Y-134

Y134; Y 134 — a raloxifene-derived benzothiophene selective estrogen receptor modulator (SERM), ER-alpha-selective. CAS 849662-80-2. NOT an aromatase inhibitor

Y-134 (Y134; Y 134 — a raloxifene-derived benzothiophene selective estrogen receptor modulator (SERM), ER-alpha-selective. CAS 849662-80-2. NOT an aromatase inhibitor) is a hormonal & sexual research compound. A raloxifene-derived benzothiophene that blocks the estrogen receptor rather than lowering estrogen — it is not an aromatase inhibitor. Y-134 keeps raloxifene's 6-hydroxy-2-(4-hydroxyphenyl)benzothiophene core and swaps raloxifene's piperidine side chain for an isopropyl-piperazine; that side chain is what the series was built around, and the series was reported as high-affinity ER-alpha-selective ligands. In CV-1 cells cotransfected with ER-alpha or ER-beta plus an estrogen-response-element luciferase reporter, Y-134 antagonized with an estimated IC50 of 0.52 nM at ER-alpha and 2.94 nM at ER-beta. Like its parent it is tissue-selective rather than uniformly blocking: antagonist in reproductive tissue, while the piperazine benzothiophene series it comes from was reported as potent agonists in bone. In ovariectomized rats it arrested estrogen-driven mammary terminal end bud outgrowth and mammary DNA synthesis more effectively than raloxifene at the same dose, with comparable uterine suppression. It also activates the aryl hydrocarbon receptor.

How Y-134 works

A raloxifene-derived benzothiophene that blocks the estrogen receptor rather than lowering estrogen — it is not an aromatase inhibitor. Y-134 keeps raloxifene's 6-hydroxy-2-(4-hydroxyphenyl)benzothiophene core and swaps raloxifene's piperidine side chain for an isopropyl-piperazine; that side chain is what the series was built around, and the series was reported as high-affinity ER-alpha-selective ligands. In CV-1 cells cotransfected with ER-alpha or ER-beta plus an estrogen-response-element luciferase reporter, Y-134 antagonized with an estimated IC50 of 0.52 nM at ER-alpha and 2.94 nM at ER-beta. Like its parent it is tissue-selective rather than uniformly blocking: antagonist in reproductive tissue, while the piperazine benzothiophene series it comes from was reported as potent agonists in bone. In ovariectomized rats it arrested estrogen-driven mammary terminal end bud outgrowth and mammary DNA synthesis more effectively than raloxifene at the same dose, with comparable uterine suppression. It also activates the aryl hydrocarbon receptor.

Proposed benefits

Researched as an ER-alpha-selective estrogen receptor modulator, studied in cells and rats for mammary antiproliferative activity and for the bone-agonist, reproductive-tissue-antagonist profile that defines the SERM class.

Where to get Y-134

The evidence for Y-134

Graded by what exists behind each claim.

✅ Clinically validated

• No human study of Y-134 exists — no trial, no case series, no pharmacokinetics in any species. The compound has been in the literature since 2005 as a chemical entity and since 2007 as a characterized SERM, and in roughly two decades nobody has published a human exposure to it.
• A transdermal SERM has been tried in humans, with a different molecule, and the trial did not meet its endpoint. A randomized presurgical trial in women with ductal carcinoma in situ compared oral tamoxifen citrate 20 mg/day against 4-hydroxytamoxifen gel 2 mg/day per breast. The gel did what a topical route is supposed to do — systemic endoxifen was minimal, median 0.3 ng/g against 13.0 ng/g for oral — and antiproliferative noninferiority of the gel was not confirmed, which the authors attribute to exactly that exposure difference. That is a different molecule and a breast application rather than general transdermal use, so it is not a result about Y-134. It is the closest human evidence anywhere near the route this product uses, and its direction is that low systemic exposure came at the cost of the biological effect.

📊 Correlative data

• Nothing. There is no human observational, association or uncontrolled data on Y-134 either. This tier is empty rather than thin, and saying so is more useful than filling it with raloxifene's epidemiology, which belongs to a different molecule that has been through phase 3 and has a label.

