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Status:
US Approved Rx
(1998)
Source:
ANDA064210
(1998)
Source URL:
First approved in 1946
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Streptomycin is a water-soluble aminoglycoside derived from Streptomyces griseus. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like Streptomycin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically Streptomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.
Streptomycin is indicated for the treatment of tuberculosis. May also be used in combination with other drugs to treat tularemia (Francisella tularensis), plague (Yersia pestis), severe M. avium complex, brucellosis, and enterococcal endocarditis (e.g. E. faecalis, E. faecium).
Status:
US Approved Rx
(2019)
Source:
ANDA211455
(2019)
Source URL:
First approved in 1946
Source:
METHERGINE by EDISON THERAPS LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Methylergometrine (other names include methylergonovine, methylergobasin, methergine, and D-lysergic acid 1-butanolamide) is a synthetic analogue of ergonovine, a psychedelic alkaloid found in ergot, and many species of morning glory. In general, the effects of all the ergot alkaloids appear to results from their actions as partial agonists or antagonists at adrenergic, dopaminergic, and tryptaminergic receptors. The spectrum of effects depends on the agent, dosage, species, tissue, and experimental or physiological conditions. All of the alkaloids of ergot significantly increase the motor activity of the uterus. After small doses contractions are increased in force or frequency, or both, but are followed by a normal degree of relaxation. As the dose is increased, contractions become more forceful and prolonged, resting tonus is markedly increased, and sustained contracture can result. Methylergometrine acts directly on the smooth muscle of the uterus and increases the tone, rate, and amplitude of rhythmic contractions through binding and the resultant antagonism of the dopamine D1 receptor. Thus, it induces a rapid and sustained tetanic uterotonic effect which shortens the third stage of labor and reduces blood loss. Methylergometrine is used for the prevention and control of excessive bleeding following vaginal childbirth.
Status:
US Approved Rx
(2019)
Source:
ANDA211455
(2019)
Source URL:
First approved in 1946
Source:
METHERGINE by EDISON THERAPS LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Methylergometrine (other names include methylergonovine, methylergobasin, methergine, and D-lysergic acid 1-butanolamide) is a synthetic analogue of ergonovine, a psychedelic alkaloid found in ergot, and many species of morning glory. In general, the effects of all the ergot alkaloids appear to results from their actions as partial agonists or antagonists at adrenergic, dopaminergic, and tryptaminergic receptors. The spectrum of effects depends on the agent, dosage, species, tissue, and experimental or physiological conditions. All of the alkaloids of ergot significantly increase the motor activity of the uterus. After small doses contractions are increased in force or frequency, or both, but are followed by a normal degree of relaxation. As the dose is increased, contractions become more forceful and prolonged, resting tonus is markedly increased, and sustained contracture can result. Methylergometrine acts directly on the smooth muscle of the uterus and increases the tone, rate, and amplitude of rhythmic contractions through binding and the resultant antagonism of the dopamine D1 receptor. Thus, it induces a rapid and sustained tetanic uterotonic effect which shortens the third stage of labor and reduces blood loss. Methylergometrine is used for the prevention and control of excessive bleeding following vaginal childbirth.
Status:
US Approved Rx
(2018)
Source:
ANDA207264
(2018)
Source URL:
First approved in 1946
Source:
D.H.E. 45 by BAUSCH
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dihydroergotamine (DHE) is a semisynthetic, hydrogenated ergot alkaloid,
synthesized by reducing an unsaturated bond in ergotamine. Dihydroergotamine was originally envisaged as an antihypertensive agent, but it was later shown to be highly effective in treating migraine.
Dihydroergotamine was first used to treat migraine in 1945 by Horton, Peters, and Blumenthal at the Mayo Clinic. In 1986, Raskin and Callaham reconfirmed
the effectiveness of DHE for both intermittent and intractable migraine. The use of DHE was reviewed by Scott in 1992. In 1997, a nasal spray
version was approved for use in migraine. Dihydroergotamine is indicated for the acute treatment of migraine headaches with or without aura and the acute treatment of cluster headache episodes. Dihydroergotamine binds with high affinity to 5-HT1Dα and 5-HT1Dβ receptors. It also binds with high
affinity to serotonin 5-HT1A, 5-HT2A, and 5-HT2C receptors, noradrenaline α2A, α2B and α, receptors, and dopamine D2L and D3 receptors.
