Resiniferatoxin

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Resiniferatoxin
Identifiers
CAS number 57444-62-9
Properties
Molecular formula C37H40O9
Molar mass 628.71 g/mol
Density 1.35 ± 0.1 g/cm³
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)
Infobox disclaimer and references

Resiniferatoxin (RTX) is a naturally occurring, ultrapotent capsaicin analog that activates the vanilloid receptor in a subpopulation of primary afferent sensory neurons involved in nociception (the transmission of physiological pain).[1][2] RTX causes a novel ion channel in the plasma membrane of sensory neurons — the transient receptor potential vanilloid 1 — to become permeable to cations, most particularly the calcium cation; this evokes a powerful irritant effect followed by desensitization and analgesia.[3][4]

Research is being conducted at the National Institutes of Health[5][6] and the University of Pennsylvania[7] to design a novel class of analgesics from the latex of resin spurge (Euphorbia resinifera), a cactus-like plant commonly found in Morocco that contains high concentrations of RTX.

A total synthesis of (+)-resiniferatoxin was completed by the Wender group at Stanford University in 1997.[8] As of 2007, this represents the only complete total synthesis of any member of the daphnane family of molecules.[9]

[edit] See also

[edit] References

 The references in this article would be clearer with a different or consistent style of citation, footnoting, or external linking.
  1. ^ Szallasi A, Blumberg PM (1989) Resiniferatoxin, a phorbol-related diterpene, acts as an ultrapotent analog of capsaicin, the irritant constituent in red pepper. Neuroscience 30(2): 515-20.
  2. ^ Szallasi A, Blumberg PM (1990) Resiniferatoxin and its analogs provide novel insights into the pharmacology of the vanilloid (capsaicin) receptor. Life Sci. 47(16): 1399-408.
  3. ^ Szallasi A, Blumberg PM (1992) Vanilloid receptor loss in rat sensory ganglia associated with long term desensitization to resiniferatoxin. Neurosci Lett. 140(1): 51-4.
  4. ^ Olah Z et al. (2001) Ligand-induced dynamic membrane changes and cell deletion conferred by vanilloid receptor 1. J Biol Chem. 276(14): 11021-30.
  5. ^ Neubert JK et al. (2003) Peripherally induced resiniferatoxin analgesia. Pain 104(1-2): 219-28.
  6. ^ Karai L et al. (2004) Deletion of vanilloid receptor 1-expressing primary afferent neurons for pain control. J Clin Invest. 113(9): 1344-52.
  7. ^ Brown DC et al. (2005) Physiologic and antinociceptive effects of intrathecal resiniferatoxin in a canine bone cancer model. Anesthesiology 103(5): 1052-9.
  8. ^ J. Am. Chem. Soc. 1997, 119, 12976-12977.
  9. ^ http://www.scripps.edu/chem/baran/images/grpmtgpdf/Seiple_Mar_07.pdf
  • Christopher S. J. Walpole, et al (1996). "Similarities and Differences in the Structure-Activity Relationships of Capsaicin and Resiniferatoxin Analogues". J. Med. Chem. 39: 2939–2952. doi:10.1021/jm960139d. 

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