🧪 Theoretical / extrapolated

• Potent ER antagonism with a measured selectivity ratio. In CV-1 cells cotransfected with ER-alpha or ER-beta and an estrogen-response-element-driven luciferase reporter, the estimated IC50 was 0.52 nM at ER-alpha and 2.94 nM at ER-beta, which the authors call comparable to raloxifene. Five analogs from two structural series were evaluated and all bound ER-alpha more tightly than ER-beta.
• The mammary-selectivity claim, which is the reason the compound has a name. In ovariectomized rats given the same dose, Y-134 was more effective than raloxifene at arresting estrogen-induced outgrowth of mammary terminal end buds and mammary gland DNA synthesis, while the two drugs' inhibitory effects on the uterus were comparable. Better selectivity meant more mammary effect at equal uterine effect — not less uterine effect. Y-134 also suppressed estrogen-stimulated proliferation of ER-positive MCF-7 and T47D human breast cancer cells, with little cytotoxicity below 10 microM.
• Bone agonism belongs to the series, not yet to this molecule. The 2005 synthesis paper describing the piperazine-side-chain benzothiophenes reports them as high-affinity, ER-alpha-selective and potent agonists in bone tissue. That abstract does not name Y-134. The 2007 pharmacology paper that does name Y-134 measured uterus and mammary gland, not bone. So the bone half of the SERM profile is a property of the chemical family that nobody has published for this member.
• A second receptor, and it is not an estrogen receptor. Y-134 was identified in a structure-activity screen of seven raloxifene analogs as an aryl hydrocarbon receptor (AhR) activator: it induced AhR-mediated transcriptional activity and apoptosis in MDA-MB-231 triple-negative (ER-negative) human breast cancer cells, and suppressing AhR expression strongly reduced that apoptosis — so the effect required AhR. It also induced apoptosis in hepatoma cells without affecting cell cycle regulation. In the same paper, zebrafish embryo toxicity testing found Y-134 had a significantly better safety profile than raloxifene. That is the only comparative toxicity datum that exists for this molecule, and it is in fish embryos.
• Independent use as a tool compound corroborates the ER-alpha selectivity. An unrelated group studying estrogen and dopamine neuron firing used Y134 in rats as 'a selective ERalpha antagonist' alongside raloxifene, and pretreatment with either largely attenuated cocaine-inhibited firing of ventral tegmental area dopamine neurons. Independent researchers reaching for it as a selective ER-alpha antagonist is weak evidence about efficacy and reasonable evidence that the selectivity claim survived outside the originating lab.

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What Y-134 actually does

Settle the class before the mechanism, because the wrong class is the expensive mistake here. Y-134 is a selective estrogen receptor modulator. It is not a SARM — it does not touch the androgen receptor — and it is not an aromatase inhibitor. An aromatase inhibitor lowers the amount of estrogen in circulation; a SERM leaves estrogen circulating and occupies the receptor it acts through. Those two produce different bloodwork, different bone consequences and different failure modes, and they are routinely spoken about as if interchangeable.

The structure tells you where it came from. Y-134 is [6-hydroxy-2-(4-hydroxyphenyl)benzo[b]thien-3-yl]-[4-[4-(1-methylethyl)-1-piperazinyl]phenyl]methanone, C₂₈H₂₈N₂O₃S, 472.60 g/mol, CAS 849662-80-2. That first half is raloxifene's own core: a benzothiophene bearing two phenolic hydroxyls, one at the 6-position and one on the 2-aryl ring. What differs is the basic side chain — raloxifene carries a piperidine, Y-134 carries an isopropyl-piperazine. The 2005 synthesis paper describing this series states the design intent plainly: benzothiophenes with a piperazine side chain, selected as high-affinity ligands selective for the ER-alpha subtype Yang 2005. Yang C and Wang M appear as authors on both that paper and the 2007 pharmacology paper Ning 2007, so the chemistry and the characterization come from one continuous program.

The receptor numbers, and what they are numbers from. Ning 2007 transfected CV-1 cells with plasmids carrying ER-alpha or ER-beta plus an estrogen-response-element-driven luciferase reporter and measured antagonism. The estimated IC₅₀ was 0.52 nM at ER-alpha and 2.94 nM at ER-beta — roughly a six-fold preference, which the authors describe as comparable in potency to raloxifene. Five analogs across two structural series were evaluated and all showed higher binding affinity for ER-alpha than ER-beta. Note what the readout is: transcription off a synthetic reporter in a monkey kidney cell line forced to express one receptor. It is a clean measurement of receptor-level antagonism and it is not a measurement of anything in a tissue.

