4-AMINOSALICYLIC ACID (Paser) is an anti-tuberculosis drug used to treat tuberculosis in combination with other active agents. 4-AMINOSALICYLIC ACID (Paser) is most commonly used in patients with Multi-drug Resistant TB (MDR-TB) or when isoniazid and rifampin use is not possible due to a combination of resistance and/or intolerance. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in the folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slow. Secondly, the aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.

4-AMINOSALICYLIC ACID (Paser) is an anti-tuberculosis drug used to treat tuberculosis in combination with other active agents. 4-AMINOSALICYLIC ACID (Paser) is most commonly used in patients with Multi-drug Resistant TB (MDR-TB) or when isoniazid and rifampin use is not possible due to a combination of resistance and/or intolerance. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in the folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slow. Secondly, the aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.

4-AMINOSALICYLIC ACID (Paser) is an anti-tuberculosis drug used to treat tuberculosis in combination with other active agents. 4-AMINOSALICYLIC ACID (Paser) is most commonly used in patients with Multi-drug Resistant TB (MDR-TB) or when isoniazid and rifampin use is not possible due to a combination of resistance and/or intolerance. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in the folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slow. Secondly, the aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.

4-AMINOSALICYLIC ACID (Paser) is an anti-tuberculosis drug used to treat tuberculosis in combination with other active agents. 4-AMINOSALICYLIC ACID (Paser) is most commonly used in patients with Multi-drug Resistant TB (MDR-TB) or when isoniazid and rifampin use is not possible due to a combination of resistance and/or intolerance. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against Mycobacterium tuberculosis. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in the folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slow. Secondly, the aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.

Thiamine, also known as vitamin B1, plays a key role in the human metabolism. It is present in many dietary sources such as meats, eggs, fish, beans and peas, nuts, and whole grains. Upon administration thiamine is converted by thiamine pyrophosphokinase-1 (TPK1) to the active form, thiamine pyrophosphate, which serves as a cofactor for enzymes involved in the TCA cycle and the non-oxidative part of the pentose phosphate pathway. The lack of thiamine may cause the thiamine deficiency. The classical syndrome caused primarily by thiamine deficiency in humans is beriberi, however, symptoms of thiamine deficiency also include congestive heart failure, metabolic acidosis, confusion, ataxia and seizures. Thiamine is a component of many vitamin complexes, which are approved for the treatmen and prevention of general vitamin deficiency, including the thiamine deficiency.

Thiamine, also known as vitamin B1, plays a key role in the human metabolism. It is present in many dietary sources such as meats, eggs, fish, beans and peas, nuts, and whole grains. Upon administration thiamine is converted by thiamine pyrophosphokinase-1 (TPK1) to the active form, thiamine pyrophosphate, which serves as a cofactor for enzymes involved in the TCA cycle and the non-oxidative part of the pentose phosphate pathway. The lack of thiamine may cause the thiamine deficiency. The classical syndrome caused primarily by thiamine deficiency in humans is beriberi, however, symptoms of thiamine deficiency also include congestive heart failure, metabolic acidosis, confusion, ataxia and seizures. Thiamine is a component of many vitamin complexes, which are approved for the treatmen and prevention of general vitamin deficiency, including the thiamine deficiency.

Methadone, sold under the brand names Dolophine among others, is an synthetic opioid that is used as the hydrochloride to treat pain and as maintenance therapy or to help with detoxification in people with opioid dependence. Methadone hydrochloride is a mu-agonist; a synthetic opioid analgesic with multiple actions qualitatively similar to those of morphine. Some data also indicate that methadone acts as an antagonist at the NMDA-receptor. The contribution of NMDA receptor antagonism to methadone’s efficacy is unknown. Most common adverse reactions are: lightheadedness, dizziness, sedation, nausea, vomiting, and sweating. Avoid use mixed agonist/antagonist and partial agonist opioid analgesics with DOLOPHINE because they may reduce analgesic effect of DOLOPHINE or precipitate withdrawal symptoms.

Thiamine, also known as vitamin B1, plays a key role in the human metabolism. It is present in many dietary sources such as meats, eggs, fish, beans and peas, nuts, and whole grains. Upon administration thiamine is converted by thiamine pyrophosphokinase-1 (TPK1) to the active form, thiamine pyrophosphate, which serves as a cofactor for enzymes involved in the TCA cycle and the non-oxidative part of the pentose phosphate pathway. The lack of thiamine may cause the thiamine deficiency. The classical syndrome caused primarily by thiamine deficiency in humans is beriberi, however, symptoms of thiamine deficiency also include congestive heart failure, metabolic acidosis, confusion, ataxia and seizures. Thiamine is a component of many vitamin complexes, which are approved for the treatmen and prevention of general vitamin deficiency, including the thiamine deficiency.

Thiamine, also known as vitamin B1, plays a key role in the human metabolism. It is present in many dietary sources such as meats, eggs, fish, beans and peas, nuts, and whole grains. Upon administration thiamine is converted by thiamine pyrophosphokinase-1 (TPK1) to the active form, thiamine pyrophosphate, which serves as a cofactor for enzymes involved in the TCA cycle and the non-oxidative part of the pentose phosphate pathway. The lack of thiamine may cause the thiamine deficiency. The classical syndrome caused primarily by thiamine deficiency in humans is beriberi, however, symptoms of thiamine deficiency also include congestive heart failure, metabolic acidosis, confusion, ataxia and seizures. Thiamine is a component of many vitamin complexes, which are approved for the treatmen and prevention of general vitamin deficiency, including the thiamine deficiency.

Methadone, sold under the brand names Dolophine among others, is an synthetic opioid that is used as the hydrochloride to treat pain and as maintenance therapy or to help with detoxification in people with opioid dependence. Methadone hydrochloride is a mu-agonist; a synthetic opioid analgesic with multiple actions qualitatively similar to those of morphine. Some data also indicate that methadone acts as an antagonist at the NMDA-receptor. The contribution of NMDA receptor antagonism to methadone’s efficacy is unknown. Most common adverse reactions are: lightheadedness, dizziness, sedation, nausea, vomiting, and sweating. Avoid use mixed agonist/antagonist and partial agonist opioid analgesics with DOLOPHINE because they may reduce analgesic effect of DOLOPHINE or precipitate withdrawal symptoms.