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EP-4735008-A1 - IBOGAINE TREATMENT

EP4735008A1EP 4735008 A1EP4735008 A1EP 4735008A1EP-4735008-A1

Abstract

There is disclosed a method of treatment of a patient undergoing ibogaine therapy, wherein the method comprises further administering a combination of: (a) a magnesium compound, (b) lactulose or an analog thereof, (c) sodium lactate or an analog thereof, and (d) dextrose or an analog thereof.

Inventors

  • INZUNZA, Jose

Assignees

  • Ambio Life Sciences Inc.

Dates

Publication Date
20260506
Application Date
20240627

Claims (20)

  1. 1. A method of treatment of a patient undergoing ibogaine therapy, wherein the method comprises further administering a combination of: (a) a magnesium compound, (b) lactulose or an analog thereof, (c) sodium lactate or an analog thereof, and (d) dextrose or an analog thereof.
  2. 2. The method defined in Claim 1, wherein component (a) comprises magnesium sulfate.
  3. 3. The method defined in Claim 2, wherein component (a) is administered in a dose of from about 0.2 g to about 3.0 g.
  4. 4. The method defined in Claim 2, wherein component (a) is administered in a dose of from from about 0.5 g to about 2 g.
  5. 5. The method defined in Claim 2, wherein component (a) is administered in a dose of about 1 g.
  6. 6. The method defined in any one of Claims 2-5, wherein component (a) is administered intravenously.
  7. 7. The method defined in Claim 1, wherein component (a) comprises magnesium glycinate.
  8. 8. The method defined in Claim 7, wherein component (a) is administered in a dose of from about 100 mg to about 1000 mg.
  9. 9. The method defined in Claim 7, wherein component (a) is administered in a dose of from about 200 mg to about 700 mg.
  10. 10. The method defined in Claim 7, wherein component (a) is administered in a dose of from about 300 mg to about 500 mg.
  11. 11. The method defined in any one of Claims 7-10, wherein component (a) is administered orally.
  12. 12. The method defined in Claim 1, wherein component (a) comprises magnesium L- threonate.
  13. 13. The method defined in Claim 12, wherein component (a) is administered in a dose of from about 0.5 g to about 3.0.
  14. 14. The method defined in Claim 12, wherein component (a) is administered in a dose of from about 0.7 g to about 2.5 g.
  15. 15. The method defined in Claim 12, wherein component (a) is administered in a dose of from about 1.0 g to about 2.0 g.
  16. 16. The method defined in any one of Claims 12-15, wherein component (a) is administered orally.
  17. 17. The method defined in Claim 1, wherein component (a) comprises magnesium malate.
  18. 18. The method defined in Claim 17, wherein component (a) is administered in a dose of from about 100 mg to about 1000 mg.
  19. 19. The method defined in Claim 17, wherein component (a) is administered in a dose of from about 150 mg to about 700 mg.
  20. 20. The method defined in Claim 17, wherein component (a) is administered in a dose of from about 200 mg to about 500 mg.

