Trimetrexate
Folic Acid Antagonists
Quinazolines
Pteroylpolyglutamic Acids
Tetrahydrofolate Dehydrogenase
Deoxyuridine
Methotrexate
Thymidine Monophosphate
Phosphoribosyl Pyrophosphate
Thymidylate Synthase
Sodium Azide
Drug Resistance
Folic Acid
Phosphoribosylglycinamide Formyltransferase
Drug Evaluation
Glucuronates
Structure and dynamics in solution of the complex of Lactobacillus casei dihydrofolate reductase with the new lipophilic antifolate drug trimetrexate. (1/95)
We have determined the three-dimensional solution structure of the complex of Lactobacillus casei dihydrofolate reductase and the anticancer drug trimetrexate. Two thousand seventy distance, 345 dihedral angle, and 144 hydrogen bond restraints were obtained from analysis of multidimensional NMR spectra recorded for complexes containing 15N-labeled protein. Simulated annealing calculations produced a family of 22 structures fully consistent with the constraints. Several intermolecular protein-ligand NOEs were obtained by using a novel approach monitoring temperature effects of NOE signals resulting from dynamic processes in the bound ligand. At low temperature (5 degrees C) the trimethoxy ring of bound trimetrexate is flipping sufficiently slowly to give narrow signals in slow exchange, which give good NOE cross peaks. At higher temperature these broaden and their NOE cross peaks disappear thus allowing the signals in the lower-temperature spectrum to be identified as NOEs involving ligand protons. The binding site for trimetrexate is well defined and this was compared with the binding sites in related complexes formed with methotrexate and trimethoprim. No major conformational differences were detected between the different complexes. The 2,4-diaminopyrimidine-containing moieties in the three drugs bind essentially in the same binding pocket and the remaining parts of their molecules adapt their conformations such that they can make effective van der Waals interactions with essentially the same set of hydrophobic amino acids, the side-chain orientations and local conformations of which are not greatly changed in the different complexes (similar chi1 and chi2 values). (+info)Safety and efficacy of using a single agent or a phase II agent before instituting standard combination chemotherapy in previously untreated metastatic breast cancer patients: report of a randomized study--Cancer and Leukemia Group B 8642. (2/95)
PURPOSE: We undertook a prospective, randomized phase III trial to evaluate the safety and efficacy of using a phase II agent before initiating therapy with standard combination chemotherapy in metastatic breast cancer patients. PATIENTS AND METHODS: A total of 365 women with measurable metastatic breast cancer, previously untreated with chemotherapy for their metastatic disease, were randomized to receive either immediate chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil (CAF) or up to four cycles of one of five sequential cohorts of single-agent drugs: trimetrexate, melphalan, amonafide, carboplatin, or elsamitrucin, followed by CAF. RESULTS: The toxicity of each single agent followed by CAF was comparable to that of CAF alone. The cumulative response rates for the single agent followed by CAF were not statistically different from those of CAF alone (44% v 52%; P = .24). However, in the multivariate analysis, patients with visceral disease had a trend toward lower response rates on the phase II agent plus CAF arm (P = .078). Although survival and response duration also were not statistically significantly different between the two study arms (P = .074 and P = .069, respectively), there was a suggestion of benefit for the CAF-only arm. CONCLUSION: The brief use of a phase II agent, regardless of its efficacy, followed by CAF resulted in response rates, toxicities, durations of response, and survival statistically equivalent to those seen with the use of CAF alone. These findings support the use of a new paradigm for the evaluation of phase II agents in the treatment of patients with metastatic breast cancer. (+info)Circumvention of methotrexate resistance in childhood leukemia subtypes by rationally designed antifolates. (3/95)
Cellular methotrexate (MTX) resistance may cause treatment failure in childhood common/preB-acute lymphoblastic leukemia (c/preB-ALL), T-lineage ALL (T-ALL), and acute myeloid leukemia (AML). The ex vivo potency of several antifolates (MTX, trimetrexate [TMQ], GW1843U89, multitargeted antifolate [MTA], Raltitrexed, and ZD9331) was studied via in situ inhibition of thymidylate synthase (TS). After short-term exposure, relapsed c/preB-ALL (rALL, n = 21), T-ALL (n = 22), and AML (n = 22) were 3-fold, 10-fold, and 6-fold less sensitive to MTX (P +info)Clustering of mutations in the first transmembrane domain of the human reduced folate carrier in GW1843U89-resistant leukemia cells with impaired antifolate transport and augmented folate uptake. (4/95)
