Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
Antimetabolites that are useful in cancer chemotherapy.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.
An inhibitor of nucleotide metabolism.
Any surgical procedure for treatment of glaucoma by means of puncture or reshaping of the trabecular meshwork. It includes goniotomy, trabeculectomy, and laser perforation.
Inosine 5'-Monophosphate. A purine nucleotide which has hypoxanthine as the base and one phosphate group esterified to the sugar moiety.
The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.
A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.
Leukemia L1210 is a designation for a specific murine (mouse) leukemia cell line that was originally isolated from a female mouse with an induced acute myeloid leukemia, which is widely used as a model in cancer research, particularly for in vivo studies of drug efficacy and resistance.
An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Inhibitors of the enzyme, dihydrofolate reductase (TETRAHYDROFOLATE DEHYDROGENASE), which converts dihydrofolate (FH2) to tetrahydrofolate (FH4). They are frequently used in cancer chemotherapy. (From AMA, Drug Evaluations Annual, 1994, p2033)
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
The action of a drug in promoting or enhancing the effectiveness of another drug.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Deoxycytidine is a nucleoside consisting of the pentose sugar deoxyribose linked to the nitrogenous base cytosine, which plays a crucial role in DNA replication and repair processes within cells.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
Established cell cultures that have the potential to propagate indefinitely.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
The rate dynamics in chemical or physical systems.
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
Phospholipids which have an alcohol moiety in ethereal linkage with a saturated or unsaturated aliphatic alcohol. They are usually derivatives of phosphoglycerols or phosphatidates. The other two alcohol groups of the glycerol backbone are usually in ester linkage. These compounds are widely distributed in animal tissues.
A cell line derived from cultured tumor cells.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Pyrido-CARBAZOLES originally discovered in the bark of OCHROSIA ELLIPTICA. They inhibit DNA and RNA synthesis and have immunosuppressive properties.
A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72.
A group of 20-member macrolactones in which there are three remotely substituted pyran rings that are linked by a methylene bridge and an E-disubstituted alkene, and have geminal dimethyls at C8 and C18 carbons. Some interact with PROTEIN KINASE C.
Thiadiazines are heterocyclic compounds containing a 5-membered ring made up of two nitrogen atoms and three carbon atoms, one of which is bonded to a sulfur atom, and are known for their diverse pharmacological properties, including use as anti-inflammatory, anticonvulsant, and antipsychotic agents.

Is early post-operative treatment with 5-fluorouracil possible without affecting anastomotic strength in the intestine? (1/3345)

Early post-operative local or systemic administration of 5-fluorouracil (5-FU) is under investigation as a means to improve outcome after resection of intestinal malignancies. It is therefore quite important to delineate accurately its potentially negative effects on anastomotic repair. Five groups (n = 24) of rats underwent resection and anastomosis of both ileum and colon: a control group and four experimental groups receiving daily 5-FU, starting immediately after operation or after 1, 2 or 3 days. Within each group, the drug (or saline) was delivered either intraperitoneally (n = 12) or intravenously (n = 12). Animals were killed 7 days after operation and healing was assessed by measurement of anastomotic bursting pressure, breaking strength and hydroxyproline content. In all cases, 5-FU treatment from the day of operation or from day 1 significantly (P<0.025) and severely suppressed wound strength; concomitantly, the anastomotic hydroxyproline content was reduced. Depending on the location of the anastomosis and the route of 5-FU administration, even a period of 3 days between operation and first dosage seemed insufficient to prevent weakening of the anastomosis. The effects of intravenous administration, though qualitatively similar, were quantitatively less dramatic than those observed after intraperitoneal delivery. Post-operative treatment with 5-FU, if started within the first 3 days after operation, is detrimental to anastomotic strength and may compromise anastomotic integrity.  (+info)

Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (2/3345)

Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency.  (+info)

Dihydropyrimidine dehydrogenase deficiency and fluorouracil-related toxicity. (3/3345)

Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. We report lymphocytic DPD data concerning a group of 53 patients (23 men, 30 women, mean age 58, range 36-73), treated by 5-FU-based chemotherapy in different French institutions and who developed unanticipated 5-FU-related toxicity. Lymphocyte samples (standard collection procedure) were sent to us for DPD determination (biochemical method). Among the whole group of 53 patients, 19 had a significant DPD deficiency (DD; below 150 fmol min(-1) mg(-1) protein, i.e. less than 70% of the mean value observed from previous population study). There was a greater majority of women in the DD group (15 out of 19, 79%) compared with the remaining 34 patients (15 out of 34, 44%, P<0.014). Toxicity was often severe, leading to patient death in two cases (both women). The toxicity score (sum of WHO grading, theoretical range 0-20) was twice as high in patients with marked DD (below 100 pmol min(-1) mg(-1) protein, n = 11, mean score = 13.2) compared with patients with moderate DD (between 150 and 100 pmol min(-1) mg(-1) protein, n = 8, mean score = 6.8), P = 0.008. In the DD group, there was a high frequency of neurotoxic syndromes (7 out of 19, 37%). The two deceased patients both had severe neurotoxicity. The occurrence of cardiac toxicity was relatively rare (1 out of 19, 5%). These data suggest that women are particularly prone to DPD deficiency and allow a more precise definition of the DD toxicity profile.  (+info)

[3H]gemcitabine uptake by nucleoside transporters in a human head and neck squamous carcinoma cell line. (4/3345)

Cellular uptake of many chemotherapeutic nucleoside analogs is dependent on the activity of a family of nucleoside transport proteins located in the cell plasma membrane. In the present study, we examined the role of these transporters in the accumulation of gemcitabine by a human head and neck squamous carcinoma cell line. The uptake of [3H]gemcitibine was compared with that of [3H]uridine and [3H]formycin B in the parent cell line (HN-5a) and in a gemcitabine-resistant variant (GEM-8e). The HN-5a and GEM-8e cells were similar in their transport characteristics and expressed predominantly the es (equilibrative, inhibitor-sensitive) transporter subtype; less than 10% of the influx of [3H]formycin B or [3H]uridine was mediated by the ei (equilibrative inhibitor-resistant) system, and there was no evidence for Na+-dependent nucleoside transporters. [3H]Gemcitabine (10 microM) entered these cells via both the es and ei transporters with an initial rate of uptake similar to that seen with the use of [3H]formycin B or [3H]uridine. In addition, ATP-replete cells accumulated significantly less [3H]gemcitabine than did ATP-depleted cells, which is indicative of an active efflux mechanism for gemcitabine. These results show that gemcitabine is a substrate for both the es and ei nucleoside transporters of HN-5a and GEM-8e cells and that gemcitabine resistance of the GEM-8e cells cannot be attributed to changes in transporter activity. Further studies to define the characteristics of the putative efflux mechanism are clearly warranted because this system has the potential to significantly affect the clinical efficacy of gemcitabine.  (+info)