Description

IBOGAINE TREATMENT CROSS-REFERENCE TO RELATED APPLICATION [0001] The present application claims the benefit under 35 U.S.C. §119(e) of provisional patent application S.N. 63/523,774, filed June 28, 2024, the contents of which are hereby incorporated by reference. BACKGROUND OF THE INVENTION FIELD OF THE INVENTION [0002] In one of its aspects, the present invention relates to ibogaine treatment. More particularly, the present invention relates to ibogaine treament using a safety protocol that obviates or mitigates deleterious side effects associated with ibogaine treatment. DESCRIPTION OF THE PRIOR ART [0003] Ibogaine is a naturally occurring, psychoactive indole alkaloid derived from the root bark of the African shrub Tabernanthe iboga. In West Central Africa, low dosages of Tabernanthe iboga root bark have been employed by indigenous people against fatigue, hunger and thirst. Higher dosages are used for initiation rituals during religious ceremonies. Ibogaine ingestion can lead to intense visions with closed eyes reminding of a waking dream, often accompanied by a vivid recall of autobiographical visual memories (Alper, K.R.; Stajic, M.; Gill, J.R. Fatalities Temporally Associated with the Ingestion of Ibogaine. J. Forensic. Sci. 2012, 57, 398-412 (Alper et al.)). [0004] The mechanisms by which ibogaine exerts its psychoactive effects in the brain are only poorly understood, which is attributable to the alkaloid’s complex pharmacology. Effects on multiple neurotransmitter systems via numerous brain targets have been reported. Among those, ibogaine interacts with neurotransmitter transporters, opioid receptors, sigma receptors, glutamate receptors, and nicotinic receptors in low micromolar concentrations (Alper, K.R. Ibogaine: A review. Alkaloids Chem. Biol. 2001, 56. 1-38 (Alper)). Long- lasting effects after ibogaine intake areattributed to the alkaloid’s long-lived active metabolite noribogaine (Baumann, M.H.; Pablo, J.P.; Ah, S.F.; Rothman, R.B.; Mash, D.C. Noribogaine (12-hydroxyibogamine): A biologically active metabolite of the antiaddictive drug ibogaine. Ann. N. Y. Acad. Set. 2000, 914, 354-368). [0005] Ibogaine’s medical history in the Western world began in the early 1900s when the substance was indicated for the treatment of asthenia and as a neuromuscular stimulant (Alper, ibid). In the 1940s and 1950s, ibogaine’s suitability as potential cardiovascular drug was studied (e.g., Schneider, J.A.; Rinehart, R.K. Analysis of the cardiovascular action of ibogaine hydrochi orid. Arch. Ini. Pharmacodyn. Ther. 1957, 110, 92-102). Later, following a discovery in in the 1960s, the drug received much attention because of its potential applicability as an anti-addiction medication. In animal studies, ibogaine has shown promising anti-addictive properties [Alper et al, ibid}. [0006] Thus, ibogaine-treated rodents exhibit attenuated opioid withdrawal symptoms, and diminished self-administration of a variety of drugs of abuse including opioids, cocaine, nicotine, and alcohol (Glick, S.D.; Maisonneuve, I.S. Mechanisms of antiaddictive actions of ibogaine. Ann. N. Y. Acad. Sci. 1998, 844, 214-226). Anecdotal evidence suggests that ibogaine is also anti-addictive in humans. When ibogaine is administered to treat drug dependence, typically as single one-time dose (Alper, ibid), patients commonly report sustained resolution of the withdrawal syndromes within 12-18 h, and a reduction in drug craving for prolonged time periods up to several weeks (Brown, T.K. Ibogaine in the treatment of substance dependence. Curr. Drug Abuse Rev. 2013, 6, 3-16). [0007] In 1993, the U.S. Food and Drug Administration (FDA) approved a clinical trial in humans to study the effects of ibogaine. The sudden death of a female patient, however, dampened further interest, and the National Institute on Drug Abuse (NIDA), critically advised by pharmaceutical industry consultants, opted not to fund additional human studies in 1995. Ibogaine was stigmatized as hallucinogen and stimulant with a possible abuse potential, and consequently classified as a Schedule 1 substance in the U.S. (Brown, ibid). [0008] Mostly because of ibogaine’s status as a banned substance in the U.S., the development of the drug’s use in addiction treatment took then place outside conventional clinical and medical settings. The great and rapidly growing popularity of ibogaine as antiaddiction medication in alternative medicine prompted Frank Vocci, former director of NIDA’s anti-addiction drug development, to term ibogaine therapy “a vast, uncontrolled experiment” (Vastag, B. Addiction research. Ibogaine therapy: A “vast, uncontrolled experiment”. Science 2005, 308, 345-346). [0009] Since that time the ibogaine “medical subculture” has continued to expand [Brown, ibid], and today, the alkaloid is used as an anti-addiction medication in alternative medicine in dozens of clinics worldwide [Apler et al., ibid; Brown, ibid], [0010] Ibogaine’s complex pharmacology entails a