.5 (±9.5)μg/mL. In renal transplant patients 5 days post-transplant, Cmax was 12.0 (±3.82) μg/mL, increasing to 24.1 (±12.1)μg/mL 3 months after transplantation. AUC values were 63.9 (±16.2) μg•h/mL in healthy volunteers after one dose, and 40.8 (±11.4) μg•h/mL, and 65.3 (±35.4)μg•h/mL 5 days and 3 months after a renal transplant, respectively. The absorption of mycophenolate mofetil is not affected by food.|A small amount of drug is excreted as MPA in the urine (less than 1%). When mycophenolate mofetil was given orally in a pharmacokinetic study, it was found to be 93% excreted in urine and 6% excreted in feces. Approximately 87% of the entire administered dose is found to be excreted in the urine as MPAG, an inactive metabolite.|The volume of distribution of mycophenolate mofetil is 3.6 (±1.5) to 4.0 (±1.2) L/kg.|Plasma clearance of mycophenolate mofetil is 193 mL/min after an oral dose and 177 (±31) mL/min after an intravenous dose.|/Absorption/ is rapid and extensive after oral administration.|In 12 healthy volunteers, the mean absolute bioavailability of oral mycophenolate mofetil relative to intravenous mycophenolate mofetil (based on MPA AUC) was 94%. The area under the plasma-concentration time curve (AUC) for MPA appears to increase in a dose-proportional fashion in renal transplant patients receiving multiple doses of mycophenolate mofetil up to a daily dose of 3 g.|Protein binding: To plasma albumin: High (97% for mycophenolic acid (MPA) at concentration ranges normally seen in stable renal transplant patients). At higher mycophenolic acid glucuronide (MPAG) concentrations (e.g., in patients with renal impairment or delayed graft function), binding of MPA may be decreased as a result of competition between MPA and MPAG for binding sites.|The mean (+/-SD) apparent volume of distribution of MPA in 12 healthy volunteers is approximately 3.6 (+/-1.5) and 4.0 (+/-1.2) L/kg following intravenous and oral administration, respectively. MPA, at clinically relevant concentrations, is 97% bound to plasma albumin. MPAG is 82% bound to plasma albumin at MPAG concentration ranges that are normally seen in stable renal transplant patients; however, at higher MPAG concentrations (observed in patients with renal impairment or delayed renal graft function), the binding of MPA may be reduced as a result of competition between MPAG and MPA for protein binding. Mean blood to plasma ratio of radioactivity concentrations was approximately 0.6 indicating that MPA and MPAG do not extensively distribute into the cellular fractions of blood.|For more Absorption, Distribution and Excretion (Complete) data for MYCOPHENOLATE MOFETIL (9 total), please visit the HSDB record page.

After both oral and intravenous administration mycophenolate mofetil is entirely metabolized by liver carboxylesterases 1 and 2 to mycophenolic acid (MPA), the active parent drug. It is then metabolized by the enzyme glucuronyl transferase, producing the inactive phenolic glucuronide of MPA (MPAG). The glucuronide metabolite is important, as it is then converted to MPA through enterohepatic recirculation. Mycophenolate mofetil that escapes metabolism in the intestine enters the liver via the portal vein and is transformed to pharmacologically active MPA in the liver cells.N-(2-carboxymethyl)-morpholine, N-(2-hydroxyethyl)-morpholine, and the N-oxide portion of N-(2-hydroxyethyl)-morpholine are additional metabolites of MMF occurring in the intestine as a result of liver carboxylesterase 2 activity. UGT1A9 and UGT2B7 in the liver are the major enzymes contributing to the metabolism of MPA in addition to other UGT enzymes, which also play a role in MPA metabolism. The four major metabolites of MPA are 7-O-MPA-β-glucuronide (MPAG, inactive), MPA acyl-glucuronide (AcMPAG), produced by uridine 5ʹ-diphosphate glucuronosyltransferases (UGT) activities, 7-O-MPA glucoside produced via UGT, and small amounts 6-O-des-methyl-MPA (DM-MPA) via CYP3A4/5 and CYP2C8 enzymes.|Following oral and intravenous dosing, mycophenolate mofetil undergoes complete metabolism to MPA /mycophenolic acid/, the active metabolite. Metabolism to MPA occurs presystemically after oral dosing. MPA is metabolized principally by glucuronyl transferase to form the phenolic glucuronide of MPA (MPAG) which is not pharmacologically active. In vivo, MPAG is converted to MPA via enterohepatic recirculation. The following metabolites of the 2- hydroxyethyl-morpholino moiety are also recovered in the urine following oral administration of mycophenolate mofetil to healthy subjects: N-(2-carboxymethyl)-morpholine, N-(2- hydroxyethyl)-morpholine, and the N-oxide of N-(2-hydroxyethyl)-morpholine.

