clomid
| Product dosage: 100mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 10 | $5.51 | $55.07 (0%) | 🛒 Add to cart |
| 20 | $3.75 | $110.14 $75.10 (32%) | 🛒 Add to cart |
| 30 | $2.84 | $165.21 $85.11 (48%) | 🛒 Add to cart |
| 60 | $1.67 | $330.42 $100.13 (70%) | 🛒 Add to cart |
| 90 | $1.22 | $495.63 $110.14 (78%) | 🛒 Add to cart |
| 120 | $1.08 | $660.84 $130.17 (80%) | 🛒 Add to cart |
| 180 | $0.83 | $991.26 $150.19 (85%) | 🛒 Add to cart |
| 270 | $0.78 | $1486.89 $210.27 (86%) | 🛒 Add to cart |
| 360 | $0.71
Best per pill | $1982.51 $255.32 (87%) | 🛒 Add to cart |
| Product dosage: 25mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 20 | $2.75 | $55.07 (0%) | 🛒 Add to cart |
| 30 | $2.17 | $82.60 $65.08 (21%) | 🛒 Add to cart |
| 60 | $1.34 | $165.21 $80.10 (52%) | 🛒 Add to cart |
| 90 | $1.00 | $247.81 $90.11 (64%) | 🛒 Add to cart |
| 120 | $0.83 | $330.42 $100.13 (70%) | 🛒 Add to cart |
| 180 | $0.64 | $495.63 $115.15 (77%) | 🛒 Add to cart |
| 270 | $0.48 | $743.44 $130.17 (82%) | 🛒 Add to cart |
| 360 | $0.43
Best per pill | $991.26 $155.20 (84%) | 🛒 Add to cart |
| Product dosage: 50mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 10 | $4.51 | $45.06 (0%) | 🛒 Add to cart |
| 20 | $3.25 | $90.11 $65.08 (28%) | 🛒 Add to cart |
| 30 | $2.50 | $135.17 $75.10 (44%) | 🛒 Add to cart |
| 60 | $1.50 | $270.34 $90.11 (67%) | 🛒 Add to cart |
| 90 | $1.11 | $405.51 $100.13 (75%) | 🛒 Add to cart |
| 120 | $0.88 | $540.69 $105.13 (81%) | 🛒 Add to cart |
| 180 | $0.72 | $811.03 $130.17 (84%) | 🛒 Add to cart |
| 270 | $0.65 | $1216.54 $175.22 (86%) | 🛒 Add to cart |
| 360 | $0.60
Best per pill | $1622.06 $215.27 (87%) | 🛒 Add to cart |
Synonyms
| |||
Clomiphene citrate, commonly known by its brand name Clomid, represents one of the most foundational and extensively studied oral ovulation induction agents in reproductive medicine. As a selective estrogen receptor modulator (SERM), its primary mechanism involves blocking estrogen receptors in the hypothalamus, which tricks the body into perceiving low estrogen levels. This prompts increased gonadotropin-releasing hormone (GnRH) secretion, subsequently elevating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) production from the pituitary gland. The resulting hormonal cascade stimulates ovarian follicular development and maturation, making it a first-line treatment for anovulatory infertility, particularly in women with polycystic ovary syndrome (PCOS). Despite newer agents like letrozole gaining traction, clomiphene citrate remains a cornerstone due to its decades of clinical use, predictable response profile, and relatively favorable safety spectrum when monitored appropriately. Its role extends beyond simple ovulation induction, sometimes being used in male infertility for hypogonadism and occasionally in assisted reproductive technology cycles for controlled ovarian stimulation, though its anti-estrogenic effects on the endometrium can sometimes limit its utility in certain patient populations.
1. Introduction: What is Clomid? Its Role in Modern Medicine
What is Clomid? Clomiphene citrate is a non-steroidal, triphenylethylene derivative that functions as a mixed estrogen agonist/antagonist. Approved by the FDA in 1967, it was originally developed as an investigational contraceptive but paradoxically found its niche in treating infertility. What is Clomid used for primarily? It’s indicated for the treatment of ovulatory dysfunction in women desiring pregnancy. The benefits of Clomid are well-documented: it’s orally administered, relatively inexpensive, and has a straightforward monitoring protocol. Its medical applications have solidified its position in clinical guidelines worldwide, despite the emergence of aromatase inhibitors like letrozole. For many clinicians, it remains the initial intervention for WHO Group II anovulation, characterized by normogonadotropic normoestrogenic anovulation.
2. Key Components and Bioavailability of Clomid
The composition of Clomid is a racemic mixture of two stereoisomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene), which have different pharmacokinetic properties and estrogen receptor binding affinities. Enclomiphene is the more potent anti-estrogenic isomer with a shorter half-life (approximately 6-8 hours), while zuclomiphene has weaker anti-estrogenic effects but a much longer elimination half-life (up to several weeks), leading to cumulative effects with repeated cycles. The standard release form is 50 mg tablets, though compounding to lower doses (12.5 mg, 25 mg) is sometimes utilized for minimal stimulation protocols.
