clomid
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| Product dosage: 50mg | |||
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Synonyms
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Clomiphene citrate, commonly known by its brand name Clomid, represents one of the foundational pillars in reproductive medicine. As a selective estrogen receptor modulator (SERM), it occupies this unique niche where it essentially tricks the body into thinking estrogen levels are lower than they actually are. This triggers a cascade of hormonal responses, primarily increasing follicle-stimulating hormone (FSH) secretion from the pituitary gland, which then stimulates ovarian follicular development. It’s fascinating how a molecule originally investigated for other purposes became the go-to first-line oral ovulation induction agent worldwide. Its significance lies not just in its efficacy, but in its accessibility and the decades of clinical data backing its use.
Key Components and Bioavailability of Clomid
The active pharmaceutical ingredient is clomiphene citrate, a racemic mixture of two isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). This composition is critical. Enclomiphene is the potent, short-lived isomer responsible for the majority of the ovulatory stimulus. Zuclomiphene, on the other hand, has a much longer half-life and accumulates over successive treatment cycles. It’s less potent but can contribute to some of the estrogenic effects and potentially side effects. We used to think it was inert, but now we know it’s more of a minor player with a persistent presence.
Bioavailability is excellent—it’s well-absorbed orally, which is a huge part of its appeal. You don’t need injections for a first-line treatment. It undergoes enterohepatic circulation and is metabolized in the liver. The zuclomiphene isomer can be detected in the feces for up to a month after you stop a course, which is something we don’t always emphasize enough to patients. It’s formulated almost universally as a 50 mg tablet, making dosing straightforward.
Mechanism of Action of Clomid: Scientific Substantiation
So how does Clomid actually work? It’s a masterclass in endocrine feedback loops. It competes with endogenous estrogen for binding sites at the level of the hypothalamus and pituitary. By blocking these receptors, it creates a perceived state of hypoestrogenism. The hypothalamus gets this false signal and, in response, pulses out more gonadotropin-releasing hormone (GnRH). This, in turn, prompts the anterior pituitary to secrete more FSH and, to a lesser extent, luteinizing hormone (LH).
The increased FSH is the key. It recruits a cohort of ovarian follicles, with one or more becoming dominant and progressing to maturity. This whole process mimics the natural follicular phase, just with a bit of a hormonal push. It’s not creating ovulation from nothing; it’s augmenting an existing, albeit dysfunctional, system. The zuclomiphene component has a weaker estrogenic effect itself, which can sometimes modulate the overall anti-estrogenic effect, making the response a bit unpredictable in some women.
Indications for Use: What is Clomid Effective For?
Clomid for Ovulatory Dysfunction
This is its primary and most evidence-backed indication. For women with anovulation or oligo-ovulation, particularly in the context of polycystic ovary syndrome (PCOS), it’s the first-line pharmacological intervention. The goal is to initiate a single ovulation event per cycle, restoring cyclicity.
Clomid for Unexplained Infertility
We use it quite a bit here as well. The theory is that even with documented ovulation, a “boost” in follicular development and hormonal milieu might improve egg quality or endometrial receptivity, though the evidence for this is less robust than for anovulation. It’s a low-risk intervention to try before moving to more invasive options like IVF.
Clomid for Male Infertility (Off-label)
This is a classic off-label use that’s fallen in and out of favor. The concept is the same—blocking estrogen receptors in the hypothalamic-pituitary axis to increase GnRH and, consequently, FSH and LH. In men, this can stimulate spermatogenesis and increase testosterone production. I’ve seen it work wonders for some men with hypogonadotropic hypogonadism, but the results are highly variable.
Clomid for Luteal Phase Defect
By enhancing follicular development, you often get a more robust corpus luteum, which can correct a lagging luteal phase. It’s a secondary benefit that can be quite significant.
Instructions for Use: Dosage and Course of Administration
The standard protocol is to start low and go slow. We almost always initiate at 50 mg daily for 5 days, typically starting on day 3, 4, or 5 of the menstrual cycle. You need some baseline estrogen activity for it to work effectively, hence not starting on day 1.
If ovulation occurs but pregnancy doesn’t, you can continue at the same dose. If there’s no ovulation, we titrate up in 50 mg increments per cycle to a maximum of 150 mg daily. I rarely go beyond that; the side effect profile escalates and the endometrial thinning becomes a real concern. The data is very clear that conception rates are best in the first 3-6 ovulatory cycles. After that, the success rate plateaus dramatically, and it’s time to re-evaluate the treatment plan.
Here’s a typical dosing table:
| Indication | Starting Dose | Duration | Cycle Day Start | Max Dose |
|---|---|---|---|---|
| Female Anovulation | 50 mg | 5 days | 3-5 | 150 mg |
| Unexplained Infertility | 50 mg | 5 days | 3-5 | 100 mg |
| Male Infertility (Off-label) | 25-50 mg | Daily or EOD | N/A | 50 mg |
Monitoring is key. We use cycle day 21 progesterone levels to confirm ovulation and often do baseline and mid-cycle ultrasounds to track follicular growth and endometrial thickness, especially at higher doses or if there’s a history of cysts.
Contraindications and Drug Interactions with Clomid
You absolutely cannot use it in pregnancy—it’s Category X. It’s also contraindicated in patients with liver disease, abnormal uterine bleeding of undetermined origin, ovarian cysts (unrelated to PCOS), or hormone-sensitive tumors.
Drug interactions are relatively minimal due to its mechanism, but it’s always wise to be cautious. We watch for interactions with other medications metabolized by the CYP450 system. One thing we learned the hard way is that using it concurrently with other ovulation-inducing agents like letrozole doesn’t add benefit and significantly increases the risk of ovarian hyperstimulation syndrome (OHSS) and multiple gestation.
