Suzetrigine for Oral Contraceptive Interaction
Recruiting in Palo Alto (17 mi)
Age: 18 - 65
Sex: Female
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 1
Recruiting
Sponsor: Vertex Pharmaceuticals Incorporated
Must be taking: Oral contraceptives
Disqualifiers: Hypertension, Cardiovascular disease, Cancer, others
No Placebo Group
Trial Summary
What is the purpose of this trial?
The purpose of this study is to evaluate the effect of SUZ on the pharmacokinetics of oral contraceptives.
Will I have to stop taking my current medications?
The trial information does not specify if you need to stop taking your current medications. However, if you have conditions that affect how drugs are absorbed or processed in your body, you might not be eligible to participate.
How does the drug Suzetrigine differ from other treatments for oral contraceptive interaction?
Eligibility Criteria
This trial is for healthy female participants who don't smoke or haven't smoked in the last year, have a body mass index (BMI) between 18.0 and 30.0, and weigh over 50 kilograms. It's designed to see how Suzetrigine affects the way their bodies process birth control pills.Inclusion Criteria
Key
My BMI is between 18.0 and 30.0.
I have not smoked for at least a year.
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Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Treatment Part A
Participants receive a single dose of DRSP/EE on Days 1 and 20, and SUZ every 12 hours from Days 7 through 25
4 weeks
Treatment Part B
Participants receive a single dose of NGM/EE on Days 1 and 22, and SUZ every 12 hours from Days 9 through 29
4 weeks
Follow-up
Participants are monitored for safety and effectiveness after treatment
4 weeks
Treatment Details
Interventions
- Suzetrigine (Other)
Trial OverviewThe study is testing Suzetrigine (SUZ), a medication intended for pain management, to understand its impact on oral contraceptives specifically DRSP/EE and NGM/EE which are common forms of birth control pills.
Participant Groups
2Treatment groups
Experimental Treatment
Group I: Part B: SUZ with Norgestimate/Ethinyl Estradiol (NGM/EE)Experimental Treatment2 Interventions
Participants will receive a single dose NGM/EE on Days 1 and 22. Participants will also receive SUZ every 12 hours (q12h) from Days 9 through 29.
Group II: Part A: SUZ with Drospirenone/Ethinyl Estradiol (DRSP/EE)Experimental Treatment2 Interventions
Participants will receive a single dose of DRSP/EE on Days 1 and 20. Participants will also receive SUZ every 12 hours (q12h) from Days 7 through 25.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Celerion - TempeTempe, AZ
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Who Is Running the Clinical Trial?
Vertex Pharmaceuticals IncorporatedLead Sponsor
References
The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects. [2018]To assess the pharmacokinetic and pharmacodynamic effects of co-administration of a combined oral contraceptive (ethinyloestradiol plus levonorgestrel) and lamotrigine.
Effect of protease inhibitors on steady-state pharmacokinetics of oral norethindrone contraception in HIV-infected women. [2021]Pharmacokinetic interactions exist between combined oral contraceptives and protease inhibitors (PI). However, such information is lacking for progestin-only oral contraception. We sought to define the steady-state pharmacokinetic interaction between norethindrone (NET) and PI in HIV-infected women.
Tazarotene does not affect the pharmacokinetics and efficacy of a norethindrone/ethinylestradiol oral contraceptive. [2018]To determine the pharmacokinetic and pharmacodynamic interaction between oral tazarotene and an oral contraceptive containing norethindrone 1mg and ethinylestradiol 0.035 mg (Ortho-Novum 1/35).
