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Mycophenolic acid

Inosine monophosphatase dehydrogenase inhibitor CAS# 24280-93-1

Mycophenolic acid

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Product Name & Size Price Stock
Mycophenolic acid:50mg $67.00 In stock
Mycophenolic acid:100mg $114.00 In stock
Mycophenolic acid:250mg $268.00 In stock
Mycophenolic acid:500mg $469.00 In stock
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Chemical structure

Mycophenolic acid

3D structure

Chemical Properties of Mycophenolic acid

Cas No. 24280-93-1 SDF Download SDF
PubChem ID 446541 Appearance Powder
Formula C17H20O6 M.Wt 320.34
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Mycophenolate
Solubility DMSO : ≥ 100 mg/mL (312.17 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.
Chemical Name (E)-6-(4-hydroxy-6-methoxy-7-methyl-3-oxo-1H-2-benzofuran-5-yl)-4-methylhex-4-enoic acid
SMILES CC1=C(C(=C(C2=C1COC2=O)O)CC=C(C)CCC(=O)O)OC
Standard InChIKey HPNSFSBZBAHARI-RUDMXATFSA-N
Standard InChI InChI=1S/C17H20O6/c1-9(5-7-13(18)19)4-6-11-15(20)14-12(8-23-17(14)21)10(2)16(11)22-3/h4,20H,5-8H2,1-3H3,(H,18,19)/b9-4+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Mycophenolic acid

DescriptionImmunosuppressive agent with antiviral and antitumor effects in vitro and in vivo. Potently inhibits inosine monophosphate dehydrogenase, thus inhibiting de novo GTP synthesis leading to decreased RNA and DNA synthesis. Reversibly inhibits proliferation of T and B lymphocytes and antibody formation.

Mycophenolic acid Dilution Calculator

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Mycophenolic acid Molarity Calculator

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Preparing Stock Solutions of Mycophenolic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.1217 mL 15.6084 mL 31.2168 mL 62.4337 mL 78.0421 mL
5 mM 0.6243 mL 3.1217 mL 6.2434 mL 12.4867 mL 15.6084 mL
10 mM 0.3122 mL 1.5608 mL 3.1217 mL 6.2434 mL 7.8042 mL
50 mM 0.0624 mL 0.3122 mL 0.6243 mL 1.2487 mL 1.5608 mL
100 mM 0.0312 mL 0.1561 mL 0.3122 mL 0.6243 mL 0.7804 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Mycophenolic acid

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References on Mycophenolic acid

Influence of Proton Pump Inhibitors on Mycophenolic Acid Pharmacokinetics in Patients With Renal Transplantation and the Relationship With Cytochrome 2C19 Gene Polymorphism.[Pubmed:28340819]

Transplant Proc. 2017 Apr;49(3):490-496.

BACKGROUND: Most patients have serious digestive complications after renal transplantation. Therefore, it is important to protect gastrointestinal function to improve the survival rate of transplant patients. Proton pump inhibitors (PPIs) such as lansoprazole and rabeprazole are widely administered to renal transplant patients with Mycophenolic acid (MPA) in the perioperative period. PPIs are metabolized by cytochrome (CYP) 2C19 enzymes. Mycophenolate sodium (MYF) and mycophenolate mofetil (MMF) have been used in immunosuppression. Clinically relevant drug-drug interactions have been described between immunosuppressive drugs. In the present study, we investigated the drug interaction between MPA and lansoparazole or rabeprazole and the impact of CYP2C19 polymorphisms on these drug interactions after renal transplantation. MATERIALS AND METHODS: A total of 125 renal transplant patients taking MPA derivatives between 2012 and 2016 were included in this study. The 125 patients were divided into 6 groups: MMF/tacrolimus/steroid together with lansoprazole or rabeprazole; MYF/tacrolimus/steroid together with lansoprazole or rabeprazole and without PPI. The single nucleotide polymorphisms of CYP2C19 were determined by the polymerase chain reaction-restriction fragment length polymorphism. Plasma concentrations of MPA were measured by cloned enzyme donor immunoassay. Clinical parameters such as incidence of delayed graft function and acute rejection, the rate of change of serum creatinine, toxicity, and gastrointestinal adverse effects were analyzed retrospectively. RESULTS: The mean concentrations of MPA in the MYF group were higher than those in the MMF group. The mean dose-adjusted blood concentration of MPA coadministered with lansoprazole was lower than that of MPA with rabeprazole or without PPI in MMF and MYF groups (P < .05). In patients with the CYP2C19*2/*2 genotype, the mean concentrations of MMF with lansoprazole were significantly lower than those with rabeprazole with MMF or without PPI (P < .05). Gastrointestinal side effects were significantly higher in MMF with lansoprazole group than in MYF with lansoprazole group (P < .05). However, no differences were found according to genotype distribution in all groups (P > .05). CONCLUSION: Polymorphisms in CYP2C19 are related to the metabolic oxidation of drugs to varying degrees. Both genetic and clinical factors in pharmacokinetics may help to make further progress toward individualized therapy to yield maximum efficacy with minimal side effects.