Tissue selectivity is the definition of the class, and it is a property of coregulators rather than of the drug. The same ligand reads as antagonist in one tissue and agonist in another because the receptor's bound conformation recruits different coactivator and corepressor complexes, and which of those are locally abundant differs by tissue. For this series the published pattern is antagonist in reproductive tissue, agonist in bone Yang 2005 — which is why no single sentence covers what one of these does to a person.

The mammary claim, stated the way the paper states it, because the direction is often reversed in the retelling. In ovariectomized rats given Y-134 and raloxifene at an identical dose, Y-134 was more effective than raloxifene at arresting estrogen-induced outgrowth of mammary terminal end buds and mammary gland DNA synthesis, while their inhibitory effects on the uterus were comparable Ning 2007. So “better mammary selectivity” here means more mammary effect at the same uterine effect — not less uterine effect. The uterus is suppressed either way.

There is a second receptor in this molecule's file, and it is not an estrogen receptor. A structure-activity study of seven raloxifene analogs identified Y-134 as an activator of the aryl hydrocarbon receptor: it drove AhR-mediated transcriptional activity and induced apoptosis in MDA-MB-231 triple-negative, ER-negative human breast cancer cells, and suppressing AhR expression strongly reduced that apoptosis, establishing the receptor as required rather than incidental Jang 2017. It also killed hepatoma cells without affecting cell cycle regulation. AhR is the xenobiotic-sensing transcription factor that drives the CYP1A arm of drug metabolism, so this is not a footnote — it is a second pharmacology with its own consequences, running in a molecule sold on the first one.

Cell, rodent, human — and where it stops

The chain for this compound is short and it stops early: reporter cell → human cancer cell line → zebrafish embryo → ovariectomized rat → nothing. Worth walking, because each rung measured something different and none of them measured a person.

Reporter cells — receptor-level antagonism. CV-1 cells, a monkey kidney line, cotransfected with ER-alpha or ER-beta and an estrogen-response-element luciferase construct. IC₅₀ 0.52 nM at ER-alpha, 2.94 nM at ER-beta Ning 2007. This establishes that the molecule engages the receptor and blocks transcription from it. It establishes nothing about tissue, absorption or duration.

Human cancer cell lines — the antiproliferative claim. Y-134 suppressed estrogen-stimulated proliferation of ER-positive MCF-7 and T47D human breast cancer cells, with little cytotoxicity below 10 microM Ning 2007. Separately, and through the other receptor entirely, it induced apoptosis in MDA-MB-231 cells, which are ER-negative — an effect that disappeared when AhR expression was suppressed Jang 2017. Two distinct mechanisms, two distinct cell contexts, both in dishes.

Zebrafish embryos — the only comparative safety datum in existence. Toxicity testing in zebrafish embryos found Y-134 had a significantly better safety profile than raloxifene Jang 2017. That is a genuine finding and it is a fish embryo. It is not a mammalian toxicology package, it says nothing about repeat dosing, and it must not be read as evidence that this compound is safer than a drug with a label and two decades of postmarketing surveillance.

Ovariectomized rats — the only in vivo efficacy work. Female rats, ovaries removed so that endogenous estrogen is out of the picture, then estrogen stimulation plus drug, with three readouts: wet weight, BrdU incorporation and terminal end bud counts Ning 2007. Y-134 beat raloxifene on mammary terminal end bud outgrowth and mammary DNA synthesis at the same dose, and matched it on the uterus. A second group independently used Y134 as a pretreatment in rats, describing it as a selective ERalpha antagonist, and found that it (like raloxifene) largely attenuated cocaine-inhibited firing of ventral tegmental area dopamine neurons Zhang 2008 — a different question entirely, and useful here mainly as outside corroboration that the selectivity label held up in another lab's hands.

Humans — and this is where the chain ends rather than narrows. Zero. No phase 1, no single-dose exposure, no case report. There is no obstacle to describe in the usual sense of a species difference or a dosing problem, because the step was never attempted.