Modulation of the cytotoxicity of 3'-azido-3'-deoxythymidine and methotrexate after transduction of folate receptor cDNA into human cervical carcinoma: identification of a correlation between folate receptor expression and thymidine kinase activity. (5/3345)

Cervical carcinoma is an AIDS-defining illness. The expression of folate receptors (FRs) in cervical carcinoma (HeLa-IU1) cells was modulated by stable transduction of FR cDNA encapsidated in recombinant adeno-associated virus-2 in the sense and antisense orientation (sense and antisense cells, respectively). Although sense cells proliferated slower than antisense or untransduced cells in vivo and in vitro in 2% (but not 10%) FCS, [methyl-3H]thymidine incorporation into DNA was significantly increased in sense cells in 10% serum; therefore, the basis for this discrepancy was investigated. The activity of thymidine kinase (TK) was subsequently directly correlated with the extent of FR expression in single cell-derived clones of transduced cells. This elevated TK activity was not a result of recruitment of the salvage pathway based on the presence of adequate dTTP pools, normal thymidylate synthase (TS) activity, persistence of increased thymidine incorporation despite the exogenous provision of excess 5,10-methylene-tetrahydrofolate, and documentation of adequate folates in sense cells. The increase in TK activity conferred significant biological properties to sense cells (but not antisense or untransduced cells) as demonstrated by augmented phosphorylation of 3'-azido-3'-deoxythymidine (AZT) and concomitantly greater sensitivity to the cytotoxic effects of AZT. Conversely, sense cells were highly resistant to methotrexate, but this was reversed by the addition of AZT. The direct correlation of FR expression and TK activity indicates a previously unrecognized consequence of FR overexpression.  (+info)

Role of folylpolyglutamate synthetase and folylpolyglutamate hydrolase in methotrexate accumulation and polyglutamylation in childhood leukemia. (6/3345)

Inefficient polyglutamylation is a mechanism of resistance to methotrexate (MTX) in childhood T-lineage acute lymphoblastic leukemia (T-ALL) and in acute myeloid leukemia (AML) in comparison with childhood c/preB-ALL. We analyzed the profile of MTX polyglutamylation in childhood c/preB-ALL, T-ALL, and AML (n = 45, 15, and 14, respectively), the activity of the MTX-polyglutamate synthesizing enzyme folylpolyglutamate synthetase (FPGS) (n = 39, 11, and 19, respectively) and of the MTX-polyglutamate breakdown enzyme folylpolyglutamate hydrolase (FPGH) (n = 98, 25, and 34, respectively). MTX-Glu4-6 accumulation after 24 hours exposure to 1 micromol/L [3H]-MTX in vitro was lower in T-ALL (threefold) and AML (fourfold) compared with c/preB-ALL (P +info)

Phase I study of eniluracil, a dihydropyrimidine dehydrogenase inactivator, and oral 5-fluorouracil with radiation therapy in patients with recurrent or advanced head and neck cancer. (7/3345)

5-Fluorouracil (5-FU) is an effective enhancer of radiation therapy (RT) in head and neck cancers. Due to rapid, predominantly hepatic metabolism by dihydropyrimidine dehydrogenase (DPD) and suggested clinical benefit from prolonged drug exposure, 5-FU is commonly given by continuous infusion. Eniluracil is a novel DPD-inactivator designed to prolong the half-life of 5-FU and provide sustained plasma concentrations of 5-FU with oral dosing. We conducted a Phase I study of the safety and efficacy of eniluracil given with oral 5-FU in patients receiving concurrent RT for recurrent or advanced squamous cell carcinomas of the head and neck. Thirteen patients with recurrent, metastatic, or high-risk (defined as an expected 2-year survival rate of <10%) head and neck cancer were enrolled and treated with concomitant chemoradiotherapy on an every-other-week schedule. Eniluracil at a fixed dose [20 mg twice a day (BID)] was given for 7 consecutive days (days 1-7). 5-FU and RT were given on 5 consecutive days (days 2-6). One patient was treated with once-daily RT (2.0 Gy fractions). The remaining patients received hyperfractionated RT (1.5-Gy fractions BID). The initial dose of 5-FU was 2.5 mg/m2 given BID. Dose escalation in patient cohorts was scheduled at 2.5-mg/m2 increments, with intrapatient dose escalation permitted. Lymphocyte DPD activity and serum 5-FU and uracil concentrations were monitored during two cycles. DPD activity was completely or nearly completely inactivated in all patients. Sustained, presumed therapeutic concentrations of 5-FU were observed at a dose of 5.0 mg/m2 given BID. Cumulative dose-limiting myelosuppression (both neutropenia and thrombocytopenia) was observed during the fourth and fifth cycles following administration of 5.0 mg/m2 5-FU BID. One patient died of neutropenic sepsis during cycle 4. Other late cycle toxicities included diarrhea, fatigue, and mucositis. Grade 3 mucositis was observed in 4 patients, but no grade 4 mucositis or grade 3 or 4 dermatitis was observed. A second patient death occurred during cycle 1 of treatment. No specific cause of death was identified. The study was subsequently discontinued. Cumulative myelosupression was the significant dose-limiting toxicity of oral 5-FU given with the DPD-inactivator eniluracil on an every-other-week schedule. Clinical radiation sensitization was not observed, based on the absence of dose-limiting mucositis and dermatitis. Alternative dosing schedules need to be examined to determine the most appropriate use of eniluracil and 5-FU as radiation enhancers.  (+info)

Colorectal liver metastasis thymidylate synthase staining correlates with response to hepatic arterial floxuridine. (8/3345)

We assessed whether intensity of colorectal liver metastasis staining with the thymidylate synthase (TS) antibody TS106 predicted response to hepatic arterial infusion (HAI) of floxuridine chemotherapy. Liver metastasis biopsies were taken during laparotomy for hepatic arterial cannulation and stained using the TS106 monoclonal antibody. Staining intensity was designated at histological examination by two independent assessors as either "high" or "low." Patients were treated by HAI, and liver metastasis response was assessed by comparison of computed tomography scan tumor volume before and after 4 months of treatment. A significant correlation (Fisher's exact test, P = 0.01) was noted between partial response to HAI and TS106 staining intensity in patients with colorectal liver metastases. Seventy-five percent of patients with evidence of a partial response had low TS staining compared with 29% of nonresponders. There was a significant difference (Fisher's exact test, P = 0.01) in the proportion of low (9 of 16) compared with high (3 of 20) TS staining tumors in which a partial response occurred. There was no significant difference (logrank test, P = 0.4) in survival from hepatic cannulation and HAI treatment of high (median, 322 days; interquartile range, 236-411) compared with low (median, 335 days; interquartile range, 301-547) TS staining patients. This study demonstrates an inverse correlation between TS immunohistochemical staining intensity in colorectal liver metastases and response to HAI. The results suggest that a prospective assessment of TS staining intensity in colorectal liver metastases would be useful to determine whether this method can be used to define patients who will benefit from HAI chemotherapy.  (+info)

Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.

Antimetabolites are a class of antineoplastic (chemotherapy) drugs that interfere with the metabolism of cancer cells and inhibit their growth and proliferation. These agents are structurally similar to naturally occurring metabolites, such as amino acids, nucleotides, and folic acid, which are essential for cellular replication and growth. Antimetabolites act as false analogs and get incorporated into the growing cells' DNA or RNA, causing disruption of the normal synthesis process, leading to cell cycle arrest and apoptosis (programmed cell death).

Examples of antimetabolite drugs include:

1. Folate antagonists: Methotrexate, Pemetrexed
2. Purine analogs: Mercaptopurine, Thioguanine, Fludarabine, Cladribine
3. Pyrimidine analogs: 5-Fluorouracil (5-FU), Capecitabine, Cytarabine, Gemcitabine

These drugs are used to treat various types of cancers, such as leukemias, lymphomas, breast, ovarian, and gastrointestinal cancers. Due to their mechanism of action, antimetabolites can also affect normal, rapidly dividing cells in the body, leading to side effects like myelosuppression (decreased production of blood cells), mucositis (inflammation and ulceration of the gastrointestinal tract), and alopecia (hair loss).

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

Floxuridine is a chemotherapeutic antimetabolite medication that is primarily used in the treatment of colon cancer. It is a fluorinated pyrimidine nucleoside analogue, which means it is similar in structure to the building blocks of DNA and RNA, and can be incorporated into these molecules during cell division, disrupting their normal function and preventing cell replication.

Floxuridine works by inhibiting the enzyme thymidylate synthase, which is necessary for the synthesis of thymidine, a nucleoside that is essential for DNA replication. By blocking this enzyme, floxuridine can prevent the growth and proliferation of cancer cells.

Floxuridine is often used in combination with other chemotherapy drugs as part of a treatment regimen for colon cancer. It may be administered intravenously or via continuous infusion, depending on the specific treatment plan. As with all chemotherapy drugs, floxuridine can have significant side effects, including nausea, vomiting, diarrhea, and myelosuppression (suppression of bone marrow function), which can lead to anemia, neutropenia, and thrombocytopenia.

Tetrahydrouridine (THU) is not a medication itself, but rather a metabolic inhibitor. It is a derivative of the nucleoside uridine and has been studied in the context of its ability to inhibit the enzyme cytidine deaminase. This enzyme is responsible for the breakdown of certain antiviral medications, such as zidovudine (AZT) and stavudine (d4T), which are used in the treatment of HIV infection.

By inhibiting cytidine deaminase, THU can help to increase the levels and effectiveness of these antiviral drugs, while also reducing some of their side effects. However, it is important to note that THU is not currently approved for use as a medication by itself and is typically used in research or experimental settings in combination with other antiretroviral therapies.

A trabeculectomy is a surgical procedure performed on the eye to treat glaucoma, an eye condition characterized by increased pressure within the eye that can lead to optic nerve damage and vision loss. The main goal of this operation is to create a new channel for the aqueous humor (the clear fluid inside the eye) to drain out, thus reducing the intraocular pressure (IOP).

During the trabeculectomy procedure, a small flap is made in the sclera (the white part of the eye), and a piece of the trabecular meshwork (a structure inside the eye that helps regulate the flow of aqueous humor) is removed. This opening allows the aqueous humor to bypass the obstructed drainage system and form a bleb, a small blister-like sac on the surface of the eye, which absorbs the fluid and reduces IOP.

The success of trabeculectomy depends on various factors, including the patient's age, type and severity of glaucoma, previous treatments, and overall health. Potential complications may include infection, bleeding, cataract formation, hypotony (abnormally low IOP), or failure to control IOP. Regular follow-up appointments with an ophthalmologist are necessary to monitor the eye's response to the surgery and manage any potential issues that may arise.

Inosine monophosphate (IMP) is a nucleotide that plays a crucial role in the metabolic pathways of energy production and purine synthesis in cells. It is an ester of the nucleoside inosine and phosphoric acid. IMP is an important intermediate in the conversion of adenosine monophosphate (AMP) to guanosine monophosphate (GMP) in the purine nucleotide cycle, which is critical for maintaining the balance of purine nucleotides in the body. Additionally, IMP can be converted back to AMP through the action of the enzyme adenylosuccinate lyase. IMP has been studied for its potential therapeutic benefits in various medical conditions, including neurodegenerative disorders and ischemia-reperfusion injury.

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.

Fluorouracil is a antineoplastic medication, which means it is used to treat cancer. It is a type of chemotherapy drug known as an antimetabolite. Fluorouracil works by interfering with the growth of cancer cells and ultimately killing them. It is often used to treat colon, esophageal, stomach, and breast cancers, as well as skin conditions such as actinic keratosis and superficial basal cell carcinoma. Fluorouracil may be given by injection or applied directly to the skin in the form of a cream.

It is important to note that fluorouracil can have serious side effects, including suppression of bone marrow function, mouth sores, stomach and intestinal ulcers, and nerve damage. It should only be used under the close supervision of a healthcare professional.

Leukemia L1210 is not a medical definition itself, but it refers to a specific mouse leukemia cell line that was established in 1948. These cells are a type of acute myeloid leukemia (AML) and have been widely used in cancer research as a model for studying the disease, testing new therapies, and understanding the biology of leukemia. The L1210 cell line has contributed significantly to the development of various chemotherapeutic agents and treatment strategies for leukemia and other cancers.

Mitomycin is an antineoplastic antibiotic derived from Streptomyces caespitosus. It is primarily used in cancer chemotherapy, particularly in the treatment of various carcinomas including gastrointestinal tract malignancies and breast cancer. Mitomycin works by forming cross-links in DNA, thereby inhibiting its replication and transcription, which ultimately leads to cell death.

In addition to its systemic use, mitomycin is also used topically in ophthalmology for the treatment of certain eye conditions such as glaucoma and various ocular surface disorders. The topical application of mitomycin can help reduce scarring and fibrosis by inhibiting the proliferation of fibroblasts.

It's important to note that mitomycin has a narrow therapeutic index, meaning there is only a small range between an effective dose and a toxic one. Therefore, its use should be closely monitored to minimize side effects, which can include myelosuppression, mucositis, alopecia, and potential secondary malignancies.

6-Mercaptopurine (6-MP) is a medication used primarily in the treatment of cancer, specifically acute lymphoblastic leukemia (ALL), and to prevent rejection in organ transplantation. It is an antimetabolite that works by interfering with the synthesis of DNA and RNA, thereby inhibiting cell division and growth.

6-MP is a prodrug, meaning it requires metabolic activation in the body to exert its therapeutic effects. Once absorbed, 6-MP is converted into several active metabolites, including thioguanine nucleotides (TGN), which are incorporated into DNA and RNA, leading to cytotoxicity and cell death.

Common side effects of 6-MP include nausea, vomiting, diarrhea, mouth sores, and increased susceptibility to infections. Long-term use of the medication can also lead to liver toxicity, pancreatitis, and anemia. Regular monitoring of blood counts, liver function tests, and TGN levels is necessary during treatment with 6-MP to minimize potential side effects and ensure safe and effective dosing.

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.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

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.

Purines are heterocyclic aromatic organic compounds that consist of a pyrimidine ring fused to an imidazole ring. They are fundamental components of nucleotides, which are the building blocks of DNA and RNA. In the body, purines can be synthesized endogenously or obtained through dietary sources such as meat, seafood, and certain vegetables.

Once purines are metabolized, they are broken down into uric acid, which is excreted by the kidneys. Elevated levels of uric acid in the body can lead to the formation of uric acid crystals, resulting in conditions such as gout or kidney stones. Therefore, maintaining a balanced intake of purine-rich foods and ensuring proper kidney function are essential for overall health.

Drug screening assays for antitumor agents are laboratory tests used to identify and evaluate the effectiveness of potential drugs or compounds that can inhibit the growth of tumor cells or induce their death. These assays are typically performed in vitro (in a test tube or petri dish) using cell cultures of various types of cancer cells.

The assays measure different parameters such as cell viability, proliferation, apoptosis (programmed cell death), and cytotoxicity to determine the ability of the drug to kill or inhibit the growth of tumor cells. The results of these assays can help researchers identify promising antitumor agents that can be further developed for clinical use in cancer treatment.

There are different types of drug screening assays for antitumor agents, including high-throughput screening (HTS) assays, which allow for the rapid and automated testing of a large number of compounds against various cancer cell lines. Other types of assays include phenotypic screening assays, target-based screening assays, and functional screening assays, each with its own advantages and limitations.

Overall, drug screening assays for antitumor agents play a critical role in the development of new cancer therapies by providing valuable information on the activity and safety of potential drugs, helping to identify effective treatments and reduce the time and cost associated with bringing new drugs to market.

Drug synergism is a pharmacological concept that refers to the interaction between two or more drugs, where the combined effect of the drugs is greater than the sum of their individual effects. This means that when these drugs are administered together, they produce an enhanced therapeutic response compared to when they are given separately.

Drug synergism can occur through various mechanisms, such as:

1. Pharmacodynamic synergism - When two or more drugs interact with the same target site in the body and enhance each other's effects.
2. Pharmacokinetic synergism - When one drug affects the metabolism, absorption, distribution, or excretion of another drug, leading to an increased concentration of the second drug in the body and enhanced therapeutic effect.
3. Physiochemical synergism - When two drugs interact physically, such as when one drug enhances the solubility or permeability of another drug, leading to improved absorption and bioavailability.

It is important to note that while drug synergism can result in enhanced therapeutic effects, it can also increase the risk of adverse reactions and toxicity. Therefore, healthcare providers must carefully consider the potential benefits and risks when prescribing combinations of drugs with known or potential synergistic effects.

Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.

Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.

Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.

Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.

In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.

It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.

Preclinical drug evaluation refers to a series of laboratory tests and studies conducted to determine the safety and effectiveness of a new drug before it is tested in humans. These studies typically involve experiments on cells and animals to evaluate the pharmacological properties, toxicity, and potential interactions with other substances. The goal of preclinical evaluation is to establish a reasonable level of safety and understanding of how the drug works, which helps inform the design and conduct of subsequent clinical trials in humans. It's important to note that while preclinical studies provide valuable information, they may not always predict how a drug will behave in human subjects.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Deoxycytidine is a chemical compound that is a component of DNA, one of the nucleic acids in living organisms. It is a nucleoside, consisting of the sugar deoxyribose and the base cytosine. Deoxycytidine pairs with guanine via hydrogen bonds to form base pairs in the double helix structure of DNA.

In biochemistry, deoxycytidine can also exist as a free nucleoside, not bound to other molecules. It is involved in various cellular processes related to DNA metabolism and replication. Deoxycytidine can be phosphorylated to form deoxycytidine monophosphate (dCMP), which is an important intermediate in the synthesis of DNA.

It's worth noting that while deoxycytidine is a component of DNA, its counterpart in RNA is cytidine, which contains ribose instead of deoxyribose as the sugar component.

The cell cycle is a series of events that take place in a cell leading to its division and duplication. It consists of four main phases: G1 phase, S phase, G2 phase, and M phase.

During the G1 phase, the cell grows in size and synthesizes mRNA and proteins in preparation for DNA replication. In the S phase, the cell's DNA is copied, resulting in two complete sets of chromosomes. During the G2 phase, the cell continues to grow and produces more proteins and organelles necessary for cell division.

The M phase is the final stage of the cell cycle and consists of mitosis (nuclear division) and cytokinesis (cytoplasmic division). Mitosis results in two genetically identical daughter nuclei, while cytokinesis divides the cytoplasm and creates two separate daughter cells.

The cell cycle is regulated by various checkpoints that ensure the proper completion of each phase before progressing to the next. These checkpoints help prevent errors in DNA replication and division, which can lead to mutations and cancer.

Cell division is the process by which a single eukaryotic cell (a cell with a true nucleus) divides into two identical daughter cells. This complex process involves several stages, including replication of DNA, separation of chromosomes, and division of the cytoplasm. There are two main types of cell division: mitosis and meiosis.

Mitosis is the type of cell division that results in two genetically identical daughter cells. It is a fundamental process for growth, development, and tissue repair in multicellular organisms. The stages of mitosis include prophase, prometaphase, metaphase, anaphase, and telophase, followed by cytokinesis, which divides the cytoplasm.

Meiosis, on the other hand, is a type of cell division that occurs in the gonads (ovaries and testes) during the production of gametes (sex cells). Meiosis results in four genetically unique daughter cells, each with half the number of chromosomes as the parent cell. This process is essential for sexual reproduction and genetic diversity. The stages of meiosis include meiosis I and meiosis II, which are further divided into prophase, prometaphase, metaphase, anaphase, and telophase.

In summary, cell division is the process by which a single cell divides into two daughter cells, either through mitosis or meiosis. This process is critical for growth, development, tissue repair, and sexual reproduction in multicellular organisms.

Antibiotics are a type of medication used to treat infections caused by bacteria. They work by either killing the bacteria or inhibiting their growth.

Antineoplastics, also known as chemotherapeutic agents, are a class of drugs used to treat cancer. These medications target and destroy rapidly dividing cells, such as cancer cells, although they can also affect other quickly dividing cells in the body, such as those in the hair follicles or digestive tract, which can lead to side effects.