The average apparent half-life of mycophenolate mofetil is 17.9 (±6.5) hours after oral administration and 16.6 (±5.8) hours after intravenous administration.|For mycophenolic acid (MPA):Mean apparent: Approximately 17.9 hours after oral administration and 16.6 hours after intravenous administration.|Mean (+/-SD) apparent half-life and plasma clearance of MPA are 17.9 (+/-6.5) hours and 193 (+/-48) mL/min following oral administration and 16.6 (+/-5.8) hours and 177 (+/-31) mL/min following intravenous administration, respectively.

The active metabolite of mycophenolate, mycophenolic acid, prevents T-cell and B-cell proliferation and the production of cytotoxic T-cells and antibodies. Lymphocyte and monocyte adhesion to endothelial cells of blood vessels that normally part of inflammation is prevented via the glycosylation of cell adhesion molecules by MPA. MPA inhibits de novo purine biosynthesis (that promotes immune cell proliferation) by inhibiting inosine 5’-monophosphate dehydrogenase enzyme (IMPDH), with a preferential inhibition of IMPDH II. IMPDH normally transforms inosine monophosphate (IMP) to xanthine monophosphate (XMP), a metabolite contributing to the production of guanosine triphosphate (GTP). GTP is an important molecule for the synthesis of ribonucleic acid (RNA), deoxyribonucleic acid (DNA), and protein. As a result of the above cascade of effects, mycophenolate mofetil reduces de-novo production of guanosine nucleotides, interfering with the synthesis of DNA, RNA, and protein required for immune cell production. Further contributing to the above anti-inflammatory effects, MMF depletes tetrahydrobiopterin, causing the decreased function of inducible nitric oxide synthase enzyme, in turn decreasing the production of peroxynitrite, a molecule that promotes inflammation.|As a potent, selective, noncompetitive, and reversible, inhibitor of inosine monophosphate dehydrogenase (IMPDH), mycophenolic acid (MPA), the active metabolite /of mycophenolate mofetil/, inhibits the de novo synthesis pathway of guanosine nucleotides without being incorporated into DNA. Because T and B lymphocytes are critically dependent for their proliferation on de novo synthesis of purines, while other cell types can utilize salvage pathways, MPA has potent cytostatic effects on lymphocytes. MPA inhibit proliferative responses of T and B lymphocytes to both mitogenic and allospecific stimulation. The addition of guanosine or deoxyguanosine reverses the cytostatic effects of MPA on lymphocytes. MPA also suppresses antibody formation by B lymphocytes. MPA prevents the glycosylation of lymphocytes and monocyte glycoproteins that are involved in intercellular adhesion of these cells to endothelial cells, and may inhibit recruitment of leukocytes into sites of inflammation and graft rejection. Mycophenolate mofetil dose not inhibit the early events in the activation of human peripheral blood mononuclear cells, such as the production of interleukin-1 and interleukin-2, but does block the coupling of these events to DNA synthesis and proliferation.

/SRP:/ Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poison A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poison A and B/

/CASE REPORTS/ Mycophenolate mofetil (MMF) is one of the new immunosuppressive drugs used in renal transplantation. MMF inhibits the de novo purine synthesis. Since this purine synthesis in lymphocytes entirely depends on the de novo pathway, MMF is considered to cause a selective inhibition of T- and B lymphocytes. Recently, 4 transplant patients out of 30 developed a severe anemia in the early post-transplantation period. Their immediate post-transplantation immunosuppression consisted of corticosteroids, cyclosporine and MMF. They all received anti-T-lymphocyte globulin (ATG) as induction treatment or because of rejection. In all 4 patients, iron supplementation and a treatment with erythropoietin were started. Blood loss, deficiencies, hemolysis, drug interactions or viral infections were excluded as causes of the anemia. Bone marrow biopsies were carried out, showing pure red cell aplasia that was ascribed to the use of MMF. Cessation or reduction of MMF was followed by a hematological improvement after 5-9 days. We hypothesized that MMF has a broader antiproliferative effect than its proposed lymphocyte-specific effect.

Cellcept

Parenteral: For injection: 500 mg (of mycophenolate mofetil), CellCept ( contains polysorbate 80), (Roche). /Mycophenolate mofetil hydrochloride/|Oral: Capsules: 250 mg, CellCept, (Roche); For oral suspension: 200 mg/mL , CellCept ( contains aspartame), (Roche); Tablets: 500 mg, CellCept, (Roche).

Human drugs -> Myfenax -> EMA Drug Category|Immunosuppressants -> Human pharmacotherapeutic group|Human drugs -> Mycophenolate mofetil Teva -> EMA Drug Category|Human drugs -> CellCept -> EMA Drug Category|Human drugs -> Myclausen -> EMA Drug Category|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients