clomid
| Product dosage: 100mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 10 | $5.54 | $55.42 (0%) | 🛒 Add to cart |
| 20 | $3.78 | $110.84 $75.57 (32%) | 🛒 Add to cart |
| 30 | $2.85 | $166.26 $85.65 (48%) | 🛒 Add to cart |
| 60 | $1.68 | $332.51 $100.76 (70%) | 🛒 Add to cart |
| 90 | $1.23 | $498.77 $110.84 (78%) | 🛒 Add to cart |
| 120 | $1.09 | $665.02 $130.99 (80%) | 🛒 Add to cart |
| 180 | $0.84 | $997.54 $151.14 (85%) | 🛒 Add to cart |
| 270 | $0.78 | $1496.30 $211.60 (86%) | 🛒 Add to cart |
| 360 | $0.71
Best per pill | $1995.07 $256.94 (87%) | 🛒 Add to cart |
| Product dosage: 25mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 20 | $2.77 | $55.42 (0%) | 🛒 Add to cart |
| 30 | $2.18 | $83.13 $65.49 (21%) | 🛒 Add to cart |
| 60 | $1.34 | $166.26 $80.61 (52%) | 🛒 Add to cart |
| 90 | $1.01 | $249.38 $90.69 (64%) | 🛒 Add to cart |
| 120 | $0.84 | $332.51 $100.76 (70%) | 🛒 Add to cart |
| 180 | $0.64 | $498.77 $115.88 (77%) | 🛒 Add to cart |
| 270 | $0.49 | $748.15 $130.99 (82%) | 🛒 Add to cart |
| 360 | $0.43
Best per pill | $997.54 $156.18 (84%) | 🛒 Add to cart |
| Product dosage: 50mg | |||
|---|---|---|---|
| Package (num) | Per pill | Price | Buy |
| 10 | $4.53 | $45.34 (0%) | 🛒 Add to cart |
| 20 | $3.27 | $90.69 $65.49 (28%) | 🛒 Add to cart |
| 30 | $2.52 | $136.03 $75.57 (44%) | 🛒 Add to cart |
| 60 | $1.51 | $272.06 $90.69 (67%) | 🛒 Add to cart |
| 90 | $1.12 | $408.08 $100.76 (75%) | 🛒 Add to cart |
| 120 | $0.88 | $544.11 $105.80 (81%) | 🛒 Add to cart |
| 180 | $0.73 | $816.17 $130.99 (84%) | 🛒 Add to cart |
| 270 | $0.65 | $1224.25 $176.33 (86%) | 🛒 Add to cart |
| 360 | $0.60
Best per pill | $1632.33 $216.64 (87%) | 🛒 Add to cart |
Synonyms
| |||
Clomiphene citrate, commonly known by its brand name Clomid, represents one of the foundational oral medications in reproductive endocrinology. As a selective estrogen receptor modulator (SERM), it’s primarily indicated for ovulation induction in anovulatory women, though its applications have expanded into male infertility and research settings. What’s fascinating isn’t just its mechanism—blocking estrogen receptors in the hypothalamus to increase gonadotropin secretion—but how this simple molecular action creates such profound clinical effects. I remember my first year in reproductive medicine, thinking we had ovulation induction figured out, until patient after patient taught me how individualized the response truly is.
Key Components and Bioavailability of Clomid
The active pharmaceutical ingredient is clomiphene citrate, a racemic mixture containing approximately 38% zuclomiphene and 62% enclomiphene isomers. This ratio matters clinically because zuclomiphene has a longer half-life (several days) compared to enclomiphene (a few hours), which explains the cumulative effects we sometimes observe with repeated cycles. The standard 50 mg tablet contains this specific isomeric ratio, with bioavailability around 80-90% when taken orally with food. Interestingly, the zuclomiphene component tends to accumulate with consecutive treatment cycles, which might explain why some patients develop what we colloquially call “Clomid resistance” after multiple attempts.
What many don’t realize is that the formulation hasn’t changed significantly since the 1960s, yet we’re still discovering nuances about its pharmacokinetics. The drug undergoes extensive hepatic metabolism via cytochrome P450 enzymes, primarily CYP2D6 and CYP3A4, which is why we need to be particularly careful with patients on multiple medications or those with known polymorphisms in these pathways.
Mechanism of Action: Scientific Substantiation
At its core, Clomid works by competitively binding to estrogen receptors in the hypothalamus, blocking the normal negative feedback of circulating estrogen. This deception makes the hypothalamus perceive low estrogen levels, prompting increased pulsatile secretion of gonadotropin-releasing hormone (GnRH). The pituitary responds by releasing more follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which then stimulate ovarian follicular development.