Antibiotics and antineoplastics are two different classes of drugs with distinct mechanisms of action and uses. It is important to use them appropriately and under the guidance of a healthcare professional.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Antineoplastic agents, phytogenic, also known as plant-derived anticancer drugs, are medications that are derived from plants and used to treat cancer. These agents have natural origins and work by interfering with the growth and multiplication of cancer cells, helping to slow or stop the spread of the disease. Some examples of antineoplastic agents, phytogenic include paclitaxel (Taxol), vincristine, vinblastine, and etoposide. These drugs are often used in combination with other treatments such as surgery, radiation therapy, and other medications to provide a comprehensive approach to cancer care.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Antineoplastic agents, alkylating, are a class of chemotherapeutic drugs that work by alkylating (adding alkyl groups) to DNA, which can lead to the death or dysfunction of cancer cells. These agents can form cross-links between strands of DNA, preventing DNA replication and transcription, ultimately leading to cell cycle arrest and apoptosis (programmed cell death). Examples of alkylating agents include cyclophosphamide, melphalan, and cisplatin. While these drugs are designed to target rapidly dividing cancer cells, they can also affect normal cells that divide quickly, such as those in the bone marrow and digestive tract, leading to side effects like anemia, neutropenia, thrombocytopenia, and nausea/vomiting.

Doxorubicin is a type of chemotherapy medication known as an anthracycline. It works by interfering with the DNA in cancer cells, which prevents them from growing and multiplying. Doxorubicin is used to treat a wide variety of cancers, including leukemia, lymphoma, breast cancer, lung cancer, ovarian cancer, and many others. It may be given alone or in combination with other chemotherapy drugs.

Doxorubicin is usually administered through a vein (intravenously) and can cause side effects such as nausea, vomiting, hair loss, mouth sores, and increased risk of infection. It can also cause damage to the heart muscle, which can lead to heart failure in some cases. For this reason, doctors may monitor patients' heart function closely while they are receiving doxorubicin treatment.

It is important for patients to discuss the potential risks and benefits of doxorubicin therapy with their healthcare provider before starting treatment.

I'm sorry for any confusion, but "Leukemia P388" is not a widely recognized medical term or a specific type of leukemia. The term "P388" is often used to refer to a particular type of mouse leukemia that is commonly used in laboratory research for testing potential anti-cancer drugs.

Leukemia, in general, is a type of cancer that originates in the bone marrow and results in an overproduction of abnormal white blood cells (leukocytes). These abnormal cells crowd out the healthy cells in the bone marrow, leading to a weakened immune system and various complications.

There are many different types of leukemia, classified based on the type of white blood cell affected (myeloid or lymphocytic) and the speed of progression (acute or chronic). If you're looking for information about a specific type of leukemia, I would be happy to help if you could provide more details.

Antineoplastic combined chemotherapy protocols refer to a treatment plan for cancer that involves the use of more than one antineoplastic (chemotherapy) drug given in a specific sequence and schedule. The combination of drugs is used because they may work better together to destroy cancer cells compared to using a single agent alone. This approach can also help to reduce the likelihood of cancer cells becoming resistant to the treatment.

The choice of drugs, dose, duration, and frequency are determined by various factors such as the type and stage of cancer, patient's overall health, and potential side effects. Combination chemotherapy protocols can be used in various settings, including as a primary treatment, adjuvant therapy (given after surgery or radiation to kill any remaining cancer cells), neoadjuvant therapy (given before surgery or radiation to shrink the tumor), or palliative care (to alleviate symptoms and prolong survival).

It is important to note that while combined chemotherapy protocols can be effective in treating certain types of cancer, they can also cause significant side effects, including nausea, vomiting, hair loss, fatigue, and an increased risk of infection. Therefore, patients undergoing such treatment should be closely monitored and managed by a healthcare team experienced in administering chemotherapy.

Phospholipid ethers are a type of phospholipid in which the traditional fatty acid chains are replaced by alkyl or alkenyl groups linked to the glycerol backbone via an ether bond. They are a significant component of lipoproteins and cell membranes, particularly in archaea, where they contribute to the stability and rigidity of the membrane at extreme temperatures and pressures.

The two main types of phospholipid ethers are plasmalogens and diether lipids. Plasmalogens contain a vinyl ether bond at the sn-1 position, while diether lipids have an ether bond at both the sn-1 and sn-2 positions. These unique structures give phospholipid ethers distinct chemical and biological properties compared to conventional phospholipids with ester-linked fatty acids.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Ellipticines are a class of naturally occurring alkaloids that have been isolated from various plants, including those in the family Apocynaceae. These compounds have been found to exhibit various biological activities, including anti-cancer and anti-microbial properties.

Ellipticines have a unique chemical structure, characterized by a planar, aromatic core with two side chains that contain nitrogen atoms. This structure allows ellipticines to intercalate into DNA, disrupting its normal function and leading to cell death. As a result, ellipticines have been studied as potential anti-cancer agents, particularly for the treatment of drug-resistant cancers.

In addition to their anti-cancer properties, ellipticines have also been found to exhibit antibacterial, antifungal, and antiparasitic activities. However, further research is needed to fully understand the mechanisms behind these effects and to determine the safety and efficacy of ellipticines as therapeutic agents.

Gallium is not a medical term, but it's a chemical element with the symbol Ga and atomic number 31. It is a soft, silvery-blue metal that melts at a temperature just above room temperature. In medicine, gallium compounds such as gallium nitrate and gallium citrate are used as radiopharmaceuticals for diagnostic purposes in nuclear medicine imaging studies, particularly in the detection of inflammation, infection, and some types of cancer.

For example, Gallium-67 is a radioactive isotope that can be injected into the body to produce images of various diseases such as abscesses, osteomyelitis (bone infection), and tumors using a gamma camera. The way gallium distributes in the body can provide valuable information about the presence and extent of disease.

Therefore, while gallium is not a medical term itself, it has important medical applications as a diagnostic tool in nuclear medicine.

Bryostatins are a class of naturally occurring marine-derived macrolide lactones that have been isolated from the Bugula neritina, a species of bryozoan. These compounds have attracted significant interest in the medical community due to their potent bioactivities, particularly their ability to modulate various signaling pathways involved in cancer, inflammation, and neurological disorders.

One of the most notable properties of bryostatins is their capacity to act as protein kinase C (PKC) agonists. PKC is a family of enzymes that play critical roles in various cellular processes, including cell growth, differentiation, and apoptosis. By activating PKC, bryostatins can induce differentiation and inhibit proliferation of certain types of cancer cells, making them promising candidates for anti-cancer therapy.

In addition to their effects on PKC, bryostatins have also been shown to modulate other signaling pathways, such as the nuclear factor kappa B (NF-κB) and Akt pathways, which are involved in inflammation and cell survival. These pleiotropic effects make bryostatins interesting targets for the development of novel therapeutic strategies for a range of diseases.

Despite their promising potential, the clinical application of bryostatins has been limited by their low natural abundance and challenging chemical synthesis. Nevertheless, ongoing research efforts continue to explore new methods for large-scale production and optimization of these compounds, with the ultimate goal of harnessing their unique biological activities for medical benefit.