We have studied the molecular basis for the resistance of human CEM leukemia cells to GW1843, a thymidylate synthase inhibitor. GW1843-resistant cells displayed a approximately 100-fold resistance to GW1843 and methotrexate but were collaterally sensitive to the lipophilic antifolates trimetrexate and AG337, which enter cells by diffusion. These cells exhibited a 12-fold decreased methotrexate influx but surprisingly had a 2-fold decreased folic acid growth requirement. This was associated with a 4-fold increased influx of folic acid, a 3.5-fold increased steady-state level of folic acid, and a 2.3-fold expansion of the cellular folate pool. Characterization of the transport kinetic properties revealed that GW1843-resistant cells had the following alterations: (a) 11-fold decreased transport K(m) for folic acid; (b) 6-fold increased transport K(m) for GW1843; and (c) a slightly increased transport V(max) for folic acid. Sequence analysis showed that GW1843-resistant cells contained the mutations Val-29 --> Leu, Glu-45 --> Lys, and Ser-46 --> Ile in the first transmembrane domain of the reduced folate carrier. Transfection of the mutant-reduced folate carrier cDNA into methotrexate transport null cells conferred resistance to GW1843. This is the first demonstration of multiple mutations in a confined region of the human reduced folate carrier in an antifolate-resistant mutant. We conclude that certain amino acid residues in the first transmembrane domain play a key role in (anti)folate binding and in the conferring of drug resistance. (+info)Retroviral vectors containing a variant dihydrofolate reductase gene for drug protection and in vivo selection of hematopoietic cells. (5/95)
Transfer of drug resistance genes to hematopoietic cells is being studied as a means to protect against the myelosuppression associated with cancer chemotherapy and as a strategy for the in vivo selection and amplification of genetically modified cells. The goal of this study was to test if retroviral-mediated gene transfer of a dihydrofolate reductase (DHFR) variant (L22Y) could be used for in vivo selection of transduced myeloid cells and to determine what proportion of transduced cells was required for protection from myelosuppression. Based on previous work suggesting that selection with antifolates may also require inhibition of nucleoside transport mechanisms, mice transplanted with DHFR-transduced bone marrow cells were treated with trimetrexate and the nucleoside transport inhibitor prodrug nitrobenzylmercaptopurine riboside phosphate. In vivo selection of transduced myeloid progenitors was seen in the bone marrow and in circulating mature peripheral blood cells following drug treatment. These results show that the novel combination of the L22Y-DHFR cDNA, trimetrexate and nitrobenzylmercaptopurine riboside phosphate can be used to select for transduced myeloid cells, and that this approach warrants further study in large animal models. A bicistronic vector containing a human CD24 reporter gene was used to determine the number of modified cells needed for chemoprotection. Partial protection from neutropenia was seen when greater than 10% of myeloid cells expressed the vector, and high levels of protection were obtained when the proportion exceeded 30%. These results suggest that gene transfer may be useful for myeloprotection in certain pediatric cancers, but that more efficient gene transfer will be required to apply this approach to adult cancer patients. (+info)Sequence-dependent enhancement of cytotoxicity produced by ecteinascidin 743 (ET-743) with doxorubicin or paclitaxel in soft tissue sarcoma cells. (6/95)
Ecteinascidin 743 (ET-743) is a potent antitumor agent from the Caribbean tunicate Ecteinascidin turbinata and is presently in clinical trials for human cancers. To better understand how ET-743 might be used clinically, the present study used SRB assays to examine the cytotoxicity resulting from combining ET-743 with three other antineoplastic agents: doxorubicin (DXR), trimetrexate, and paclitaxel in different administration schedules in two soft tissue sarcoma cell lines, HT-1080 and HS-18, in vitro. Concurrent exposure of ET-743 with DXR resulted in synergistic interactions in both cell lines. Addition of ET-743 for 24 h before DXR was the most effective cytotoxic regimen against both cell lines. Morphological study by fluorescence microscopy revealed that combination treatment of both cells with ET-743 and DXR induced apoptosis. Exposure to paclitaxel before ET-743 was also an effective regimen. These results encourage studies of the combination of ET-743 and DXR in the treatment of soft tissue sarcoma, because each of these agents have activity in this disease. (+info)In vivo selection of antifolate-resistant transgenic hematopoietic stem cells in a murine bone marrow transplant model. (7/95)