Simultaneous Determination of Protein-Unbound Cyclosporine A and Mycophenolic Acid in Kidney Transplant Patients Using Liquid Chromatography-Tandem Mass Spectrometry.[Pubmed:28328764]

Ther Drug Monit. 2017 Jun;39(3):211-219.

BACKGROUND: Therapeutic drug monitoring (TDM) of immunosuppressants is essential to optimize patient care after organ transplantation. In blood, most immunosuppressive drugs are bound to plasma proteins or located inside blood cells. However, it is generally assumed that only protein-unbound (free) drug concentrations are pharmacologically active and could therefore better reflect the clinical outcome. Study data are still limited due to lacking rapid analytical methods. Therefore, a simple multiplex method for direct measurement of free cyclosporine A (CsA) and Mycophenolic acid (MPA) has been developed. METHODS: The sample preparation included ultracentrifugation, followed by liquid-liquid extraction. Stable isotope labeled analogues of CsA and MPA were used as internal standards. The LC-MS/MS analysis was performed on a triple quadrupole mass spectrometer in the multiple reaction monitoring mode. The validated assay was used in a study of 40 blood samples from kidney transplant patients. RESULTS: The lower limits of quantification were 0.1 (CsA) and 0.5 ng/mL (MPA). Assay linearity was confirmed in the concentration ranges of 0.1-10.0 ng/mL (CsA) and 0.5-100 ng/mL (MPA). For both analytes, inaccuracy was

Production of mycophenolic acid by Penicillium brevicompactum-A comparison of two methods of optimization.[Pubmed:28352543]

Biotechnol Rep (Amst). 2016 Aug 4;11:77-85.

Production of Mycophenolic acid (MPA) by submerged fermentation using the microfungus Penicillium brevicompactum MTCC 8010 is reported here. Screening experiments were used to identify: the suitable media composition; the optimal initial pH; and the optimal incubation temperature to maximize the production of MPA in batch cultures. The initial concentrations of the selected sources of carbon (glucose), nitrogen (peptone) and the precursors (methionine, glycine) were then optimized by: (1) one-at-a-time variation of factors; and (2) a central composite design (CCD) of experiments, in a 12-day batch culture at an initial pH of 5.0, an incubation temperature of 25 degrees C, and an agitation speed of 200 rpm. The medium optimized using the one-at-a-time variation yielded a peak MPA titer of 1232 +/- 90 mg/L. The medium optimized by the CCD method yielded a 40% higher MPA titer of 1737 +/- 55 mg/L. The latter value was nearly 9-fold greater than the titer achieved prior to optimization.

Evaluation of tolerance and safety of conversion from mycophenolate mofetil to enteric-coated mycophenolic acid in renal transplant recipients.[Pubmed:28337883]

J Biol Regul Homeost Agents. 2017 Jan-Mar;31(1):141-146.

