Eribulin is an analog of halichondrin B, which is a macrocycle, a polyether, a polycyclic ether, a cyclic ketone, a primary amine compound, and a cyclic ketal. Eribulin is a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. The trade name is Halaven. Eribulin is also known as E7389 and ER-086526, with the name NSC-707389 of US NCI. It is used to treat some patients with breast cancer and liposarcoma.

Mechanism of Action

Eribulin is a completely synthetic macrocyclic ketone analog of marine natural product HalichondrinB. The parent molecule is a powerful natural mitotic inhibitor. Eribulin is a unique microtubule kinetic inhibitor, which mainly binds to a few high-affinity sites at the positive end of the microtubule. It has the mechanism of cytotoxicity and non-cytotoxicity. Its cytotoxicity is related to its antimitotic activity, under which apoptosis of cancer cells occurs after prolonged and irreversible mitotic blocking. In addition to its cytotoxicity and antimitotic mechanisms, preclinical studies in human breast cancer models have shown that Ricin also has complex effects on the biology of surviving cancer cells and residual tumors that do not seem to be related to their antimitotic effects. These non-mitotic mechanisms include vascular remodeling that leads to increased tumor perfusion and alleviates tumor hypoxia, phenotypic changes consistent with the reversal of epithelial-interstitial transition (EMT). And the decrease of migration and invasion ability, which led to a decrease of metastasis ability, was measured in the preclinical experimental metastasis model. In other studies, the expression of differentiation antigens in smooth muscle cells and adipocytes increased after Eribulin treatment of leiomyosarcoma and liposarcoma cells, respectively. Taxol-resistant tumors often do not respond to Eribulin. Some study found that this resistance is due to the expression of multidrug resistance protein 1 (MDR1). Fluorescently labeled eribulin has been used to study the pharmacokinetics and pharmacodynamics at single cell level in vivo.


Eribulin can dilate cerebral vessels, reduce cerebral vascular resistance, increase cerebral blood flow, improve microcirculation, and antagonize platelet aggregation. Therefore, it can be used to treat ischemic cerebrovascular diseases, such as cerebral thrombosis, cerebral embolism, cerebral hemorrhage, and other sequela paralysis patients, has a better effect, the course of the disease within 6 months is better than more than 6 months.

Common side effects

  • Increased risk of getting an infection
  • Breathlessness
  • Loss of appetite
  • Numbness or tingling in fingers and toes
  • Headaches
  • Breathlessness and cough
  • Feeling or being sick
  • Constipation or diarrhea
  • Hair loss
  • Pain in different parts of the body
  • Fatigue
  • High temperature (fever)
  • Weight loss


Eribulin is an anticancer drug approved for the treatment of metastatic breast cancer resistant to anthracyclines and paclitaxel. It comes from a Japanese sponge and its function is to interfere with the growth of microtubule. Neutropenia, neuropathy and prolonged QT are the most common adverse events associated with the drug. It has a low incidence of hypersensitivity and convenient administration and is useful even in paclitaxel-resistant cases. It is a valuable antineoplastic drug for oncologists.


1. Smith, J. A., Wilson, L., Azarenko, O., Zhu, X., Lewis, B. M., Littlefield, B. A., & Jordan, M. A. (2010). Eribulin binds at microtubule ends to a single site on tubulin to suppress dynamic instability. Biochemistry49(6), 1331-1337.

2. Dybdal-Hargreaves, N. F., Risinger, A. L., & Mooberry, S. L. (2015). Eribulin mesylate: mechanism of action of a unique microtubule-targeting agent. Clinical Cancer Research21(11), 2445-2452.

3. Swami, U., Chaudhary, I., Ghalib, M. H., & Goel, S. (2012). Eribulin-a review of preclinical and clinical studies. Critical reviews in oncology/hematology81(2), 163-184.

Related Drug target

PI3K              Raf             mTOR          JAK 

FGFR           CDK           VEGFR        mTOR