Gentamicin is an antibiotic of the aminoglycoside group, is derived by the growth of Micromonospora purpurea, an actinomycete. Gentamicin is a complex of three different closely related aminoglycoside sulfates, Gentamicins C1, C2, and C1a. Gentamicin is a broad-spectrum antibiotic, but may cause ear and kidney damage. Gentamicin binds to the prokaryotic ribosome, inhibiting protein synthesis in susceptible bacteria. It is bactericidal in vitro against Gram-positive and Gram-negative bacteria. Adverse reactions include adverse renal effects, neurotoxicity (dizziness, vertigo, tinnitus, roaring in the ears, hearing loss, peripheral neuropathy or encephalopathy), respiratory depression, lethargy, confusion, depression, visual disturbances, etc.

Colistimethate is a methanesulfonate of polymyxin antibacterial colistin. Colistimethate is a nonactive prodrug. In aqueous solutions, colistimethate is hydrolyzed and forms a complex mixture of partially sulfomethylated derivatives and colistin. The antimicrobial activity of colistin is similar to that of polymyxin B and is restricted to gram-negative bacteria, including P aeruginosa, Acinetobacter species, Enterobacter-Klebsiella tribe, Escherichia coli, Salmonella and Shigella species, Citrobacter species, Yersinia pseudotuberculosis, Morganella morganii and Haemophilus influenzae. Colistin has also been shown to possess considerable in vitro activity against Stenotrophomonas maltophilia. Colistin and polymyxin B, however, do not have activity against Proteus, Providencia, Serratia species, Pseudomonas mallei, Burkholderia cepacia, Brucella species, most gram-positive bacteria, gram-negative cocci, anaerobes, fungi and parasites. Parenteral or nebulized colistimethate is indicated for the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli. It is particularly indicated when the infection is caused by sensitive strains of Pseudomonas aeruginosa.

Neomycin is an aminoglycoside antibiotic found in many topical medications such as creams, ointments, and eye drops. In vitro tests have demonstrated that neomycin is bactericidal and acts by inhibiting the synthesis of protein in susceptible bacterial cells. It is effective primarily against gram-negative bacilli but does have some activity against gram-positive organisms. Neomycin is active in vitro against Escherichia coli and the Klebsiella-Entero. Topical uses include treatment for superficial eye infections caused by susceptible bacteria (used in combination with other anti-infective), treatment of otitis externa caused by susceptible bacteria, treatment or prevention of bacterial infections in skin lesions, and use as a continuous short-term irrigant or rinse to prevent bacteriuria and gram negative rod bacteremia in bacteriuria patients with indwelling catheters. May be used orally to treat hepatic encephalopathy, as a perioperative prophylactic agent, and as an adjunct to fluid and electrolyte replacement in the treatment of diarrhea caused to enter pathogenic E. coli (EPEC). Neomycin sulfate has been shown to be effective adjunctive therapy in hepatic coma by reduction of the ammonia forming bacteria in the intestinal tract. The subsequent reduction in blood ammonia has resulted in neurologic improvement. To reduce the development of drug-resistant bacteria and maintain the effectiveness of Neomycin Sulfate Oral Solution and other antibacterial drugs, susceptible bacteria should use Neomycin Sulfate Oral Solution only to treat or prevent infections that are proven or strongly suspected to be caused. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. Neomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site near 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

Magnesium diamide is used as a chemical intermediate. Magnesium diamide is spontaneously combustible. It is toxic by inhalation. Skin or eye contact may cause severe burns.

Gonadorelin is a synthetic decapeptide prepared using solid phase peptide synthesis. GnRH is responsible for the release of follicle stimulating hormone and leutinizing hormone from the anterior pitutitary. In the pituitary GnRH stimulates synthesis and release of FSH and LH, a process that is controlled by the frequency and amplitude of GnRH pulses, as well as the feedback of androgens and estrogens. The pulsatility of GnRH secretion has been seen in all vertebrates, and it is necessary to ensure a correct reproductive function. Thus a single hormone, GnRH, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male. Its short half life requires infusion pumps for its clinical use. Gonadorelin is used for the treatment of amenorrhea, delayed puberty, and infertility the administration of gonadorelin is used to simulate the physiologic release of GnRH from the hypothalamus in treatment of delayed puberty, treatment of infertility caused by hypogonadotropic hypogonadism, and induction of ovulation in those women with hypothalamic amenorrhea. This results in increased levels of pituitary gonadotropins LH and FSH, which subsequently stimulate the gonads to produce reproductive steroids.

Sulfomyxin is an antibacterial sulfonamide. It is intended for use in chickens and turkeys as an aid in the treatment of disease caused or complicated by E. coli, such as colibacillosis and complicated chronic respiratory disease.

