Temodox is an antibacterial agent that was studied as a veterinary growth stimulant. Information about the current use of this compound is not available.

Ciadox is Quinoxaline 1,4-dioxide derivative with antimicrobial and promoting activities. Cyadox supplied as premix in the final feed in Eastern Europe and may be used in pigs up to four months of age. Some evidence demonstrated that the mechanism of Ciadox for improving pig growth performance was correlated with several metabolic hormones and growth factors. Cyadox also did not show any adverse effects in carcinogenicity tests with rats and long-term toxicity tests with mice and rats. Cyadox subchronic oral toxicity evaluation shows mild toxicity in non-rodents animals. Metabolic transformation of Ciadox leads to three major metabolites, including 1,4-bisdesoxycyadox, 4-desoxycyadox, and quinoxaline-2-carboxylic acid. Ciadox and metabolites shows virtually no toxic effects in the acute and subchronic oral toxicity study and no mutagenic, carcinogenic activivt.

Cletoquine is a metabolite of a disease-modifying anti-rheumatic and antimalarial drug hydroxychloroquine. It is produced by oxidative N-deethylation of hydroxychloroquine.

Fumoxicillin was developed as an antibacterial agent that binds to penicillin-binding protein and inhibits the bacterial cell wall biosynthesis. Information about the current development of this compound is not available.

Clodacaine is a local anesthetic drug, invented by Cilag AG in the late 1950s.

FLOPRISTIN is one of the components of the experimental drug NXL103 (XRP 2868), along with linopristin. Both are semi-synthetic streptogramin antibiotics derived from the Streptomyces genus. NXL103 has a spectrum of antibacterial activity that indicates it has the potential to be effective in the treatment of skin and skin structure infections, including those caused by methicillin-resistant Staphylococcus aureus, as well as community-acquired pneumonia. NXL103 has completed Phase II trials.

Esmirtazapine (S-(+)mirtazapine or ORG-50081) is an enantiomer of mirtazapine (REMERON®), a high-affinity antagonist at 5-HT2/5-HT3 and H1 receptors, used in the treatment of depression. Esmirtazapine has a shorter plasma half-life than the R(−) enantiomer. Esmirtazapine is preferentially metabolized into an 8-hydroxy glucuronide. Organon was developing esmirtazapine for the treatment of hot flushes (vasomotor symptoms) associated with the menopause and insomnia.

Sivifene (also known as A-007), a triaryl hydrazone that produced objective responses when applied topically. During preclinical studies, sivifene was observed to upregulate both cutaneous and systemic T-lymphocytes, in particular, CD4/8+ lymphocyte subtypes. The current mechanism of action for the drug is unknown however is assumed that it can show its immunomodulating properties through the upregulation of the CD45 T lymphocyte cell surface receptor. Sivifene was being evaluated for its anticancer activities in melanoma, breast cancer, Kaposi's sarcoma, and lymphoproliferative disorders. The drug as a 0.25% gel is confirmed as an effective palliative treatment option for cutaneous metastases from cancers. Skin reactions were minimal, tolerated, and no cessation of treatment was required. However, the further development of this drug apparently has been discontinued.

Tucaresol, a substituted benzaldehyde, was being developed by Glaxo Wellcome for the prevention of sickle cell disease. Tucaresol was designed to interact with haemoglobin to increase oxygen affinity and has been shown to inhibit sickling in vitro. Tucaresol is also a low-molecular-weight compound that enhances co-stimulatory signaling to CD4 cells. Immune induction is dependent on transient covalent bonding (Schiff base formation) between carbonyls and amines expressed on antigen presenting cell (APC) and T-cell surfaces. Tucaresol substitutes for the natural donor of carbonyl groups to mimic the transient bonding that is essential for T-cell activation. In preliminary studies, tucaresol has been shown to stimulate HIV-specific cytotoxic T lymphocyte responses and generation of naive T cells via thymopoiesis in patients receiving ART who have suppressed viremia. Tucaresol appears to specifically increase type 1 cytokine production. Tucaresol has been used in trials studying the treatment of HIV infections. However, the development of tucaresol for HIV, Hepatitis B and sickle cell diseas treatment has been discontinued.

Nafazatrom [BAY G 6575] is a leukotriene synthesis inhibitor that was being developed by Bayer in Germany. It is a pyrazolinone derivative with potential antimetastatic activities. Nafazatrom, originally developed as an antithrombotic agent, inhibits the key prostaglandin catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase, which prolongs the biological half-life of prostacyclin (prostaglandin I2; PGI2) and prevents intravascular coagulation. Nafazatrom, in the micromolar range, inhibits the metabolism of PGs (prostaglandins) by 15-OH PGDH in a dose-dependent manner. The IC50 for inhibition of 15-OH PGDH was estimated to be 18.5 uM when [3H]PGF2 alpha was used as substrate. This agent also serves as a reducing cofactor with the hydroperoxidase moiety of cyclooxygenase and accelerates the conversion of arachidonic acid into precursors of PGI2. An elevated level of PGI2 prevents aggregation of platelets; subsequently it decreases the formation of tumor cell-platelet aggregates as well as their sequestration in blood vessels, which is an important initiating step in the development of metastasis. Nafazatrom may have had potential as an antithrombotic, anti-ischaemic and antiasthmatic agent. However, the development of nafazatrom was discontinued.