Noscapine (also known as Narcotine, Nectodon, Nospen, Anarcotine and (archaic) Opiane) is a benzylisoquinoline alkaloid from plants of the poppy family, without painkilling properties. This agent is primarily used for its antitussive (cough-suppressing) effects. Noscapine is often used as an antitussive medication. A 2012 Dutch guideline, however, does not recommend its use for coughing. Noscapine can increase the effects of centrally sedating substances such as alcohol and hypnotics. Noscapine should not be taken in conjunction with warfarin as the anticoagulant effects of warfarin may be increased. Noscapine, and its synthetic derivatives called noscapinoids, are known to interact with microtubules and inhibit cancer cell proliferation. Mechanisms for its antitussive action are unknown, although animal studies have suggested central nervous system as a site of action. Furthermore, noscapine causes apoptosis in many cell types and has potent antitumor activity against solid murine lymphoid tumors (even when the drug was administered orally) and against human breast and bladder tumors implanted in nude mice. Because noscapine is water-soluble and absorbed after oral administration, its chemotherapeutic potential in human cancer merits thorough evaluation. Antifibrotic effect of noscapine based on novel mechanism, which it shows through EP2 prostaglandin E2 receptor-mediated activation of protein kinase A.

Vinflunine (Javlor) is the first fluorinated microtubule inhibitor belonging to the Vinca alkaloids family. Vinflunine, at the lowest effective concentrations, interacts with the Vinca alkaloid binding site on tubulin, suppresses microtubule dynamics (switching at microtubule ends between phases of slow growth and rapid shortening) and microtubule treadmilling (growth at the plus end and shortening at the minus end of the microtubule), causes cell cycle arrest which appears on fluorescence-activated cell sorting analysis as a G2 + M phase arrest, and is associated with an accumulation of cells in mitosis leading to cell death via apoptosis. Vinflunine has been been approved for advanced or metastatic transitional cell carcinoma of the urothelial tract. Pierre Fabre submitted an extension to the EU authorisation to add treatment of advanced breast cancer.

Vindesine (desacetyl vinblastine amide sulfate) is a synthetic derivative of vinblastine. Vindesine acts by causing the arrest of cells in metaphase mitosis through its inhibition tubulin mitotic funcitoning. Vindesine is an anti-neoplastic drug for intravenous use which can be used alone or in combination with other oncolytic drugs. Information available at present suggests that Eldisine as a single agent may be useful for the treatment of: acute lymphoblastic leukaemia of childhood resistant to other drugs; blastic crises of chronic myeloid leukaemia; malignant melanoma unresponsive to other forms of therapy; advanced carcinoma of the breast, unresponsive to appropriate endocrine surgery and/or hormonal therapy. Adverse effects associated with the use of vindesine include cellulitis and phlebitis, gastrointestinal bleeding, chills, and fever. It may increase the neuropathy associated with Charcot-Marie-Tooth syndrome. Vindesine may interact with mitomycin-C (brand name Mutamycin), causing acute bronchospasm within minutes or hours following administration. Phenytoin (brand name Dilantin) may also interact with vindesine, leading to decreased serum levels of phenytoin.

Demecolcine, also called Colcemid, was isolated from the autumn crocus in 1950 and commercialized by Ciba. Initially, it was explored as a cancer drug due to its low toxicity. Demecolcine depolymerizes microtubules and limits microtubule formation (inactivates spindle fiber formation), thus arresting cells in metaphase and allowing cell harvest and karyotyping to be performed. Today, it is only used as a research tool mainly to overcome limitations of colchicine due to its very slow association and dissociation rate constants. It binds to tubulin at the same site as colchicine, but ~10-fold faster, and it also dissociates faster. Demecolcine main use has been to arrest cells in mitosis for cytogenetic analysis, though to our knowledge it offers no special advantages over other drugs in this application.