Gonadorelin is a synthetic decapeptide prepared using solid phase peptide synthesis. GnRH is responsible for the release of follicle stimulating hormone and leutinizing hormone from the anterior pitutitary. In the pituitary GnRH stimulates synthesis and release of FSH and LH, a process that is controlled by the frequency and amplitude of GnRH pulses, as well as the feedback of androgens and estrogens. The pulsatility of GnRH secretion has been seen in all vertebrates, and it is necessary to ensure a correct reproductive function. Thus a single hormone, GnRH, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male. Its short half life requires infusion pumps for its clinical use. Gonadorelin is used for the treatment of amenorrhea, delayed puberty, and infertility the administration of gonadorelin is used to simulate the physiologic release of GnRH from the hypothalamus in treatment of delayed puberty, treatment of infertility caused by hypogonadotropic hypogonadism, and induction of ovulation in those women with hypothalamic amenorrhea. This results in increased levels of pituitary gonadotropins LH and FSH, which subsequently stimulate the gonads to produce reproductive steroids.

Gonadorelin is a synthetic decapeptide prepared using solid phase peptide synthesis. GnRH is responsible for the release of follicle stimulating hormone and leutinizing hormone from the anterior pitutitary. In the pituitary GnRH stimulates synthesis and release of FSH and LH, a process that is controlled by the frequency and amplitude of GnRH pulses, as well as the feedback of androgens and estrogens. The pulsatility of GnRH secretion has been seen in all vertebrates, and it is necessary to ensure a correct reproductive function. Thus a single hormone, GnRH, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male. Its short half life requires infusion pumps for its clinical use. Gonadorelin is used for the treatment of amenorrhea, delayed puberty, and infertility the administration of gonadorelin is used to simulate the physiologic release of GnRH from the hypothalamus in treatment of delayed puberty, treatment of infertility caused by hypogonadotropic hypogonadism, and induction of ovulation in those women with hypothalamic amenorrhea. This results in increased levels of pituitary gonadotropins LH and FSH, which subsequently stimulate the gonads to produce reproductive steroids.

Hyaluronic acid (HA) is a high molecular weight biopolysacharide, discovered in 1934, by Karl Meyer and his assistant, John Palmer in the vitreous of bovine eyes. Hyaluronic acid is a naturally occurring biopolymer, which has important biological functions in bacteria and higher animals including humans. It is found in most connective tissues and is particularly concentrated in synovial fluid, the vitreous fluid of the eye, umbilical cords and chicken combs. It is naturally synthesized by a class of integral membrane proteins called hyaluronan synthases, and degraded by a family of enzymes called hyaluronidases. Hyaluronan synthase enzymes synthesize large, linear polymers of the repeating disaccharide structure of hyaluronan by alternating addition of glucuronic acid and N-acetylglucosamine to the growing chain using their activated nucle¬otide sugars (UDP – glucuronic acid and UDP-N-acetlyglucosamine) as substrates. The number of repeat disaccharides in a completed hyaluronan molecule can reach 10 000 or more, a molecular mass of ~4 million daltons (each disaccharide is ~400 daltons). The average length of a disaccharide is ~1 nm. Thus, a hyaluronan molecule of 10 000 repeats could ex¬tend 10 μm if stretched from end to end, a length approximately equal to the diameter of a human erythrocyte. Although the predominant mechanism of HA is unknown, in vivo, in vitro, and clinical studies demonstrate various physiological effects of exogenous HA. Hyaluronic acid possesses a number of protective physiochemical functions that may provide some additional chondroprotective effects in vivo and may explain its longer term effects on articular cartilage. Hyaluronic acid can reduce nerve impulses and nerve sensitivity associated with pain. In experimental osteoarthritis, this glycosaminoglycan has protective effects on cartilage. Exogenous HA enhances chondrocyte HA and proteoglycan synthesis, reduces the production and activity of proinflammatory mediators and matrix metalloproteinases, and alters the behavior of immune cells. In addition to its function as a passive structural molecule, hyaluronan also acts as a signaling molecule by interacting with cell surface receptors and regulating cell proliferation, migration, and differentiation. Hyaluronan is essential for embryogenesis and is likely also important in tumorigenesis. HA plays several important organizational roles in the extracellular matrix (ECM) by binding with cells and other components through specific and nonspecific interactions. Hyaluronan-binding pro¬teins are constituents of the extracellular matrix, and stabilize its integrity. Hyaluronan receptors are involved in cellular signal transduction; one receptor family includes the binding proteins aggrecan, link protein, versican and neurocan and the receptors CD44, TSG6, GHAP and LYVE-1. The chondroprotective effects of hyaluronic acid, e.g., that it stimulates the production of tissue in¬hibitors of matrix metalloproteineses (TIMP-1) by chondrocytes, inhibits neutrophil-mediated cartilage degradation and attenuates IL-1 induced matrix de¬generation and chondrocyte cytotoxicity have been observed in vitro. Articular chondrocytes cultured in the presence of HA have a significantly greater rate of DNA proliferation and ex¬tracellular matrix production, compared with chon¬drocytes cultured without HA.