This study was designed to evaluate the curative effect of conversion from mycophenolate mofetil (MMF) to enteric-coated mycophenolate sodium tablets (EC-MPS) and its safety. One hundred and twenty renal transplant recipients who developed MMF-associated chronic diarrhea were selected as research subjects and treated with EC-MPS. The patients were followed up for 12 months to compare the improvement of gastrointestinal symptoms and the indexes such as carbon dioxide combining power (CO2CP), serum sodium, serum potassium, serum creatinine (Scr) and 24-h urine protein before and after conversion treatment. One hundred and ten of the 120 patients tolerated the conversion treatment and the dose increment of EC-MPS at week 28. After initiating the conversion treatment, the improvement rate of diarrhea within 2 weeks was 95% (114/120). Indexes, such as CO2CP, serum sodium, serum potassium, after conversion treatment were higher than those before treatment (P less than 0.05). No acute rejection reactions were observed in the 12-month follow-up. Indexes of Scr and 24-h urine protein had significant improvement after conversion treatment compared to before conversion treatment (P less than 0.05). Compared to before treatment, the average values of indexes in gastrointestinal symptom rating scale in the 12th month remained stable, except for the increase of dose. For renal transplant recipients who received suboptimal EC-MPS treatment due to gastrointestinal symptoms, conversion from MMF to EC-MPS can significantly lower gastrointestinal symptom load, improve quality of life, relieve electrolyte disturbance and improve the injured functions of transplanted kidney, without increasing the risks of acute rejection reactions.

Pharmacological characterization of endomorphin-1 and endomorphin-2 in mouse brain.[Pubmed:9694962]

J Pharmacol Exp Ther. 1998 Aug;286(2):1007-13.

The recently isolated peptides endomorphin-1 and endomorphin-2 have been suggested to be the endogenous ligands for the mu receptor. In traditional opioid receptor binding assays in mouse brain homogenates, both endomorphin-1 and endomorphin-2 competed both mu1 and mu2 receptor sites quite potently. Neither compound had appreciable affinity for either delta or kappa1 receptors, confirming an earlier report. However, the two endomorphins displayed reasonable affinities for kappa3 binding sites, with Ki values between 20 and 30 nM. Both endomorphins competed 3H-[D-Ala2, MePhe4,Gly(ol)5] enkephalin binding to MOR-1 receptors expressed in CHO cells with high affinity. In mouse brain homogenates 125I-endomorphin-1 and 125I-endomorphin-2 binding was selectively competed by mu ligands. 125I-Endomorphin-1 and 125I-endomorphin-2 also labeled MOR-1 receptors expressed in CHO cells with high affinity. Autoradiography of the two 125I-labeled endomorphins demonstrated regional patterns in the brain similar to those previously observed for mu drugs. Pharmacologically, the endomorphins were potent analgesics. Although they were equipotent supraspinally, endomorphin-1 was more potent spinally. Endomorphin analgesia was effectively blocked by naloxone, as well as the mu-selective antagonists beta-funaltrexamine and naloxonazine. In CXBK mice, which are insensitive to supraspinal morphine, neither endomorphin was active, consistent with a mu mechanism of action. Finally, the endomorphins inhibited gastrointestinal transit. In conclusion, these results support the mu selectivity of these agents.

Distinct inhibitory effects of spinal endomorphin-1 and endomorphin-2 on evoked dorsal horn neuronal responses in the rat.[Pubmed:9422796]

Br J Pharmacol. 1997 Dec;122(8):1537-9.

Intrathecal endomorphin-1 and endomorphin-2 (0.25-50 micrograms) dose-relatedly reduced all components of electrical evoked C-fibre responses of spinal neurones. These effects were partially reversed by naloxone. Endomorphin-1, but not endomorphin-2, dose-relatedly reduced the A beta-fibre evoked responses. Peak inhibitory effects of endomorphin-1 and -2 were at 15-20 min post-administration. Thus spinal endomorphin-2 had selective effects on noxious responses, whereas endomorphin-1 was non-selective.

A potent and selective endogenous agonist for the mu-opiate receptor.[Pubmed:9087409]

Nature. 1997 Apr 3;386(6624):499-502.