Currently, low levels of stable gene transfer into hematopoietic tissues of large animals and humans continues to limit the clinical application of gene therapy. One strategy for overcoming this problem is to selectively expand, in vivo, the population of successfully gene-modified cells. Recent work has shown that nucleoside transport inhibition in combination with antifolates can be used to select in vivo for hematopoietic stem cells expressing drug-resistant dihydrofolate reductase (DHFR). In this study we investigated whether trimetrexate (TMTX) and the nucleoside transport inhibitor prodrug nitrobenzylmercaptopurine ribose phosphate (NBMPR-P) can be used to select for tyr22-variant DHFR expressing transgenic hematopoietic cells in a murine bone marrow transplant model. Our results indicate that 40 mg/kg TMTX and 20 mg/kg NBMPR-P can be used in combination to expand transgene-positive progenitor cells 3- to 4-fold immediately following drug administration. In addition, long-term progenitor populations were expanded 2- to 3-fold in primary recipients, to approximately 5 months following drug administration. Secondary transplants conducted with marrow from primary recipients 5 months following drug administration revealed a statistically significant selective expansion of transgene-positive cells in the spleens and peripheral blood of these animals. No such expansion was observed in groups of mice treated with TMTX alone or NBMPR-P alone. We conclude that TMTX + NBMPR-P can be used to selectively expand transgenic tyr22-variant DHFR expressing murine hematopoietic stem cells in vivo. (+info)A double-blind placebo-controlled randomized phase III trial of 5-fluorouracil and leucovorin, plus or minus trimetrexate, in previously untreated patients with advanced colorectal cancer. (8/95)
BACKGROUND: Trimetrexate (TMTX) biochemically modulates 5-fluorouracil (5-FU) and leucovorin (LCV). Two phase II trials demonstrated promising activity for TMTX/5-FU/LCV in patients with untreated advanced colorectal cancer (ACC). This trial was designed to demonstrate the safety and efficacy of TMTX/5-FU/LCV as first-line treatment in ACC. PATIENTS AND METHODS: Eligible patients with ACC were randomized in double-blind fashion to receive placebo or TMTX (110 mg/m2) intravenously (i.v.) followed 24 h later by i.v. LCV 200 mg/m2, and 5-FU 500 mg/m2 plus oral LCV rescue. Both schedules were given weekly for 6 weeks every 8 weeks. Patients were evaluated for progression-free survival (PFS), overall survival (OS), tumor response, quality of life (QoL) and toxicity. RESULTS: A total of 382 eligible patients were randomized. Significant toxicities were noted more frequently with TMTX/5-FU/LCV. Diarrhea was the most common grade 3 or 4 side-effect (41% and 28% on the TMTX and placebo arms, respectively). QoL scores and response rates did not differ between treatment arms. PFS was 5.3 months and 4.4 months in the TMTX and placebo arms, respectively (P = 0.77; Wilcoxon). OS was 15.8 months and 16.8 months, respectively (P = 0.73; Wilcoxon). CONCLUSIONS: The addition of TMTX to a weekly regimen of 5-FU/LCV worsened grade 3 or 4 diarrhea. The inclusion of TMTX did not yield any significant improvements in response rate, PFS or OS. (+info)Trimetrexate is a antifolate drug, which means it interferes with the use of folic acid in the body. It is primarily used in the treatment of certain types of cancer and parasitic infections. Trimetrexate works by blocking the action of an enzyme called dihydrofolate reductase, which is necessary for the production of DNA and RNA, the genetic material found in cells. By inhibiting this enzyme, trimetrexate can help to stop the growth and multiplication of cancer cells or parasites.
In medical terms, Trimetrexate is classified as an antineoplastic agent and an antiprotozoal agent. It may be used to treat certain types of cancer such as non-Hodgkin's lymphoma, and it may also be used to treat parasitic infections caused by Pneumocystis jirovecii (formerly known as Pneumocystis carinii) in patients with weakened immune systems.
It is important to note that Trimetrexate can have significant side effects and should only be used under the close supervision of a healthcare provider.
Folic acid antagonists are a class of medications that work by inhibiting the action of folic acid or its metabolic pathways. These drugs are commonly used in the treatment of various types of cancer and certain other conditions, such as rheumatoid arthritis. They include drugs such as methotrexate, pemetrexed, and trimetrexate.