Bioavailability of Clomid is nearly complete with oral administration, with peak serum concentrations reached within 4-6 hours. The extensive enterohepatic recirculation and long half-life of zuclomiphene contribute to its prolonged action, which can be both therapeutic and problematic. The component zuclomiphene accumulation is why many reproductive endocrinologists recommend breaks between treatment cycles to prevent excessive endometrial suppression. Understanding this isomer-specific pharmacology is crucial for optimizing treatment protocols and minimizing side effects.
3. Mechanism of Action of Clomid: Scientific Substantiation
How Clomid works centers on its competitive binding to estrogen receptors throughout the body, particularly in the hypothalamus. By occupying these receptors without activating them, it creates a false signal of hypoestrogenism. The hypothalamus responds by increasing pulsatile GnRH secretion, which stimulates the anterior pituitary to produce more FSH and LH. This heightened gonadotropin release then drives ovarian follicular recruitment and development.
The mechanism of action involves complex feedback systems. In the hypothalamic-pituitary-ovarian axis, the reduced negative estrogen feedback allows for enhanced FSH production during the early follicular phase, promoting the growth of multiple follicles. The effects on the body extend beyond the reproductive axis, however, as estrogen receptors are ubiquitous. This explains why some patients experience hot flashes (central thermoregulatory centers), visual disturbances (CNS effects), or mood changes. The scientific research behind these mechanisms is robust, with studies dating back to the 1960s confirming its central action on gonadotropin secretion through hypothalamic estrogen receptor blockade.
4. Indications for Use: What is Clomid Effective For?
Clomid for Ovulatory Dysfunction
The primary indication remains anovulatory infertility, particularly in PCOS patients. Multiple randomized controlled trials demonstrate ovulation rates of 60-85% and pregnancy rates of 30-40% within 6 cycles for appropriately selected patients.
Clomid for Unexplained Infertility
Though less common today with the shift toward letrozole and gonadotropins, Clomid was historically used for unexplained infertility, often combined with intrauterine insemination (IUI) to enhance pregnancy rates over timed intercourse alone.
Clomid for Luteal Phase Defect
By enhancing follicular development and subsequent corpus luteum function, Clomid can improve inadequate luteal phase progesterone production in some patients, though this remains a controversial diagnosis.
Clomid for Male Infertility
At lower doses (12.5-25 mg daily), Clomid can stimulate endogenous testosterone production in hypogonadal men, potentially improving semen parameters in select cases of secondary hypogonadism.
5. Instructions for Use: Dosage and Course of Administration
Standard instructions for use for Clomid typically involve initiating treatment on cycle days 3-5, though some protocols use day 2 or even day 1 starts. The starting dosage is usually 50 mg daily for 5 days, with incremental increases in subsequent cycles if ovulation doesn’t occur. Maximum recommended daily dose is 150-200 mg, though many clinicians will reconsider the treatment approach if 100 mg fails to induce ovulation.
| Indication | Typical Dosage | Duration | Timing | Monitoring |
|---|---|---|---|---|
| First-line ovulation induction | 50 mg | 5 days | Cycle days 3-7 | Mid-cycle ultrasound + progesterone |
| CC-resistant anovulation | 100-150 mg | 5 days | Cycle days 3-7 | Enhanced monitoring with estrogen levels |
| Male hypogonadism | 25 mg | Daily or EOD | Continuous | Testosterone levels at 4-6 weeks |
The recommended course of administration is typically 3-6 ovulatory cycles before reassessing treatment strategy, as approximately 75% of pregnancies occur within the first three treatment cycles. Beyond 6-12 cycles, cumulative pregnancy rates plateau while potential side effects may increase.
6. Contraindications and Drug Interactions with Clomid
Absolute contraindications include pregnancy (Category X), liver disease, abnormal uterine bleeding of undetermined origin, ovarian cysts unrelated to PCOS, and uncontrolled thyroid or adrenal dysfunction. Relative contraindications include endometriosis, previous ectopic pregnancy, and personal history of hormone-sensitive cancers.
Important drug interactions with Clomid involve medications that induce or inhibit CYP450 enzymes, particularly CYP2D6 and CYP3A4, which metabolize clomiphene. Concomitant use with tamoxifen may have additive anti-estrogenic effects. Drugs like rifampin can decrease clomiphene levels, while ketoconazole may increase them.
Regarding safety, is it safe during pregnancy? Absolutely not—Clomid is pregnancy Category X and must be discontinued immediately once pregnancy is confirmed due to potential teratogenic risks.
7. Clinical Studies and Evidence Base for Clomid
The clinical studies on Clomid foundation is extensive. A landmark 2014 NEJM study comparing letrozole versus clomiphene for infertility in PCOS patients found higher ovulation and live birth rates with letrozole, yet clomiphene still achieved respectable outcomes. Multiple Cochrane reviews have confirmed its efficacy for ovulation induction while highlighting the importance of appropriate patient selection.
The scientific evidence spans decades, with meta-analyses demonstrating cumulative pregnancy rates of approximately 45-50% after 3 cycles and 60-65% after 6 cycles in anovulatory women. The effectiveness appears highest in younger women with pure anovulation rather than those with additional infertility factors. Physician reviews consistently note its value as a first-line option, particularly in resource-limited settings where cost and monitoring capabilities are considerations.
