Oxfenicine is a CPT-1b-specific inhibitor. It must be transaminated to its active form, 4-hydroxyphenyl-glyoxylate, which is competitive with carnitine, preventing the formation of acylcarnitine. Because CPT-1b shows the highest sensitivity to 4-hydroxyphenyl-glyoxylate, inhibition of fatty acid oxidation by oxfenicine takes place selectively in those tissues that express this CPT isoform. It may be effective for treating noninsulin-dependent diabetes mellitus which is characterized by elevated fatty acid levels and obesity. In 1980 it was also tested in preclinical models of angina pectoris and ischemia.

LTX109 is a synthetic antimicrobial agent and is a potent fungicide that disturbs plasma membrane integrity in a sphingolipid dependent manner. LTX109 was in clinical phase II trials for topical treatment of infections of multiresistant bacterial strains. However, the further development of this drug apparently has been discontinued.

Colforsin (NKH477) is a water-soluble forskolin derivative. NKH477, like forskolin, showed adenylate cyclase stimulant activity in guinea pig ventricular membrane but did not inhibit Na+, K(+)-ATPase or phosphodiesterase (PDE) activity. The compound was developed by a Japanese company Nippon Kayaku. Colforsin daropate, a prodrug of colforsin, is marketed in Japan for the treatment of acute heart failure under tradename Adehl.

Lycetamine is an antibacterial compound.

Thyroxine I-131 is a radiolabeled thyroid hormone that has been studied as a diagnostic agent for thyroid cancer. In pharmacokinetic studies, Thyroxine I-131 shows broad tissue distribution and 99% of the ingested radiolabeled Thyroxine may be found in the skin, intestines, muscles, blood, bones, liver, and thyroid glands of rats.

A radioconjugate of synthetic active thyroid hormone, liothyronine (T3), labeled with Iodine 131. Liothyronine involves many important metabolic functions and is essential to the proper development and differentiation of all cells. I131 liothyronine may be used in radiotherapy in thyroid cancers.

Thyroxine I-125 is a radiolabeled thyroid hormone that has been used for diagnostics of thyroid disease. Thyroxine is the main hormone secreted into the bloodstream by the thyroid gland. Thyroxine plays vital roles in digestion, heart and muscle function, brain development and maintenance of bones. A thyroxine test measures the level of Thyroxine in the plasma and Thyroxine I-125 was used as a radioiodine-labeled tracer for this assay. Currently Thyroxine I-125 primary use as a tracer for binding assays and other radiometric biological studies.

Betamicin is an aminoglycoside antibiotic

Puromycin dihydrochloride belongs to the aminonucleoside family of antibiotics and is isolated from Streptomyces alboniger. Since the partial structure of this antibiotic showed it to be a purine derivative, puromycin was assigned as its generic name. Puromycin is a broad spectrum antibiotic and antibacterial agent. It is active against Gram-positive microorganisms, less active against acid-fast bacilli, and weakly active against Gram-negative microorganisms. It acts very quickly and can kill 99% of the cells within 2 days. It also exhibits antitumor activity in studies on brain tumor cells. Puromycin is a protein synthesis inhibitor that causes premature chain termination by acting as an analog of the 3’-terminal end of aminoacyl-tRNA. It has been used to study transcriptional regulatory mechanisms that control the sequential and coordinate expression of genes during cell differentiation.

Ceronapril is a phosphonate angiotensin-converting enzyme inhibitor that was being developed by Bristol-Myers Squibb for the treatment of hypertension. In spontaneously hypertensive rats, Ceronapril narrowed the autoregulatory range and shifted it to lower pressures. In in vitro experiments, Ceronapril inhibited ACE in slices of the brain with an IC50 of approximately 34 nM, as measured by in vitro autoradiography. In C.S.F. ACE was inhibited with an IC50 of approximately 34 nM, as assessed by a fluorimetric enzyme assay. Ceronapril (100 mg/kg, p.o.) inhibited ACE in plasma, kidney, and lung rapidly (3 hr) after administration. Inhibition of ACE in kidney lasted up to 48 hr after administration of Ceronapril, whereas the activity of ACE in plasma and lung recovered rapidly (8 hr). In lung and plasma ACE was increased at 72 hr after administration. Therefore, induction of ACE in plasma and lung by the drug may partly obscure the acute inhibition and may contribute to the different time-course of inhibition of ACE from the kidney. Ceronapril inhibited ACE in the vascular organ of the lamina terminals (OVLT) and subfornical organ (SFO) of the brain slowly (onset at 8 hr) but persistently (from 24 to 48 hr). However, the drug did not inhibit ACE in structures of the brain within the blood-brain barrier, such as the caudate-putamen, choroid plexus, globus pallidus, supraoptic nucleus and paraventricular nucleus of the hypothalamus.