The three specific obstacles between what was published and what is in the bottle. First, the route does not match. The rat work delivered drug systemically and neither abstract states the route or the dose; the product is a topical solution. Nothing in the published record was applied to skin. Second, the model does not match the buyer. Every in vivo finding comes from an ovariectomized female rat under estrogen challenge — a preparation built to isolate estrogen-receptor pharmacology, and about as far from an intact adult human of either sex as an animal model gets. Third, the one human trial of a topical SERM went the unhelpful way. Khan 2023 got the low systemic exposure a topical route promises and failed to confirm noninferiority on the biological endpoint. The generous reading of this product's route is that it is untested; the evidence-based reading is that the nearest tested version of the idea did not clear its bar.

Y-134 pharmacokinetics — how much of it actually gets in

Start with the blank and then do the work the blank allows. No pharmacokinetic study of Y-134 has been published in any species: no absorption fraction, no C_max, no half-life, no clearance route, oral or topical. Not poorly characterized — absent, across two decades in which three separate groups used the compound Ning 2007 Jang 2017 Zhang 2008. What follows is the reasoning that bounds the exposure, which is the only honest substitute for a measurement.

What the structure predicts about clearance. Y-134 carries two phenolic hydroxyls. Phenols are the canonical substrate for phase II conjugation, and glucuronidation of both positions is the dominant clearance route for the benzothiophene SERM scaffold — which is precisely why an oral drug of this shape delivers so little intact molecule to the circulation, and why a route that bypasses the gut wall and liver looks attractive on paper. It also predicts the less convenient half: a conjugated bis-phenol excreted in bile can be deconjugated by gut bacteria and reabsorbed, and that enterohepatic recycling is what gives this class a long terminal half-life out of proportion to its metabolic lability. If Y-134 is absorbed at all, the prediction is accumulation across days rather than a clean daily on-off — which matters because the effects that make this class consequential, on coagulation protein synthesis and on bone turnover, integrate over weeks.

Now the route actually on sale, which is the harder problem. Passive permeation of intact stratum corneum falls off steeply above roughly 500 Da, and 472.60 g/mol sits right at that edge. Worse for flux: the isopropyl-piperazine is a basic nitrogen, protonated at skin-surface pH, and a charged species crosses a lipid barrier far less readily than a neutral one. Transdermal delivery of a molecule like this is decided almost entirely by the vehicle — the solvent system, any penetration enhancer, the occlusion — and DA's page states a concentration and a volume and no vehicle at all. That single omission makes the delivered fraction unknowable from the label rather than merely unmeasured.

The one human measurement that speaks to this route, and it is a different molecule. Khan 2023 randomized women with ductal carcinoma in situ to oral tamoxifen citrate 20 mg/day versus 4-hydroxytamoxifen gel 2 mg/day per breast before surgery. The gel behaved exactly as a topical route is meant to: systemic endoxifen was minimal — median 0.3 ng/g (IQR 0–0.3) against 13.0 ng/g (IQR 8.9–20.6) for oral. And the trial's own conclusion is that antiproliferative noninferiority of the gel was not confirmed, which the authors attribute to that exposure difference. A trial was run, and it did not show what people assume a topical SERM shows. This is 4-hydroxytamoxifen applied directly over the target tissue, not Y-134 applied to skin, so it transfers as a caution about the route rather than as a result about this compound.

The arithmetic that is actually available. 20 mg/mL × 30 mL = 600 mg of Y-134 in the bottle, a figure DA prints itself. Against a compound whose receptor IC₅₀ is sub-nanomolar, that is an enormous quantity of a potent hormonal ligand, and the honest statement is the uncomfortable one: nobody — not the vendor, not this page — can convert a volume applied to skin into a plasma concentration, because the study that would permit it has never been run in any species. That is the reason the dose field on this card is empty rather than conservative.

What would have to be true, and how you would know it was not

Four predictions. The first is the one everything else depends on, the fourth cuts against the product, and each names something a person can actually draw or measure.

1. If any clinically meaningful amount crosses the skin, SHBG moves. If SHBG does not move, nothing systemic is happening. Hepatic estrogen-receptor activity is the most sensitive routine readout of systemic estrogen-pathway engagement there is, and sex hormone binding globulin is its cheapest expression: the liver's SHBG output tracks estrogen-receptor signaling closely. Draw SHBG at baseline and six weeks. This is the load-bearing measurement on the whole page, because Khan 2023 demonstrated in humans that a topical SERM can deliver minimal systemic drug — median endoxifen 0.3 against 13.0 ng/g — while still being applied daily. A flat SHBG is the most likely result and it is informative in both directions: it means the systemic claims do not apply, and equally that the systemic fears do not. Nobody has run it.

