Fertirelin Acetate

Fertirelin acetate is a potent LHRH agonist. After a transient increase, continuous administration results in downregulation of LH and FSH levels followed by a suppression of ovarian and testicular steroid biosynthesis.

Liraglutide

Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist used clinically to treat type 2 diabetes mellitus.

Lanreotide Acetate

Lanreotide is a a synthetic cyclic octapeptide analogue of somatostatin. Lanreotide inhibits the secretion of growth hormone (GH) by binding to pituitary somatostatin receptors, and may inhibit the release of various other hormones, including thyroid stimulating hormone (TSH) and the gastroenteropancreatic hormones insulin, glucagon and gastrin.

TETA-Octreotide acetate

Pramlintide Acetate

Pramlintide acetate is a polypeptide analogue of human amylin. Pramlintide acetate, an antidiabetic agent, is antineoplastic in colorectal cancer.

Thymosin β4 Acetate

Thymosin β4 is a 43 amino acid peptide which is regarded as the main intracellular G-actin sequestering peptide. Extracellular thymosin β4 may contribute to physiological processes such as angiogenesis, wound healing and regulation of inflammation.

Thymopentin Acetate

Thymopentin, also known as TP-5, is a synthetic derivative of thymopoietin, a thymic hormone, and has immunoregulatory properties. Thymopentin interacts with T cells, reduces endocrine and behavioral responses to experimental stress. It is also found to increase the number of cells undergoing apoptosis in irradiated cells and selectively bind to apoptotic cells.

Bivalirudin

Bivalirudin, a peptide anticoagulant, is a direct thrombin inhibitor for anticoagulation in the setting of invasive cardiology, particularly percutaneous coronary intervention.

Octreotide Acetate

Octreotide is a somatostatin analog that binds to the somatostatin receptor, mainly subtypes 2, 3, and 5, increases Gi activity, and reduces intracellular cAMP production.

Goserelin Acetate

Goserelin acetate stimulates the production of the sex hormones testosterone and estrogen in a non-pulsatile (non-physiological) manner. This causes the disruption of the endogenous hormonal feedback systems, resulting in the down-regulation of testosterone and estrogen production.