Vintafolide is a water-soluble derivative of FA and the vinca alkaloid desacetylvinblastine hydrazide (DAVLBH). DAVLBH is a vinca alkaloid that disrupts the formation of the mitotic spindle, thereby inhibiting cell division and inducing cell death. FA and DAVLBH are connected through a peptide spacer and a reducible, self-immolative disulfide-linker system to form vintafolide. The disulfide linker enables the release of DAVLBH inside the cancer cell after receptor-mediated endocytosis. This is an important feature because the high affinity of FA for the FR can result in ligands remaining attached to the FR for long periods of time, which can reduce the potency of folate-targeted chemotherapeutic agents. Vintafolide was designed specifically to bind to high-affinity FR present on the surfaces of cancer cells and to release its active component, DAVLBH, once it enters the endosome of the target cell. Preclinical studies have shown that vintafolide binds to the FRα with high affinity, it has highly potent and specific antitumor activity against FRα+ tumors. The efficacy and safety of vintafolide was first assessed in 2007 in a nonrandomized trial, and a number of phase II and III clinical studies have since been conducted in patients with ovarian and lung cancer. A Marketing Authorization Application (MAA) filing for vintafolide and etarfolatide for the treatment of patients with folate receptor-positive platinum-resistant ovarian cancer in combination with doxorubicin, pegylated liposomal doxorubicin (PLD), has been accepted by the European Medicines Agency. The drug received orphan drug status in Europe in March 2012. Merck & Co. acquired the development and marketing rights to Vintafolide from Endocyte in April 2012. On 16 May 2014 Endocyte Europe B.V. officially notified the Committee for Medicinal Products for Human Use (CHMP) that it has decided to withdraw its application for a marketing authorisation for Vynfinit (Vintafolide), for the treatment of ovarian cancer which has become resistant to platinum-based cancer treatment. The preliminary data from the study could not confirm the benefit of Vynfinit in ovarian cancer patients. Endocyte and Merck are still waiting for data from a phase IIb trial of vintafolide in non-small cell lung cancer (NSCLC), called TARGET, which met its primary PFS target and is due to generate overall survival data in the coming months.

Soblidotin is a derivative of dolastatin 10, which was isolated from the Indian Ocean sea hare, Dolabella auricularia, in 1987. Soblidotin inhibits tubulin polymerization, resulting in cell cycle arrest and induction of apoptosis. It has a broad spectrum of antitumor activity against various murine tumors – P388 leukemia, Colon26 and LLC carcinomas, B16 melanoma and M5076 sarcoma – as well as human tumor xenografts, MX-1, LX-1 and SBC-3 carcinomas. Soblidotin is currently undergoing clinical evaluation and, in phase II clinical trials for solid tumours.

Paclitaxel trevatide (formerly known as ANG 1005 or GRN 1005) is a paclitaxel-peptide drug conjugate, where three paclitaxel molecules linked by a cleavable succinyl ester linkage to a brain peptide vector, Angiopep-2. Paclitaxel trevatide is an oncology product to leverage the low-density lipoprotein receptor-related protein 1 (LRP-1) pathway to cross the blood-brain barrier (BBB) and enter cancer cells. This drug successfully completed phase II clinical trials in breast cancer patients with recurrent brain metastases and in patients with high-grade glioma. 30-May-2014 Angiochem, the company that developed this drug, announced that the Food & Drug Association (FDA) had granted both orphan drug and fast track designation to paclitaxel trevatide for the treatment of glioblastoma multiforme (GBM). In addition, paclitaxel trevatide is going to be involved in phase III clinical trial to see if this drug can prolong survival compared to a Physician Best Choice control in HER2-negative breast cancer patients with the newly diagnosed leptomeningeal disease and previously treated brain metastases.

ERIBULIN MESYLATE (HALAVEN®) is a microtubule dynamics inhibitor. It is a synthetic analog of halichondrin B, a product isolated from the marine sponge Halichondria okadai. ERIBULIN MESYLATE (HALAVEN®) inhibits the growth phase of microtubules without affecting the shortening phase and sequesters tubulin into nonproductive aggregates. It exerts its effects via a tubulin-based antimitotic mechanism leading to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after the prolonged mitotic blockage. ERIBULIN MESYLATE (HALAVEN®) is indicated for the treatment of patients with metastatic breast cancer who have previously received at least two chemotherapeutic regimens for the treatment of metastatic disease. It is also indicated for the treatment of patients with unresectable or metastatic liposarcoma who have received a prior anthracycline-containing regimen.

Docetaxel was protected by patents (U.S. patent and European patent) which were owned by Sanofi-Aventis, and so was available only under the Taxotere brand name internationally. The European patent expired in 2010. Docetaxel is a clinically well-established anti-mitotic chemotherapy medication used for the treatment of patients with locally advanced or metastatic breast cancer after failure of prior chemotherapy. Also used as a single agent in the treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of prior platinum-based chemotherapy. It is also used in combination with prednisone, in the treatment of patients with androgen independent (hormone refractory) metastatic prostate cancer. Furthermore, docetaxel has uses in the treatment of gastric adenocarcinoma and head and neck cancer. Docetaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, docetaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, docetaxel binds to the β-subunit of tubulin. Tubulin is the "building block" of mictotubules, and the binding of docetaxel locks these building blocks in place. The resulting microtubule/docetaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that docetaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function.

Vinorelbine (trade name Navelbine) is a semi-synthetic vinca-alkaloid with a broad spectrum of anti-tumour activity. Vinorelbine is a mitotic spindle poison that impairs chromosomal segregation during mitosis. It blocks cells at G2/M. Microtubules (derived from polymers of tubulin) are the principal target of vinorelbine. Vinorelbine was developed by Pierre Fabre under licence from the CNRS in France. NAVELBINE (vinorelbine tartrate) as a single agent or in combination is indicated for the first line treatment of non small cell lung cancer and advanced breast cancer.