8. Comparing Clomid with Similar Products and Choosing a Quality Product
When comparing Clomid similar agents, letrozole has emerged as a strong competitor, particularly for PCOS patients, due to potentially better mono-follicular development and less endometrial thinning. Gonadotropins offer higher pregnancy rates but with increased cost, monitoring requirements, and risk of ovarian hyperstimulation syndrome (OHSS).
For which Clomid is better, the pharmaceutical quality is generally consistent among manufacturers, as it’s a well-characterized compound. The more important consideration is appropriate patient selection and monitoring rather than brand preference. How to choose between ovulation induction agents depends on multiple factors: previous response, BMI, ovarian reserve, and patient-specific considerations like medication cost and monitoring availability.
9. Frequently Asked Questions (FAQ) about Clomid
What is the recommended course of Clomid to achieve results?
Most pregnancies occur within 3-6 ovulatory cycles, with diminishing returns beyond 6 cycles. Continuing beyond 12 cycles is generally not recommended without reassessment.
Can Clomid be combined with metformin?
Yes, particularly in insulin-resistant PCOS patients, where the combination may improve ovulation rates compared to either agent alone.
Does Clomid cause multiple births?
The twin rate is approximately 5-8%, with triplets or higher occurring in <1% of cycles. This compares favorably to gonadotropins but exceeds the natural rate.
How long does Clomid stay in your system?
While enclomiphene clears quickly, zuclomiphene can be detected for weeks after discontinuation due to its long half-life and enterohepatic circulation.
10. Conclusion: Validity of Clomid Use in Clinical Practice
Despite newer alternatives, Clomid maintains an important role in reproductive medicine due to its established efficacy, favorable oral administration, and extensive clinical experience. The risk-benefit profile remains acceptable for appropriately selected patients with close monitoring. While letrozole may offer advantages in certain populations, Clomid’s decades of use, predictable response, and cost-effectiveness ensure its continued relevance in evidence-based infertility management.
I remember when we first started using Clomid back in the early 2000s—we were so optimistic about its potential, but reality quickly tempered our enthusiasm. There was this one patient, Sarah, 29-year-old with classic PCOS features: irregular cycles, hirsutism, BMI around 32. We started her on the standard 50mg days 3-7 protocol. First cycle, beautiful response—dominant follicle at 22mm, endometrial thickness 8.5mm, progesterone confirmed ovulation. We were all high-fiving in the clinic. Second cycle, same protocol, but the endometrium barely hit 6mm. By the third cycle, it was down to 5mm despite good follicular growth. We had a team meeting about whether to continue—I was pushing to switch to letrozole, but our senior partner, Dr. Evans, argued for adding vaginal estrogen and continuing with Clomid since she was ovulating well. We compromised by doing one more cycle with estrogen priming, which got the lining to 7mm, but no pregnancy. Ultimately switched to letrozole cycle 5 and she conceived that first cycle. What that taught me was that the zuclomiphene accumulation is real and can really sabotage endometrial receptivity in some patients, something they don’t emphasize enough in the textbooks.
Then there was Mark, 34-year-old with borderline low testosterone and suboptimal sperm parameters. We tried him on 25mg Clomid daily for 3 months—his testosterone went from 280 to 650 ng/dL, but his sperm count actually decreased slightly. We had heated debates in our andrology meetings about whether the estrogenic effects in the testes were counteracting the systemic testosterone boost. We ended up dropping the dose to 25mg every other day, which brought his testosterone to 480 but improved sperm concentration by 30% over the next 3 months. It was a good reminder that the hypothalamic-pituitary-testicular axis responds differently than the ovarian axis, and sometimes less is more with men.
The failed insights really accumulated over the years. We had this hypothesis that overweight patients might need higher doses due to increased volume of distribution—turned out BMI didn’t correlate well with response, but insulin resistance status did. The unexpected finding was that some patients with “Clomid resistance” actually had subtle hypothyroidism that wasn’t picked up on initial screening—once we optimized their levothyroxine, they started responding to lower Clomid doses. We now check TSH and anti-TPO antibodies on everyone before starting ovulation induction.
Longitudinal follow-up has been revealing too. We recently reviewed our 10-year data and found that about 15% of our Clomid successes later developed diminished ovarian reserve earlier than expected—can’t prove causation of course, but it makes you wonder about the long-term effects of multiple stimulated cycles. Meanwhile, I’ve got patients like Jessica who did 6 cycles back in 2015, had twins, and recently returned at 39 for a second child—we were able to get her ovulating again with the same 50mg dose that worked years earlier. She told me last visit, “I know there’s newer stuff out there, but this old faithful worked for me before and it’s working again.”
The professional shorthand we use now reflects these hard-earned lessons: “She’s a zuclomiphene accumulator” or “He’s a testosterone responder but spermatogenesis non-responder.” The art has become knowing when to push through and when to pivot—something that comes only from seeing hundreds of these cases over the years. The research gives you the framework, but the clinical nuance comes from all the individual variations that never make it into the published studies.