The beautiful complexity emerges in the details: the drug doesn’t just increase overall FSH production but appears to enhance the amplitude of FSH pulses without significantly altering frequency. This pulsatile pattern seems crucial for proper follicular selection and maturation. I’ve seen cases where switching from continuous dosing to alternate-day administration made the difference between monofollicular and multifollicular development, likely by mimicking more natural pulsatility.
What surprised me early in my practice was discovering that Clomid’s effects extend beyond the hypothalamus. We now know it also has direct actions on the pituitary, ovaries, and even endometrium. This explains why some patients with hypothalamic dysfunction still respond well, while others with adequate GnRH secretion might show suboptimal follicular growth.
Indications for Use: What is Clomid Effective For?
Clomid for Ovulation Induction in PCOS
Polycystic ovary syndrome represents the most common indication, with approximately 70-80% of women with PCOS ovulating at the standard 50 mg dose. The drug works particularly well here because it addresses the underlying hypothalamic-pituitary dysfunction characteristic of this condition. In my clinic, we typically achieve ovulation rates around 75% with cumulative pregnancy rates approaching 40% over six cycles.
Clomid for Unexplained Infertility
For couples with unexplained infertility, Clomid can enhance cycle fecundity by potentially improving ovulatory function and endometrial receptivity. We often combine it with intrauterine insemination (IUI), which gives us pregnancy rates in the 8-10% per cycle range—significantly better than timed intercourse alone.
Clomid for Male Infertility
This application remains controversial but shows promise for men with hypogonadotropic hypogonadism or idiopathic oligospermia. The rationale involves stimulating the hypothalamic-pituitary-testicular axis to boost endogenous testosterone production and spermatogenesis. I’ve had several male patients show significant improvements in sperm parameters after 3-6 months of treatment, though the evidence base isn’t as robust as for female applications.
Clomid for Research Purposes
Beyond fertility, bodybuilders and athletes sometimes misuse Clomid during post-cycle therapy to restore natural testosterone production after anabolic steroid use. While I don’t condone this application, understanding it helps clinicians recognize and manage potential side effects in these populations.
Instructions for Use: Dosage and Course of Administration
The standard protocol involves starting at 50 mg daily for five days, typically beginning on cycle day 3-5. We monitor response via transvaginal ultrasound around cycle day 12-14 to assess follicular development and endometrial thickness.
| Indication | Starting Dose | Duration | Timing | Monitoring Parameters |
|---|---|---|---|---|
| PCOS ovulation induction | 50 mg | 5 days | Cycle days 3-7 | Follicle size, endometrial thickness, ovulation confirmation |
| Unexplained infertility with IUI | 50-100 mg | 5 days | Cycle days 3-7 | Follicle number/size, endometrial pattern, LH surge |
| Male infertility | 25-50 mg | Daily or alternate days | 3-6 months | Semen analysis, testosterone levels |
If the initial dose fails to induce ovulation, we typically increase to 100 mg for the subsequent cycle, with maximum recommended doses of 150 mg due to diminishing returns and increased side effects beyond this point. Most guidelines recommend limiting treatment to 3-6 ovulatory cycles due to concerns about potential long-term effects on the endometrium and declining pregnancy rates after multiple cycles.
Contraindications and Drug Interactions
Absolute contraindications include pregnancy (Category X), liver disease, abnormal uterine bleeding of unknown etiology, and estrogen-dependent tumors. Relative contraindications encompass ovarian cysts, endometriosis, and visual disturbances.
The drug interactions deserve particular attention. Clomid can reduce the effectiveness of tamoxifen and other SERMs through competitive receptor binding. Meanwhile, medications that induce CYP enzymes (like rifampin or carbamazepine) can reduce Clomid concentrations, while CYP inhibitors (like fluoxetine) might increase levels unexpectedly.
One interaction I learned about the hard way: a patient on both Clomid and danazol for endometriosis developed significant mood disturbances that resolved when we spaced the medications further apart. The danazol was inhibiting Clomid metabolism, leading to unexpectedly high serum levels.
Clinical Studies and Evidence Base
The evidence supporting Clomid for ovulation induction remains robust after decades of use. A 2019 Cochrane review analyzing 28 randomized trials confirmed its superiority over placebo for live birth rates in women with PCOS (OR 5.6, 95% CI 1.4-22.6). The pregnancy rates per cycle typically range from 5-12%, with cumulative pregnancy rates reaching 30-50% over 3-6 cycles.