Thiadiazines are a class of heterocyclic compounds containing a five-membered ring with two nitrogen atoms and two sulfur atoms. In the context of pharmaceuticals, thiadiazine derivatives are commonly used as therapeutic agents, particularly in the treatment of various cardiovascular diseases.

The most well-known thiadiazine derivative is hydrochlorothiazide, which is a diuretic drug used to treat hypertension and edema associated with heart failure, liver cirrhosis, and kidney disease. Hydrochlorothiazide works by inhibiting the reabsorption of sodium and chloride ions in the distal convoluted tubule of the nephron, thereby increasing water excretion and reducing blood volume and pressure.

Other thiadiazine derivatives have been investigated for their potential therapeutic benefits, including anti-inflammatory, anticonvulsant, and antimicrobial activities. However, many of these compounds have not yet been approved for clinical use due to safety concerns or lack of efficacy.

... an antimetabolite; (Ox)aliplatin - a platinum-based alkylating antineoplastic agent. GEMOX-R regimen is a highly effective ...
... an antimetabolite; Cyclophosphamide - an alkylating antineoplastic agent from the oxazafosforine group; Mitoxantrone - a ...
... is an anthracenyl bishydrazone with anthracycline-like antineoplastic activity and an antimetabolite. Bisantrene intercalates ...
Antineoplastic+Antimetabolites at the U.S. National Library of Medicine Medical Subject Headings (MeSH) "How Chemotherapy Drugs ... An antimetabolite is a chemical that inhibits the use of a metabolite, which is another chemical that is part of normal ... Anti-metabolites also affect RNA synthesis. However, because thymidine is used in DNA but not in RNA (where uracil is used ... Antimetabolites can be used in cancer treatment, as they interfere with DNA production and therefore cell division and tumor ...
v t e v t e (Antineoplastic antimetabolites, Thymidylate synthase inhibitors, All stub articles, Biochemistry stubs, Oncology ...
... a platinum-based antineoplastic agent, which inhibits DNA repair and/or DNA synthesis; IRI - irinotecan (Camptosar), a ... a pyrimidine analog and antimetabolite which incorporates into the DNA molecule and stops DNA synthesis; OX - oxaliplatin ( ...
... a platinum-based antineoplastic agent, which inhibits DNA repair and/or DNA synthesis. The regimen emerged in 2010 as a new ... a pyrimidine analog and antimetabolite which incorporates into the DNA molecule and stops DNA synthesis; IRIN - irinotecan ( ...
Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a ... which are divided into broad categories such as alkylating agents and antimetabolites. Traditional chemotherapeutic agents act ...
Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a similar structure to the ... Antineoplastic drugs may also increase the risk of learning disabilities among children of health care workers who are exposed ... Unlike alkylating agents, anti-metabolites are cell cycle dependent. This means that they only work during a specific part of ... In the 1970s, antineoplastic (chemotherapy) drugs were identified as hazardous, and the American Society of Health-System ...
... antimetabolites, antineoplastic MeSH D27.505.954.248.147 - antimitotic agents MeSH D27.505.954.248.150 - antineoplastic agents ... antimetabolites MeSH D27.888.569.042.030 - antimetabolites, antineoplastic MeSH D27.888.569.071 - antispermatogenic agents MeSH ... antimetabolites, antineoplastic MeSH D27.505.519.217 - antioxidants MeSH D27.505.519.217.500 - free radical scavengers MeSH ... antineoplastic agents MeSH D27.505.954.248.025 - angiogenesis inhibitors MeSH D27.505.954.248.106 - antibiotics, antineoplastic ...
Antineoplastic antimetabolites, Bristol Myers Squibb, IARC Group 3 carcinogens, Wikipedia medicine articles ready to translate ... 2015). Hydroxyurea is a monohydroxyl-substituted urea (hydroxycarbamate) antimetabolite. Similar to other antimetabolite anti- ... Hydroxycarbamide is in the antineoplastic family of medications. It is believed to work by blocking the making of DNA. ... Hydroxyurea has many pharmacological applications under the Medical Subject Headings classification system: Antineoplastic ...
Cladribine, also known by its brand name Mavenclad, is a purine antimetabolite and antineoplastic drug used to reduce relapse ...
... antimetabolite - antimicrotubule agent - antimitotic agent - antineoplastic - antineoplastic antibiotic - antioxidant - ...
... an antimetabolite; (P)latinol (cisplatin), a platinum-based antineoplastic, also an alkylating antineoplastic agent. Effective ...
Official information from the package insert for purinethol: Mercaptopurine is an antimetabolite antineoplastic, as such it ... Mercaptopurine is in the thiopurine and antimetabolite family of medications. Mercaptopurine was approved for medical use in ... Specifically, Mercaptopurine is a purine antimetabolite or purine antagonist as such inhibits DNA synthesis by inhibiting the ...
In the past, antimetabolites (e.g., cytarabine, hydroxyurea), alkylating agents, interferon alfa 2b, and steroids were used as ... Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes ...
G-CSF is still included, even though the "G" is taken out of the acronym.) Amsacrine is an alkylating antineoplastic agent that ... an antimetabolite that has been proven to be the most active toward AML among various cytotoxic drugs in single-drug trials; ... an antimetabolite that, while not active toward AML, increases formation of an active cytarabine metabolite, ara-CTP, in AML ...
Matera C, Gomila AM, Camarero N, Libergoli M, Soler C, Gorostiza P (November 2018). "Photoswitchable Antimetabolite for ... Antineoplastic and immunomodulating drug stubs). ...
It shows antineoplastic activity and has been used in the treatment of acute leukemia. The compound closely resembles guanine ... Timmis, G.M.; Williams, Donald Charles (1967). "Chemotherapy of Cancer: the Antimetabolite Approach". Butterworths. University ...
... is in the antimetabolite family of medications. It is a purine analogue of guanine and works by disrupting DNA and ... The second pathway is the methylation of thioguanine to 2-amino-6-methylthiopurine, which is minimally effective as an anti-neoplastic ... One route is through the deamination by the enzyme guanine deaminase to 6-thioxanthine, which has minimal anti-neoplastic ... Baca QJ, Coen DM, Golan DE (2011). "Principles of antimicrobial and antineoplastic therapy". In Golan DE, Tashjian AH, ...
The thiopurine drugs are purine antimetabolites widely used in the treatment of acute lymphoblastic leukemia, autoimmune ... Antineoplastic and immunomodulating drug stubs). ...
Pemetrexed Pemetrexed functions as an antimetabolite. Pemetrexed inhibits thymidylate synthase, dihydrofolate reductase and ... and approved pembrolizumab in combination with pemetrexed and platinum-based antineoplastic (carboplatin or cisplatin) as first ...