Folic acid is a type of B vitamin that is essential for the production of DNA and RNA, the genetic material found in cells. Folic acid antagonists work by interfering with the enzyme responsible for converting folic acid into its active form, tetrahydrofolate. This interference prevents the formation of new DNA and RNA, which is necessary for cell division and growth. As a result, these drugs can inhibit the proliferation of rapidly dividing cells, such as cancer cells.
It's important to note that folic acid antagonists can also affect normal, non-cancerous cells in the body, particularly those that divide quickly, such as cells in the bone marrow and digestive tract. This can lead to side effects such as anemia, mouth sores, and diarrhea. Therefore, these drugs must be used carefully and under the close supervision of a healthcare provider.
Quinazolines are not a medical term per se, but they are a class of organic compounds that have been widely used in the development of various pharmaceutical drugs. Therefore, I will provide you with a chemical definition of quinazolines:
Quinazolines are heterocyclic aromatic organic compounds consisting of a benzene ring fused to a pyrazine ring. The structure can be represented as follows:
Quinazoline
They are often used as building blocks in the synthesis of various drugs, including those used for treating cancer, cardiovascular diseases, and microbial infections. Some examples of FDA-approved drugs containing a quinazoline core include the tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva), which are used to treat non-small cell lung cancer, and the calcium channel blocker verapamil (Calan, Isoptin), which is used to treat hypertension and angina.
Pteroylpolyglutamic acids are forms of folic acid that are composed of multiple glutamic acid molecules linked together in a chain. This compound is also known as polyglutamated folate or folylpolyglutamates. The length of the glutamic acid chain can vary, and these compounds are often found naturally in foods such as leafy green vegetables, fruits, and dried beans.
In the body, pteroylpolyglutamic acids must be converted to the active form of folate, called tetrahydrofolate, before they can participate in various metabolic processes, including DNA synthesis and methylation reactions. Some people may have difficulty absorbing or converting these compounds due to genetic factors or certain medical conditions, which can lead to folate deficiency and related health problems.
It's worth noting that supplemental forms of folic acid are typically in the form of a single glutamate molecule (pteroylmonoglutamic acid) and may not be as effective at raising folate levels in the body as the polyglutamated forms found in food. However, the monoglutamate form is more easily absorbed and utilized by the body, making it a common choice for supplementation.
Tetrahydrofolate dehydrogenase (EC 1.5.1.20) is an enzyme involved in folate metabolism. The enzyme catalyzes the oxidation of tetrahydrofolate (THF) to dihydrofolate (DHF), while simultaneously reducing NADP+ to NADPH.
The reaction can be summarized as follows:
THF + NADP+ -> DHF + NADPH + H+
This enzyme plays a crucial role in the synthesis of purines and thymidylate, which are essential components of DNA and RNA. Therefore, any defects or deficiencies in tetrahydrofolate dehydrogenase can lead to various medical conditions, including megaloblastic anemia and neural tube defects during fetal development.
Deoxyuridine is a chemical compound that is a component of DNA. It is a nucleoside, which means it consists of a sugar (deoxyribose) linked to a nitrogenous base (uracil). In the case of deoxyuridine, the uracil is not methylated, which differentiates it from thymidine.
Deoxyuridine can be converted into deoxyuridine monophosphate (dUMP) by the enzyme thymidine kinase. The dUMP can then be converted into deoxythymidine triphosphate (dTTP), which is a building block of DNA, through a series of reactions involving other enzymes.
Deoxyuridine has been used in research and medicine as a marker for DNA synthesis and repair. It can also be used to inhibit the growth of certain types of cells, such as cancer cells, by disrupting their DNA synthesis.
Methotrexate is a medication used in the treatment of certain types of cancer and autoimmune diseases. It is an antimetabolite that inhibits the enzyme dihydrofolate reductase, which is necessary for the synthesis of purines and pyrimidines, essential components of DNA and RNA. By blocking this enzyme, methotrexate interferes with cell division and growth, making it effective in treating rapidly dividing cells such as cancer cells.
In addition to its use in cancer treatment, methotrexate is also used to manage autoimmune diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. In these conditions, methotrexate modulates the immune system and reduces inflammation.