The side effects are mostly dose-dependent. Patients frequently report hot flashes, which make perfect sense given the anti-estrogenic effect in the hypothalamus. Mood swings, breast tenderness, and nausea are also common. The two most clinically significant side effects are the risk of multiple gestation (about 8-10%, mostly twins) and the potential for Clomid to cause a thin endometrial lining at higher doses, which can ironically impair implantation even if ovulation occurs.
Clinical Studies and Evidence Base for Clomid
The evidence base is massive and spans over 50 years. A landmark study often cited is the 2014 New England Journal of Medicine article comparing Clomid to letrozole for infertility in women with PCOS. It showed letrozole had higher live birth rates (27.5% vs. 19.1%), which shifted practice patterns, but it didn’t invalidate Clomid—it just provided another effective option.
Cochrane reviews consistently affirm its efficacy over placebo for ovulation induction in PCOS. The pregnancy rates per cycle with Clomid for anovulatory women are in the 15-20% range, which is excellent for an oral medication. For male infertility, the data is murkier. Some meta-analyses show modest improvements in sperm parameters and pregnancy rates, while others show no significant benefit over placebo. It really seems to be a subset of men who respond.
Comparing Clomid with Similar Products and Choosing a Quality Product
The most direct comparison is with letrozole, an aromatase inhibitor. Letrozole works by blocking the conversion of androgens to estrogen, creating a true state of hypoestrogenism. The debate in our clinic is ongoing. Letrozole seems to have a slight edge in live birth rates for PCOS patients and is associated with less endometrial thinning. However, Clomid has a longer safety track record and is often more readily available and affordable.
Compared to injectable gonadotropins, Clomid is far less potent, has a much lower risk of severe OHSS, and is exponentially cheaper. It’s the logical first step before escalating to that level of intervention.
As for choosing a product, clomiphene citrate is a generic drug. The bioequivalence between manufacturers is generally reliable. The key isn’t the brand; it’s the prescribing and monitoring protocol. A quality product is one prescribed by a provider who understands its nuances, monitors the response with ultrasounds and progesterone levels, and knows when to stop or change course.
Frequently Asked Questions (FAQ) about Clomid
What is the recommended course of Clomid to achieve results?
We typically recommend a maximum of 3-6 ovulatory cycles. The vast majority of pregnancies that will occur with Clomid happen within this window. Continuing beyond six cycles has diminishing returns and increases cumulative side effects.
Can Clomid be combined with other fertility medications?
It can be, but this is a decision for a specialist. It’s commonly used with metformin in PCOS patients to improve insulin sensitivity and ovulatory response. Combining it with injectable gonadotropins is a more advanced protocol that significantly increases the risk of multiples and OHSS and requires intense monitoring.
Does Clomid cause birth defects?
Extensive research has not shown a significant increase in the rate of birth defects above the baseline population risk when used for ovulation induction as directed. The concern is its use during an established pregnancy, which is why confirmation of non-pregnancy before each cycle is mandatory.
Why did I ovulate on Clomid but not get pregnant?
This is incredibly common and frustrating for patients. Ovulation is just one piece of the puzzle. Other factors like sperm quality, tubal patency, and endometrial receptivity are equally critical. Clomid itself can sometimes negatively impact the endometrial lining or cervical mucus, creating barriers to conception despite successful ovulation.
Conclusion: Validity of Clomid Use in Clinical Practice
Clomid remains a valid, powerful, and essential tool in the reproductive endocrinology arsenal. Its risk-benefit profile is well-established. For the right patient—primarily the anovulatory woman—it is a safe and effective first-line treatment that can restore fertility with minimal intervention. Its limitations, particularly concerning endometrial effects and a defined window of efficacy, are now well understood, allowing clinicians to use it more judiciously. It may no longer be the only oral agent we have, but its legacy and utility are secure.
I remember one patient, Sarah, a 32-year-old with classic PCOS—anovulatory, insulin resistant. We started her on the standard 50 mg Clomid protocol. First cycle, beautiful follicle, textbook progesterone rise… but no pregnancy. Second cycle, same thing. The third cycle, we upped it to 100 mg. She came in for her mid-cycle scan, and I saw two dominant follicles. We had the talk about the increased risk of twins. She was nervous but decided to proceed. That cycle, she conceived. Not twins, but a single, healthy pregnancy. She sent a card to the clinic after her daughter was born, saying, “Thank you for not giving up after two cycles.” It was a good reminder that sometimes persistence within a reasoned protocol pays off.
Then there was Mark, a 28-year-old bodybuilder using anabolic steroids who came to us with post-cycle hypogonadism—zero sperm count. His testosterone was in the tank. We had a big debate in the practice. One of my partners was vehemently against treating him, calling it “cleaning up a self-inflicted problem.” I argued that our job was to treat the patient in front of us, not judge his past. We started Mark on 25 mg of Clomid every other day. It was a bit of a Hail Mary. Three months later, his testosterone had tripled, and his repeat semen analysis showed a few motile sperm. It wasn’t a home run, but it was a start. He was able to freeze a sample. It taught me that even in less conventional scenarios, the basic endocrine principles still apply, and you can sometimes salvage a difficult situation.
The biggest struggle we had internally was letting go of the “more is better” mentality. For years, we’d push the dose to 150 mg, even 200 mg, trying to force a response. We’d see these patients with beautiful follicles on ultrasound but a paper-thin endometrium. We were so focused on the ovary we forgot about the uterus. I had a run of three patients in a row who ovulated on 150 mg but didn’t conceive, and when we dropped them back down to 50 mg, two of them got pregnant the very next cycle. It was a humbling lesson. The goal isn’t just to make an egg; it’s to create an environment where that egg can become a baby. Sometimes the drug that fixes the first problem inadvertently creates a second one. It’s a constant balancing act.