It is classified as a purine analog, which is a type of antimetabolite. It mimics the nucleoside adenosine and thus inhibits ... Antineoplastic and immunomodulating drug stubs). ...
5-fluorouracil (5-FU), the nucleobase of doxifluridine, is currently an FDA-approved antimetabolite. 5-FU is normally ... Antineoplastic drugs, Nucleosides, Organofluorides, Fluoropyrimidines). ...
... is an antimetabolite of the antifolate type. It is thought to affect cancer and rheumatoid arthritis by two ... Antineoplastic and immunomodulating drugs, Benzamides, Chemotherapy, Disease-modifying antirheumatic drugs, Folates, ...
Antineoplastics, Antimetabolite. Class Summary. Antimetabolites interfere with nucleic acid synthesis and inhibit cell growth ...
Antineoplastics, Anti-HER2. Class Summary. Monoclonal antibodies are a form of drug delivery that specifically targets the ... Antineoplastics, VEGF Inhibitor. Class Summary. Vascular endothelial growth factor inhibitors reduce tumor vascularity and ... Antineoplastics, Antimicrotubular (Taxanes). Class Summary. Antimicrotubular agents inhibit cell growth and proliferation. ... Antineoplastics, Platinum Analog. Class Summary. Platinum compounds inhibit cell growth and proliferation. ...
Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the ...
Methotrexate is an antineoplastic agent that inhibits cell proliferation by destroying rapidly dividing cells. It acts as a ...
The antimetabolite gemcitabine remains part of the standard of care but shows very limited antitumor efficacy. Ataxia ... Antimetabolites, Antineoplastic / pharmacology * Antimetabolites, Antineoplastic / therapeutic use* * Carcinoma, Pancreatic ... The antimetabolite gemcitabine remains part of the standard of care but shows very limited antitumor efficacy. Ataxia ... plays a central role in safeguarding cells from replication stress and can therefore limit the efficacy of antimetabolite drug ...
Antimetabolites, Antineoplastic / adverse effects* * Antimetabolites, Antineoplastic / metabolism * Antimetabolites, ...
... an antimetabolite; (Ox)aliplatin - a platinum-based alkylating antineoplastic agent. GEMOX-R regimen is a highly effective ...
Drug Class: Antineoplastics, Antimetabolite. Medical Editor: John P. Cunha, DO, FACOEP Last updated on RxList: 11/28/2022 ... The mechanism of action of this antimetabolite is not completely characterized and may be multi-faceted. ... 1. Preventing Occupational Exposures to Antineoplastic and Other Hazardous Drugs in Health Care Settings. NIOSH Alert 2004-165. ... FLUDARA (fludarabine) FOR INJECTION is a potent antineoplastic agent with potentially significant toxic side effects. Patients ...
Antimetabolite. Antineoplastic. Flucytosine. Ancobon. Antifungal. Fluorouracil. Adrucil. Antineoplastic. Fluorouracil. Efudex. ...
Organic Compound; Organofluoride; Amide; Drug; Antimetabolite; Antimetabolite, Antineoplastic; Immunosuppressive Agent; ... It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deo xynucleotide, it ... IC50 value:;Target: Nucleoside antimetabolite/analog5-Fluorouracil is metabolized to ribonucleotides and deoxyribonucleotides, ...
A long-acting corticosteroid (glucocorticoid). In general, this drug is used more commonly for supportive care, and as an antiemetic than it is as hormone therapy. 25 times as potent as cortisol; used topically as an anti-inflammatory and administered orally in replacement therapy for adrenal insufficiency, as an anti-inflammatory and immunosuppressant in a wide variety of disorders, and as an antiemetic in cancer chemotherapy. Dexamethasone and other corticosteroids may be used to control white cell proliferation in hematopoietic diseases and would be coded as hormone therapy for lymphoid leukemia, lymphoma and multiple myeloma ...
ATC L01B: Antineoplastic agents. Antimetabolites. Tradenames. Main tradenames from several countries containing クロファラビン in its ...
L ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS. L01 ANTINEOPLASTIC AGENTS. L01B ANTIMETABOLITES. L01BC Pyrimidine analogues. ATC ...
An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. Terms. ... An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. Entry Term ... Antimetabolites, Antineoplastic. Registry Number. FTK8U1GZNX. Related Numbers. 154-42-7. 5580-03-0. 76078-67-6. WIX31ZPX66. CAS ...
An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by ...
antineoplastics. Pharm. Class.. antimetabolites. nucleoside analogues. Theres more to see -- the rest of this topic is ...
1400 ONCOLYTICS 1479 Antineoplastics, Miscellaneous 1480 Hormonal/Biological Response Mod. 1481 Antimetabolites 1482 ... ANTINEOPLASTIC AGENT 35500 ANTITHYROID AGENT 35505 ANTITUBERCULAR AGENT 35510 ANTIVIRAL AGENT 35530 BACTINE 35580 SLO-BID 35590 ...
Risk of additive immune system effects with etrasimod has not been studied in combination with antineoplastic, immune- ... Leucorvorin, reduced folates, and folate antimetabolites are substrates for glucarpidase (hydrolyzes glutamate residue from ... Risk of additive immune system effects with etrasimod has not been studied in combination with antineoplastic, immune- ... Leucorvorin, reduced folates, and folate antimetabolites are substrates for glucarpidase (hydrolyzes glutamate residue from ...
Methotrexate is an antimetabolite used in the treatment of certain neoplastic diseases, severe psoriasis, and adult rheumatoid ... Antineoplastic Agents. Class Summary. Antineoplastic agents inhibit cell growth and proliferation.. Cyclophosphamide *View full ...
Antimetabolite/Antirheumatic Antineoplastic Agent Antiparkinsonian Agent Antiparkinsonian Agent/Dopamine Agonist Antipsoriatic ...
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by ... An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by ...
Anti-metabolites (L01B). Main article: antimetabolite. Anti-metabolites masquerade as purine ((azathioprine, mercaptopurine)) ... See main article: antineoplastic The most important immunosuppressant from this group is dactinomycin, which is used in kidney ... Antimetabolites. Folic acid: (Aminopterin, Methotrexate, Pemetrexed, Raltitrexed). Purine:(Cladribine, Clofarabine, Fludarabine ... In popular usage, it usually refers to antineoplastic drugs used to treat cancer or the combination of these drugs into a ...
Pharma Action Antimetabolites, Antineoplastic ; Antiviral Agents ; Enzyme Inhibitors ; Immunosuppressive Agents ; Radiation- ... Pharma Action Antineoplastic Agents ; Enzyme Inhibitors Cancer Res 1982;42(8):2963 tobacco tar 0 *Tars Ribonucleotide ... Pharma Action Anti-Inflammatory Agents, Non-Steroidal ; Antineoplastic Agents, Phytogenic ; Antioxidants ; Enzyme Inhibitors ; ...
... and specifically to the group of antineoplastics known as antimetabolites. Hydroxyurea fights cancer by preventing the growth ... Hydroxyurea belongs to the group of cancer-fighting medications known as antineoplastics, ... and specifically to the group of antineoplastics known as antimetabolites. Hydroxyurea fights cancer by preventing the growth ... Hydroxyurea belongs to the group of cancer-fighting medications known as antineoplastics, ...
