Vincofos is a broad-spectrum canine anthelmintic. All or nearly all of the ascarids, hookworms, whipworms, and the tapeworm, Taenia pisiformis, were expelled following therapy with vincofos. The tapeworm, Dipylidium caninum, was also effectively removed by the vincofos treatment, but it appeared that a slightly greater dosage would be required to obtain maximum anthelmintic effect.

Rioprostil is a methylprostaglandin E1 analog. Rioprostil inhibits gastric acid secretion and enhances the gastric mucus-bicarbonate barrier. In peptic ulcer cases, it facilitates the healing process and the elimination of pain. Rioprostil can also be used to prevent recurrence of duodenal ulcers. However, its development has been discontinued in 2000.

Afuresertib (GSK2110183 ) is an orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Afuresertib binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents. Preclinically, AKT inhibition by afuresertib can reverse platinum resistance in ovarian cancer cell lines isolated from patients with platinum-resistant ovarian cancer. Afuresertib is well tolerated and demonstrates clinical activity as monotherapy in heavily pretreated MM patients. Is in phase II clinical trials for Chronic lymphocytic leukaemia; Haematological malignancies; Histiocytosis.

Meisoindigo ((E)-1,1'-dimethyl-[3,3'-biindolinylidene]-2,2'-dione) is a derivative of Indigo Naturalis, that has been used in China for chronic myeloid leukemia. In vitro cell line studies have shown that this agent might induce apoptosis and myeloid differentiation of acute myeloid leukemia (AML). Meisoindigo has been a routine therapeutic agent in the clinical treatment of chronic myelogenous leukemia (CML) in China since the 1980s. In phase III clinical trial of Meisoindigo involving 402 patients, it was shown that Meisoindigo was equally efficient for both newly diagnosed and previously treated CML patients after oral administration. The hematological complete response (CR) and partial response (PR) rates, respectively, were 45.0 and 39.3% for newly diagnosed patients and 35.9 and 41.4% for previously treated patients. Meisoindigo was generally well tolerated. The most frequent side‑effects were bone, joint and/or muscle pain of varying degrees when the dosage was more than the suitable one.

Temperocol is an investigative anti-cancer drug that inhibits the expression of survivin and CDK-1; discovered at Johns Hopkins University and under development by Erimos Pharmaceuticals. It has been tested in phase I/II clinical trials for Leukemia, and several forms of neoplasms including gliomas. Results of these clinical trials have shown promise, however treatment regimes produce several toxic side effects that need to be balanced against efficacy. Temperocol is a fully methylated derivative of the natural product Nordihydroguaiaretic acid.

Shogaol (6-Shogaol) is a bioactive ingredient of ginger root (Zingiber officinale), a medicinal plant having anti-nausea, anti-inflammatory, and anti-carcinogenic properties and a carminative effect. 6-Shogaol inhibits LPS-induced inflammation by activating PPAR-γ. As one of the main bioactive compounds of dried ginger, 6-shogaol has been widely used to alleviate many ailments. It is also a major pungent flavor component, and its precursor prior to dehydration is 6-gingerol, which is reported to be responsible for the pungent flavor and biological activity of fresh ginger. The conjugation of the α,β-unsaturated ketone skeleton in the chemical structure of 6-shogaol explicates its higher potency and efficacy than 6-gingerol in terms of antioxidant, anti-inflammatory, anticancer, antiemetic and other bioactivities. 6-Shogaol not only scavenges free radicals, such as superoxide radicals and hydroxyl radicals, but also effectively suppresses the activity of xanthine oxidase, which is an important generator of oxygen containing free radicals. 6-shogaol possesses strong metal-binding capacity to inhibit lipid peroxidation and AAPH-induced DNA damage. 6-shogaol exhibits an excellent anti-inflammatory activity in downregulation of pro-inflammatory cytokines and prevention of excessive oxidants in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells, human kidney epithelial cell 293T, mouse microglia, rat astrocytes, human keratinocytes as well as 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated mouse skin. 6-Shogaol also exerts a strong anti-inflammatory influence on acute gouty arthritis. The increased lipid peroxidation, lysosomal enzymes, inflammatory mediator tumor necrosis factor-α (TNF-α) as well as enlarged paw volume induced by monosodium urate crystals in mice can be reduced to nearly normal levels upon consuming 6-shogaol. Various molecular targets are involved in the anti-inflammatory effect of 6-shogoal. Some molecules such as TLR4 receptor and Keap1 are directly targeted by 6-shogaol, while others are indirectly mediated by various pathways. 6-shogaol also exhibits neuroprotective effects on dopaminergic neurons in both in vitro and in vivo Parkinson's disease (PD) models. In addition to anti-oxidative stress, anti-neuroinflammation and anti-Aβ toxicity activities, 6-shogaol also shows capacities to resist neuronal apoptosis and to modulate synaptic and cholinergic functions. 6-shogaol has been treated as a potent anticancer agent against multitudinous cancers including liver, colon, lung, breast, gastric, skin, kidney, ovarian, prostate, laryngeal and pancreatic cancers as well as leukemia. The anticancer activity of 6-shogaol is attributed to its ability to modulate a series of signaling molecules such as MAPK, PI3K, Akt, NF-κB, signal transducer and activator of transcription-3 (STAT3), TNF-ɑ, COX-2, cyclin D1, CDK, MMP-9, survivin, cellular inhibitor of apoptosis protein 1 (cIAP-1), X-linked inhibitor-of-apoptosis protein (XIAP), Bcl-2, and caspases. 6-Shogaol can trigger autophagy of human non-small cell lung cancer A549 cells by blocking the activation of Akt and its downstream targets, such as mTOR, forkhead in rhabdomyosarcoma (FKHR), and glycogen synthase kinase-3β (GSK-3β).