It's important to note that methotrexate can have significant side effects and should be used under the close supervision of a healthcare provider. Regular monitoring of blood counts, liver function, and kidney function is necessary during treatment with methotrexate.
Thymidine Monophosphate (TMP or dTMP) is a nucleotide that is a ester of phosphoric acid with thymidine, a nucleoside consisting of deoxyribose sugar linked to the nitrogenous base thymine. It is one of the four monophosphate nucleotides that are the building blocks of DNA, along with adenosine monophosphate (AMP), guanosine monophosphate (GMP), and cytidine monophosphate (CMP). TMP plays a crucial role in DNA replication and repair processes. It is also used as a marker in biochemical research and medical diagnostics.
Phosphoribosyl Pyrophosphate (PRPP) is defined as a key intracellular nucleotide metabolite that plays an essential role in the biosynthesis of purine and pyrimidine nucleotides, which are the building blocks of DNA and RNA. PRPP is synthesized from ribose 5-phosphate and ATP by the enzyme PRPP synthase. It contributes a phosphoribosyl group in the conversion of purines and pyrimidines to their corresponding nucleotides, which are critical for various cellular processes such as DNA replication, repair, and gene expression. Abnormal levels of PRPP have been implicated in several genetic disorders, including Lesch-Nyhan syndrome and PRPP synthetase superactivity.
Thymidylate synthase (TS) is an essential enzyme in the metabolic pathway for DNA synthesis and repair. It catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is a crucial building block for DNA replication and repair. This reaction also involves the methylation of dUMP using a methyl group donated by N5,N10-methylenetetrahydrofolate, resulting in the formation of dihydrofolate as a byproduct. The regeneration of dihydrofolate to tetrahydrofolate is necessary for TS to continue functioning, making it dependent on the folate cycle. Thymidylate synthase inhibitors are used in cancer chemotherapy to interfere with DNA synthesis and replication, leading to cytotoxic effects in rapidly dividing cells.
Sodium azide is a chemical compound with the formula NaN3. Medically, it is not used as a treatment, but it can be found in some pharmaceutical and laboratory settings. It is a white crystalline powder that is highly soluble in water and has a relatively low melting point.
Sodium azide is well known for its ability to release nitrogen gas upon decomposition, which makes it useful as a propellant in airbags and as a preservative in laboratory settings to prevent bacterial growth. However, this property also makes it highly toxic to both animals and humans if ingested or inhaled, as it can cause rapid respiratory failure due to the release of nitrogen gas in the body. Therefore, it should be handled with great care and appropriate safety measures.
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
Tetrahydrofolates (THFs) are a type of folate, which is a form of vitamin B9. Folate is essential for the production and maintenance of new cells, especially in DNA synthesis and methylation. THFs are the active forms of folate in the body and are involved in various metabolic processes, including:
1. The conversion of homocysteine to methionine, an amino acid required for protein synthesis and the formation of S-adenosylmethionine (SAM), a major methyl donor in the body.
2. The transfer of one-carbon units in various metabolic reactions, such as the synthesis of purines and pyrimidines, which are essential components of DNA and RNA.
3. The remethylation of homocysteine to methionine, a process that helps maintain normal homocysteine levels in the body. Elevated homocysteine levels have been linked to an increased risk of cardiovascular disease.
THFs can be obtained from dietary sources, such as leafy green vegetables, legumes, and fortified cereals. They can also be synthesized endogenously in the body through the action of the enzyme dihydrofolate reductase (DHFR), which reduces dihydrofolate (DHF) to THF using NADPH as a cofactor.
Deficiencies in folate or impaired THF metabolism can lead to various health issues, including megaloblastic anemia, neural tube defects during fetal development, and an increased risk of cardiovascular disease due to elevated homocysteine levels.
Folic acid is the synthetic form of folate, a type of B vitamin (B9). It is widely used in dietary supplements and fortified foods because it is more stable and has a longer shelf life than folate. Folate is essential for normal cell growth and metabolism, and it plays a critical role in the formation of DNA and RNA, the body's genetic material. Folic acid is also crucial during early pregnancy to prevent birth defects of the brain and spine called neural tube defects.
Medical Definition: "Folic acid is the synthetic form of folate (vitamin B9), a water-soluble vitamin involved in DNA synthesis, repair, and methylation. It is used in dietary supplementation and food fortification due to its stability and longer shelf life compared to folate. Folic acid is critical for normal cell growth, development, and red blood cell production."