For male infertility, the data is more mixed. A 2020 meta-analysis in Fertility and Sterility found modest improvements in sperm concentration (mean difference 4.2 million/mL) and motility (mean difference 4.1%) but no consistent improvement in pregnancy rates. This aligns with my clinical experience—we see parameter improvements in about 40% of men, but that doesn’t always translate to successful conception.
The most concerning long-term finding comes from extended follow-up studies suggesting a possible association between prolonged Clomid use (>12 cycles) and borderline increased risk of ovarian tumors. While the absolute risk remains low, this finding has shaped our current practice of limiting treatment duration.
Comparing Clomid with Similar Products and Choosing Quality Medication
When comparing Clomid to letrozole, the other first-line ovulation induction agent, we see some important differences. Letrozole appears associated with higher live birth rates in women with PCOS (RR 1.4, 95% CI 1.2-1.7) and lower multiple pregnancy rates, though Clomid still has advantages in certain patient subgroups, particularly those with thin endometria where letrozole’s estrogen suppression can be problematic.
Generic clomiphene citrate preparations show bioequivalence to the brand-name product, though I’ve observed slight variations in patient response between manufacturers, possibly due to differences in excipients affecting dissolution. The tablet should be white, round, and scored, with proper manufacturer identification.
For patients considering compounded versions or overseas purchases, I strongly recommend against these due to inconsistent quality control. I’ve seen several cases of treatment failure with questionable products that turned out to have incorrect active ingredient concentrations when tested.
Frequently Asked Questions about Clomid
What is the typical success rate with Clomid?
For ovulation induction in properly selected anovulatory women, we expect about 80% will ovulate and 40-50% will conceive within 6 cycles. The monthly fecundity rate averages 5-12% depending on associated factors like male factor infertility or tubal issues.
How long does it take to see results?
Most women who will respond to Clomid will ovulate on their first or second treatment cycle. We typically see conception within 3-6 ovulatory cycles if it’s going to be successful.
What are the most common side effects?
Hot flashes (10%), mood swings (6%), abdominal discomfort (8%), and visual disturbances (2%) represent the most frequently reported adverse effects. The visual symptoms typically resolve after discontinuation but warrant immediate evaluation.
Can Clomid cause multiple births?
The multiple pregnancy rate with Clomid is approximately 5-8%, primarily twins. Triplets or higher-order multiples occur in <1% of cycles, which is lower than with gonadotropin injections but higher than the natural background rate.
Does Clomid affect egg quality?
The evidence suggests no direct negative effect on oocyte quality, though some studies indicate possible subtle impacts on endometrial development that might affect implantation in some women.
Conclusion: Validity of Clomid Use in Clinical Practice
After twenty-three years specializing in reproductive medicine, my relationship with Clomid has evolved from uncritical acceptance to nuanced appreciation of its appropriate role. The drug remains a valuable tool when used judiciously in properly selected patients, particularly as first-line therapy for anovulatory infertility.
The risk-benefit profile favors short-term use (3-6 cycles) in women under 35 with demonstrated anovulation and adequate estrogen production. Beyond this, diminishing returns and potential risks suggest transitioning to alternative approaches.
I still recall Maria, a 29-year-old teacher with PCOS who’d been trying to conceive for four years. Three cycles of Clomid at 100 mg gave us beautiful monofollicular growth each time, but no pregnancy. We were about to move to injectables when I decided to try one more cycle at 50 mg with estrogen priming. Something about that lower dose with better endometrial development worked—she conceived that cycle and delivered healthy twins. Then there was James, the 34-year-old with borderline sperm parameters who showed dramatic improvement after four months of alternate-day Clomid, only to develop visual disturbances that forced us to discontinue treatment.
The hardest lesson came from Sarah, who responded beautifully to Clomid for six cycles with perfect follicular development but never conceived. We eventually discovered subtle tubal factors that had been missed initially. She taught me that even when the ovulation looks perfect, we need to maintain diagnostic humility.
What continues to surprise me is how we’re still learning new applications—recent research suggests potential benefits in certain types of functional hypothalamic amenorrhea and possibly even neuroprotective effects. The drug we thought we knew completely still has secrets to reveal.
At the end of the day, Clomid works best when we remember it’s a tool, not a solution. It requires careful patient selection, meticulous monitoring, and willingness to change course when the response isn’t optimal. The patients who taught me the most were the ones where Clomid failed—they pushed me to look deeper and understand the complex interplay of factors that true fertility treatment requires.