It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent ...
Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Tubulin Modulators. ... Antineoplastic Agents, Immunological. Antineoplastic Agents. Angiogenesis Inhibitors. Angiogenesis Modulating Agents. Growth ...
Keywords: Area Under Curve, Colorectal Neoplasms, Drug Monitoring, Fluorouracil, Aged, Antimetabolites, Antineoplastic, ... Antineoplastic Combined Chemotherapy Protocols, Drug Dosage Calculations, Drug-Related Side Effects and Adverse Reactions, ...
Antimetabolites, Antineoplastic - Preferred Concept UI. M0001471. Scope note. Antimetabolites that are useful in cancer ... TN 4: relation to ANTINEOPLASTIC AGENTS. Allowable Qualifiers:. AD administration & dosage. AE adverse effects. AN analysis. BL ... Antimetabolites that are useful in cancer chemotherapy.. Annotation:. ...
  • Fluorouracil is an antineoplastic anti-metabolite. (pharmacycode.com)
  • Fluorouracil Cream USP is topical preparations containing the fluorinated pyrimidine 5-fluorouracil, an antineoplastic antimetabolite. (nih.gov)
  • It is a purine nucleoside antimetabolite . (bionity.com)
  • FLUDARA (fludarabine) FOR INJECTION should be administered under the supervision of a qualified physician experienced in the use of antineoplastic therapy. (rxlist.com)
  • The antimetabolite gemcitabine remains part of the standard of care but shows very limited antitumor efficacy. (nih.gov)
  • Antineoplastic agents inhibit cell growth and proliferation. (medscape.com)
  • Antimetabolite agents are used to terminate pregnancy. (medscape.com)
  • Drugs used to manage connective tissue disease (CTD) associated with interstitial lung disease (ILD) (CTD-ILD) include nintedanib, corticosteroids, and antineoplastic agents. (medscape.com)
  • Methotrexate is an antineoplastic agent that inhibits cell proliferation by destroying rapidly dividing cells. (medscape.com)
  • Ox)aliplatin - a platinum-based alkylating antineoplastic agent. (wikipedia.org)
  • An antimetabolite antineoplastic agent with immunosuppressant properties. (online-medical-dictionary.org)
  • Azacytidine has been used as an antineoplastic agent. (umassmed.edu)
  • It is an antimetabolite and antineoplastic agent. (transparencymarketresearch.com)
  • An antineoplastic agent, it is used in the treatment of myeloid leukaemia. (pharmakb.com)
  • It has a role as an antineoplastic agent. (pharmakb.com)
  • Cisplatin is a platinum-containing compound that exerts an antineoplastic effect by covalently binding to DNA, with preferential binding to N-7 position of guanine and adenosine. (medscape.com)
  • An antineoplastic compound which also has antimetabolite action. (nih.gov)
  • Ataxia telangiectasia and Rad3-related protein (ATR), the apical kinase of the intra-S-phase DNA damage response, plays a central role in safeguarding cells from replication stress and can therefore limit the efficacy of antimetabolite drug therapies. (nih.gov)
  • In popular usage, it usually refers to antineoplastic drugs used to treat cancer or the combination of these drugs into a standardized treatment regimen . (wikidoc.org)
  • Hydroxyurea belongs to the group of cancer-fighting medications known as antineoplastics , and specifically to the group of antineoplastics known as antimetabolites . (medbroadcast.com)
  • Antimetabolites that are useful in cancer chemotherapy. (bvsalud.org)
  • The cellular kinetics of particular cancers is an important consideration in the design of antineoplastic drug regimens and may influence the dosing schedules and timing intervals of treatment. (msdmanuals.com)
  • Many antineoplastic drugs, such as antimetabolites, are most effective when cells are actively dividing. (msdmanuals.com)
  • Antineoplastic with alkylating activity. (cancer.gov)
  • Intrathecal methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in malignant cells. (medscape.com)
  • Methotrexate (MTX) is an antineoplastic antimetabolite and folic acid analogue and antagonist with antineoplastic and immunosuppressive properties from interfering with the synthesis and cellular replication of DNA. (e-lactancia.org)
  • Methotrexate is an antimetabolite, which inhibits DHFR resulting in decreased immune function and antineoplastic activity and is FDA approved for psoriasis, RA, and several cancers including choriocarcinoma, AML, lung, head and neck and epidermoid (FDA.gov). (jax.org)
  • Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and embryonic cell reproduction. (medscape.com)
  • It is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. (absource.de)
  • Hydroxyurea is an antineoplastic (anti-cancer) agent used to treat melanoma , resistant chronic myelocytic leukemia , and recurrent , metastatic, or inoperable carcinoma of the ovary and primary squamous cell (epidermoid) carcinomas of the head and neck. (rxlist.com)
  • Cytarabine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute myelogenous leukemia and meningeal leukemia. (pharmacycode.com)
  • therefore, antineoplastic agents are devoid of selective toxicity to tumour cells. (pharmacy180.com)
  • Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures. (lookformedical.com)
  • Classic antimetabolite anticancer drug with chemical structure similar to endogenous intermediates or building blocks of DNA or RNA synthesis. (medscape.com)
  • Gemcitabine belongs to the group of cancer-fighting medications known as antineoplastics , and specifically to the group of antineoplastics known as antimetabolites . (medbroadcast.com)
  • Thus, future antineoplastic treatments could combine the modulation of the microbiome and its products with immunotherapeutics and more conventional approaches that directly target malignant cells. (nature.com)
  • Doxorubicin is an anthracycline antineoplastic that causes DNA strand breakage through effects on topoisomerase II and direct intercalation into DNA, which causes DNA polymerase inhibition. (medscape.com)
  • The prominent adverse effects of antineoplastic drugs are exerted on rapidly proliferating normal tissues, in addition, to their chronic and cumulative toxicities. (pharmacy180.com)
  • It has antineoplastic properties, including inhibition of angiogenesis and induction of APOPTOSIS. (nih.gov)
  • The cellular kinetics of particular cancers is an important consideration in the design of antineoplastic drug regimens and may influence the dosing schedules and timing intervals of treatment. (msdmanuals.com)
  • Many antineoplastic drugs, such as antimetabolites, are most effective when cells are actively dividing. (msdmanuals.com)
  • Cancer cells very rapidly develop resistance to antineoplastic drugs. (pharmacy180.com)
  • An antineoplastic antimetabolite with immunosuppressant properties. (clustermed.info)
  • Bacterial products that have potential antineoplastic or immunostimulatory properties include bacterial toxins, microbial ligands of pattern recognition receptors, as well as bacterial metabolites, including butyrate, polyamines and pyridoxine. (nature.com)