Peptides have been identified in mammalian brain that are considered to be endogenous agonists for the delta (enkephalins) and kappa (dynorphins) opiate receptors, but none has been found to have any preference for the mu receptor. Because morphine and other compounds that are clinically useful and open to abuse act primarily at the mu receptor, it could be important to identify endogenous peptides specific for this site. Here we report the discovery and isolation from brain of such a peptide, endomorphin-1 (Tyr-Pro-Trp-Phe-NH2), which has a high affinity (Ki = 360 pM) and selectivity (4,000- and 15,000-fold preference over the delta and kappa receptors) for the mu receptor. This peptide is more effective than the mu-selective analogue DAMGO in vitro and it produces potent and prolonged analgesia in mice. A second peptide, endomorphin-2 (Tyr-Pro-Phe-Phe-NH2), which differs by one amino acid, was also isolated. The new peptides have the highest specificity and affinity for the mu receptor of any endogenous substance so far described and they may be natural ligands for this receptor.

Mycophenolic acid, an inhibitor of IMP dehydrogenase that is also an immunosuppressive agent, suppresses the cytokine-induced nitric oxide production in mouse and rat vascular endothelial cells.[Pubmed:7482723]

Transplantation. 1995 Nov 27;60(10):1143-8.

Mycophenolic acid (MPA), an inhibitor of IMP dehydrogenase and de novo GTP biosynthesis, also has immunosuppressive activity. The effect of MPA on nitric oxide (NO) production by rodent brain vascular endothelial cells in culture was investigated. MPA inhibited NO production by mouse and rat brain endothelial cells that had been stimulated with a combination of interferon-gamma and tumor necrosis factor-alpha. The 50% inhibitory concentration (EC50) was in the range of 0.5-1.0 microM. However, MPA had no effect on basal NO production in mouse brain vascular endothelial cells. Brequinar, an inhibitor of de novo pyrimidine synthesis, had no effect on NO production in cytokine stimulated endothelial cells. Guanosine, which can act as a salvage pathway precursor for GTP biosynthesis, reversed the inhibitory effect of MPA in a dose-dependent fashion. We suggest that inducible NO synthase activity is dependent on GTP level and can be blocked by curtailing IMP dehydrogenase activity.

Lymphocyte-selective cytostatic and immunosuppressive effects of mycophenolic acid in vitro: role of deoxyguanosine nucleotide depletion.[Pubmed:1826793]

Scand J Immunol. 1991 Feb;33(2):161-73.

Mycophenolic acid (MPA), an inhibitor of inosine monophosphate dehydrogenase, in nanomolar concentrations blocks proliferative responses of cultured human, mouse and rat T lymphocytes and B lymphocytes to mitogens or in mixed lymphocyte reactions. The inhibitory effect of MPA on lymphocyte proliferation is reversed by addition to culture media of deoxyguanosine or guanosine but not by addition of deoxyadenosine or adenosine. The findings suggest that the principal mechanism of action of low concentrations of MPA is depletion of deoxyguanosine triphosphate which is required for DNA synthesis. In immunosuppressive doses, MPA does not affect the formation of IL-1 by LPS-activated human peripheral blood monocytes. Unlike cyclosporin A and FK-506, MPA does not inhibit the formation of IL-2 and the expression of the IL-2 receptor in mitogen-activated human T lymphocytes. MPA suppresses mixed lymphocyte reactions when added 3 days after their initiation. These findings suggest that MPA does not inhibit early responses of T and B lymphocytes to mitogenic or antigenic stimulation but blocks the cells at the time of DNA synthesis. The cytostatic effect of MPA is more potent on lymphocytes than on other cell types, such as fibroblasts and endothelial cells. MPA also inhibits antibody formation by polyclonally activated human B lymphocytes. MPA is an immunosuppressive agent reversibly inhibiting proliferation of T and B lymphocytes and antibody formation, with a profile of activity different from that of other immunosuppressive drugs. Human T and B lymphocytic and promonocytic cell lines are highly sensitive to the antiproliferative effects of MPA, whereas the erythroid precursor cell line K562 is less susceptible. The effect of MPA on cells of the monocyte-macrophage lineage could exert long-acting anti-inflammatory activity. MPA or analogues may have therapeutic utility in diseases such as rheumatoid arthritis, for prevention of allograft rejection and in lymphocytic or monocytic leukaemias and lymphomas.

Description

Mycophenolic acid (Mycophenolate) is an an immunosuppresant drug and has potent anti-proliferative activity.

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