Pharmacokinetic drug interactions with oral contraceptives. [2018]Oral contraceptive steroids are used by an estimated 60 to 70 million women world-wide. Over the past 20 years there have been both case reports and clinical studies on the topic of drug interactions with these agents. Some of the interactions are of definite therapeutic relevance, whereas others can be discounted as being of no clinical significance. Pharmacological interactions between oral contraceptive steroids and other compounds may be of 2 kinds: (a) drugs may impair the efficacy of oral contraceptive steroids, leading to breakthrough bleeding and pregnancy (in a few cases, the activity of the contraceptive is enhanced); (b) oral contraceptive steroids may interfere with the metabolism of other drugs. A number of anticonvulsants (phenobarbital, phenytoin, carbamazepine) are enzyme-inducing agents and thereby increase the clearance of the oral contraceptive steroids. Valproic acid has no enzyme-inducing properties, and thus women on this anticonvulsant can rely on their low dose oral contraceptive steroids for contraceptive protection. Researchers are now beginning to unravel the molecular basis of this interaction, with evidence of specific forms of cytochrome P450 (P450IIC and IIIA gene families) being induced by phenobarbital. Rifampicin, the antituberculous drug, also induces a cytochrome P450 which is a product of the P450IIIA gene subfamily. This isozyme is one of the major forms involved in 2-hydroxylation of ethinylestradiol. Broad spectrum antibiotics have been implicated in causing pill failure; case reports document the interaction, and general practitioners are convinced that it is real. The problem remains that there is still no firm clinical pharmacokinetic evidence which indicates that blood concentrations of oral contraceptive steroids are altered by antibiotics. However, perhaps this should not be a surprise, given that the incidence of the interaction may be very low. It is suggested that an individual at risk will have a low bioavailability of ethinylestradiol, a large enterohepatic recirculation and gut flora particularly susceptible to the antibiotic being used. Two drugs, ascorbic acid (vitamin C) and paracetamol (acetaminophen), give rise to increased blood concentrations of ethinylestradiol due to competition for sulphation. The interactions could have some significance to women on oral contraceptive steroids who regularly take high doses of either drug. Although on theoretical grounds adsorbents (e.g. magnesium trisilicate, aLuminium hydroxide, activated charcoal and kaolin) could be expected to interfere with oral contraceptive efficacy, there is no firm evidence that this is the case. Similarly, there is no evidence that smoking alters the pharmacokinetics of oral contraceptive steroids. These agents are now well documented as being able to alter the pharmacokinetics of other concomitantly administered drugs.(ABSTRACT TRUNCATED AT 400 WORDS)
Clinical pharmacokinetics of contraceptive steroids. An update. [2018]The present article should be read in conjunction with the original review published in the Journal in 1983. There is no new information of major significance about the pharmacokinetics of levonorgestrel, norethisterone (norethindrone) or ethinylestradiol, although it has been shown that the concentrations of these hormones secreted in breast milk are small and mothers taking combined oral contraceptive steroids may breast-feed safely. Both levonorgestrel and ethinylestradiol can be successfully administered from appropriate vaginal formulations, but no clear advantages over oral administration have been demonstrated. Several new progestogens have been investigated. Desogestrel is a prodrug for its active metabolite 3-keto-desogestrel, gestodene is itself an active progestogen and norgestimate is a prodrug acting by conversion to norgestrel and its metabolites. All 3 compounds have good bioavailability with wide intersubject variation. The newer progestogens, like norethisterone and levonorgestrel, are bound to sex hormone binding globulin (SHBG). This causes their plasma concentrations to increase with time, since SHBG is induced by ethinylestradiol even in doses of 30 micrograms daily. The binding capacity and affinity of SHBG do not increase in direct proportion to its concentration. Further drug interactions with oral contraceptive steroids have been described. Contraceptive steroids may inhibit hepatic microsomal enzyme metabolism and increase the plasma concentration and effect of some tricyclic antidepressants, the hydroxylated benzodiazepines, some beta-blocking drugs, methylxanthines, prednisolone and cyclosporin. There are no significant effects on vitamins. Oral contraceptive steroids induce glucuronidation and hence decrease plasma concentrations of some benzodiazepines, clofibric acid, paracetamol (acetaminophen) and possibly morphine. The plasma concentration of ethinylestradiol may be increased by competitive sulphation with paracetamol. Plasma concentrations of contraceptive steroids are decreased by griseofulvin, which induces their hepatic metabolism. The role of other antibiotics remains controversial but there is probably a group of susceptible women who have lower plasma contraceptive hormone concentrations and experience breakthrough bleeding or pregnancy when given broad spectrum antibiotics. This may relate to interruption of the enterohepatic recirculation of ethinylestradiol. Anticonvulsants, other than valproic acid, all induce contraceptive steroid metabolism and therefore lower plasma hormone concentrations, thus reducing contraceptive effectiveness.