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Showing 681 - 690 of 911 results

Status:
First approved in 1964
Source:
Virac by Ruson
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)



Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.
Status:
First approved in 1964
Source:
Virac by Ruson
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)



Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.
Status:
First approved in 1964
Source:
Virac by Ruson
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)



Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.
Melphalan, also known as L-phenylalanine mustard, phenylalanine mustard, L-PAM, or L-sarcolysin, is a phenylalanine derivative of nitrogen mustard. Melphalan is a bifunctional alkylating agent which produces a number of DNA adducts with the DNA interstrand crosslink (ICL) considered to be the critical cytotoxic lesion. Melphalan is used to treat different cancers including myeloma, melanoma and ovarian cancer.
Status:
First approved in 1964
Source:
Virac by Ruson
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)



Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.
Diazepam is a benzodiazepine first discovered at Hoffman-La Roche in the late 1950s. Diazepam was approved by FDA for the treatment of anxiety disorders as well as for such conditions as skeletal muscle spasm, alcohol withdrawal syndrom and convulsions (under the most known brand Valium). The drug acts by binding to GABA-A receptors and potentiating GABA evoked current. Chronic diazepam use is associated with tolerance, dependence, and withdrawal.
Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.
Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.
Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.
Betamethasone and its derivatives, betamethasone sodium phosphate and betamethasone acetate, are synthetic glucocorticoids. Used for its antiinflammatory or immunosuppressive properties, betamethasone is combined with a mineralocorticoid to manage adrenal insufficiency and is used in the form of betamethasone benzoate, betamethasone dipropionate, or betamethasone valerate for the treatment of inflammation due to corticosteroid-responsive dermatoses. Betamethasone and clotrimazole are used together to treat cutaneous tinea infections. Betamethasone is a glucocorticoid receptor agonist. This leads to changes in genetic expression once this complex binds to the GRE. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Betamethasone binds to plasma transcortin, and it becomes active when it is not bound to transcortin.Betamethasone is used for: treating certain conditions associated with decreased adrenal gland function. It is used to treat severe inflammation caused by certain conditions, including severe asthma, severe allergies, rheumatoid arthritis, ulcerative colitis, certain blood disorders, lupus, multiple sclerosis, and certain eye and skin conditions.

Showing 681 - 690 of 911 results