The therapeutic activity of dihydroergotamine in migraine is generally attributed to the agonist effect at 5-HT1D receptors. Two current theories have been proposed to explain the efficacy of 5-HT1D receptor agonists in migraine. One theory suggests that activation of 5-HT1D receptors located on
intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache. The alternative hypothesis suggests that activation of
5-HT1D receptors on sensory nerve endings of the trigeminal system results in the inhibition of proinflammatory neuropeptide release.
Status:
US Approved Rx
(2009)
Source:
ANDA065448
(2009)
Source URL:
First approved in 1943
Class (Stereo):
CHEMICAL (ABSOLUTE)
Penicillin G, also known as benzylpenicillin, is a penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. Microbiology Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Neisseria meningitidis. Other organisms susceptible in vitro to penicillin G are Neisseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible. Adverse effects can include hypersensitivity reactions including urticaria, fever, joint pains, rashes, angioedema, anaphylaxis, serum sickness-like reaction.
Status:
US Approved Rx
(1943)
Source:
NDA005378
(1943)
Source URL:
First approved in 1943
Source:
NDA005378
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
DL-Methamphetamine (also known as +/- Methamphetamin) is a central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed. Methamphetamine is a mixture of two isomers. One isomer called Dextro, or D Methamphetamine, is active as a central nervous system stimulant and it is a DEA Schedule 2 controlled drug commonly called “Meth” or “Speed”. Desoxyn, a prescription drug also contains D Methamphetamine. The other isomer, Levo, or L Methamphetamine is not a DEA controlled drug. It is found in an over the counter medicine called “Vicks Inhaler” or as the prescription drug, Selegiline. (+)-methamphetamine is the more physiologically active isomer. In addition to some medications, L Methamphetamine can be produced in the illegal production of street Methamphetamine.
Status:
US Approved Rx
(2009)
Source:
ANDA065448
(2009)
Source URL:
First approved in 1943
Class (Stereo):
CHEMICAL (ABSOLUTE)
Penicillin G, also known as benzylpenicillin, is a penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. Microbiology Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Neisseria meningitidis. Other organisms susceptible in vitro to penicillin G are Neisseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible. Adverse effects can include hypersensitivity reactions including urticaria, fever, joint pains, rashes, angioedema, anaphylaxis, serum sickness-like reaction.
Status:
US Approved Rx
(2009)
Source:
ANDA065448
(2009)
Source URL:
First approved in 1943
Class (Stereo):
CHEMICAL (ABSOLUTE)
Penicillin G, also known as benzylpenicillin, is a penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. Microbiology Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Neisseria meningitidis. Other organisms susceptible in vitro to penicillin G are Neisseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible. Adverse effects can include hypersensitivity reactions including urticaria, fever, joint pains, rashes, angioedema, anaphylaxis, serum sickness-like reaction.
Status:
US Approved Rx
(2009)
Source:
ANDA065448
(2009)
Source URL:
First approved in 1943
Class (Stereo):
CHEMICAL (ABSOLUTE)
Penicillin G, also known as benzylpenicillin, is a penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. Microbiology Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Neisseria meningitidis. Other organisms susceptible in vitro to penicillin G are Neisseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible. Adverse effects can include hypersensitivity reactions including urticaria, fever, joint pains, rashes, angioedema, anaphylaxis, serum sickness-like reaction.
Status:
US Approved Rx
(2018)
Source:
ANDA207509
(2018)
Source URL:
First approved in 1943
Source:
HYCODAN by GENUS
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Benzhydrocodone is a prodrug of hydrocodone. Benzhydrocodone is formed by covalently bonding hydrocodone to benzoic acid. Benzhydrocodone itself is not pharmacologically active, but must be metabolized to hydrocodone by enzymes in the intestinal tract to optimally deliver its pharmacologic effects. Hydrocodone is a full agonist of the opioid receptors with a higher affinity for the mu-opioid receptor. Upon binding, hydrocodone produces an analgesic effect with no ceiling. APADAZ a combination of benzhydrocodone and acetaminophen is FDA approved and indicated for the short-term (no more than 14 days) management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. APADAZ, even when taken as recommended, can result in addiction, abuse, and misuse, which can lead to overdose and death.