Phosphoribosylglycinamide formyltransferase (PGTF) is an enzyme involved in the biosynthesis of purine nucleotides, which are essential components of DNA and RNA. The systematic medical definition of PGTF is:
"An enzyme that catalyzes the transfer of a formyl group from 10-formyltetrahydrofolate to the amino group of phosphoribosylglycinamide, forming N-formylphosphoribosylglycinamide and tetrahydrofolate as byproducts. This reaction is the fourth step in the de novo synthesis pathway of purine nucleotides."
PGTF's gene name is GART (Glycinamide Ribonucleotide Transformylase), and it is located on human chromosome 10q24.32-q25.1. Mutations in the GART gene can lead to a rare autosomal recessive disorder called Lesch-Nyhan syndrome, which is characterized by hyperuricemia, neurological symptoms, and self-mutilating behavior.
"Drug evaluation" is a medical term that refers to the systematic process of assessing the pharmacological, therapeutic, and safety profile of a drug or medication. This process typically involves several stages, including preclinical testing in the laboratory, clinical trials in human subjects, and post-marketing surveillance.
The goal of drug evaluation is to determine the efficacy, safety, and optimal dosage range of a drug, as well as any potential interactions with other medications or medical conditions. The evaluation process also includes an assessment of the drug's pharmacokinetics, or how it is absorbed, distributed, metabolized, and eliminated by the body.
The findings from drug evaluations are used to inform regulatory decisions about whether a drug should be approved for use in clinical practice, as well as to provide guidance to healthcare providers about how to use the drug safely and effectively.
Glucuronates are not a medical term per se, but they refer to salts or esters of glucuronic acid, a organic compound that is a derivative of glucose. In the context of medical and biological sciences, glucuronidation is a common detoxification process in which glucuronic acid is conjugated to a wide variety of molecules, including drugs, hormones, and environmental toxins, to make them more water-soluble and facilitate their excretion from the body through urine or bile.
The process of glucuronidation is catalyzed by enzymes called UDP-glucuronosyltransferases (UGTs), which are found in various tissues, including the liver, intestines, and kidneys. The resulting glucuronides can be excreted directly or further metabolized before excretion.
Therefore, "glucuronates" can refer to the chemical compounds that result from this process of conjugation with glucuronic acid, as well as the therapeutic potential of enhancing or inhibiting glucuronidation for various clinical applications.
Polyglutamic acid (PGA) is not a medical term per se, but it is a term used in biochemistry and cosmetics. Medically, it may be mentioned in the context of certain medical conditions or treatments. Here's a definition:
Polyglutamic acid is a polymer of glutamic acid, a type of amino acid. It is a natural substance found in various foods such as natto, a traditional Japanese fermented soybean dish. In the human body, it is produced by certain bacteria during fermentation processes.
PGA has been studied for its potential medical applications due to its unique properties, including its ability to retain moisture and form gels. It has been explored as a wound dressing material, drug delivery vehicle, and anti-aging cosmetic ingredient. However, it is not a widely used or recognized medical treatment at this time.
Trimetrexate - Wikipedia
Trimetrexate (NeuTrexin) | Davis's Drug Guide
Trimetrexate ‹ Ingredient - Unilexicon for medicines
Trimetrexate (Neutrexin) | HemOnc.org - A Hematology Oncology Wiki
DailyMed - KETOCONAZOLE tablet
Melanoma - HealthWell Foundation
CanMED: HCPCS
ITRACAP - MyDr.com.au
Medimmune Oncology Inc Product News and Research
| CureHunter
SPORANOX - Drug Information from Guideline Central
Infections After Hematopoietic Stem Cell Transplantation: Overview, Risk Factors for Infection, Assessment of Infection Risk in...
Parasites: Using Prescription Drugs Against Parasites Description
Pharmaceutical Preparations | DrugBank Online
Gdlns. Prev. Opportunistic Infections in Persons Infected w/ HIV
Intrinsic resistance to methotrexate in human soft tissue sarcoma cell lines.
US Patent for Cysteine engineered anti-MUC16 antibodies and antibody drug conjugates Patent (Patent # 7,723,485 issued May 25,...
Severe folate restriction results in depletion of and alteration in the composition of the intracellular folate pool, moderate...
Daktarin Oral Gel 15g | Medicines | Buy Online at TravelPharm
Hypothesis