2. Bone turnover markers should fall, and in a specific order, if the series' bone agonism holds for this member. The prediction from Yang 2005 is estrogen-receptor agonism in bone, which suppresses resorption. Resorption reports first: CTX (C-terminal telopeptide) down at 3 months, with P1NP as the formation marker following it downward as the coupled pair re-equilibrates. DEXA is the wrong instrument for this window — bone mineral density needs 12–24 months to move detectably, and a scan at 3 months answers nothing. The falsification is clean: a SERM that is systemically active and genuinely bone-agonist cannot leave CTX unchanged.

3. The lipid signature, which is the class's most reproducible non-skeletal effect. Hepatic estrogen-receptor engagement predicts LDL-C and ApoB down, HDL-C roughly unmoved, triglycerides variable — a pattern distinct from what an aromatase inhibitor does, since lowering estradiol tends to worsen the same panel. Baseline and 12 weeks, ApoB rather than LDL-C alone because ApoB counts particles. If lipids and SHBG both move, systemic exposure is established and the rest of this page's safety section becomes live rather than hypothetical.

4. THE PREDICTION THAT CUTS AGAINST THE PRODUCT, and it is about a lab that lies rather than a lab that moves. Receptor blockade does not lower the hormone. Y-134 occupies ER-alpha; it does not reduce aromatization, so estradiol on a sensitive assay will read normal or high while the receptor is antagonized, and loss of estrogen negative feedback predicts LH and FSH rising. Anyone managing estrogen by chasing an estradiol number will therefore conclude nothing is happening at the exact moment something is — and will be tempted to apply more. That inverted feedback loop is the specific way this molecule's pharmacology becomes dangerous in the hands of someone treating it like an aromatase inhibitor. The corollary is worse and has no marker at all: the prothrombotic liability of the SERM class arises from hepatic synthesis of coagulation proteins, and there is no blood test that predicts a venous thromboembolic event before it happens. D-dimer is not a screening test in an asymptomatic person. So the most consequential risk here is the one the bloodwork section cannot help with, which is why it is written in the safety section as a decision rather than a measurement.

What nobody has tested yet

Five experiments nobody has run. The first two are cheap enough that their absence is the most interesting fact about this product.

1. Does Y-134 cross human skin at all, from anything resembling this vehicle? A Franz diffusion cell with excised human skin, the solution applied at its stated 20 mg/mL, receptor fluid sampled over 24 hours. This is a routine formulation experiment, it costs very little, and it would convert the central question of this product from unanswerable to answered. No permeation study of Y-134 through any skin has been published, and DA states no vehicle, which is the input the experiment needs.

2. Any pharmacokinetics, in any species, by any route. One time course in rats: plasma Y-134 against time after a stated dose, with the conjugated metabolites measured alongside, since a bis-phenol's glucuronides are where most of the material will be. Never published. Everything on this page about accumulation, duration and systemic exposure is structural reasoning standing in for this one unrun study.

3. Y-134's own bone data. The bone-agonist claim for this chemical family comes from Yang 2005, whose abstract does not name Y-134; the paper that does name it measured uterus and mammary gland Ning 2007. So the obvious experiment — ovariectomized rat, Y-134, femoral bone mineral density and histomorphometry against raloxifene — has not been published for this member. Until it is, half of what makes a SERM a SERM is inherited rather than demonstrated here, and this page says so rather than rounding up.

4. Whether the aryl hydrocarbon receptor activity happens in a living animal, and what it does to drug clearance. Jang 2017 established AhR as required for Y-134-induced apoptosis in ER-negative cells, in culture. AhR activation induces the CYP1A enzymes, so the mechanistic prediction is faster clearance of CYP1A2 substrates — testable with a caffeine clearance probe, which is a standard and inexpensive human phenotyping method. Nobody has measured CYP1A induction by Y-134 in any species. For a compound applied daily by people who take other things, this is a real interaction question sitting entirely unexamined.

5. Repeat-dose toxicology, which does not exist. No NOAEL, no 28-day or 90-day study, no genotoxicity panel, no reproductive toxicity, in any species. The single comparative safety datum in the literature is zebrafish embryos, where Y-134 looked better than raloxifene Jang 2017. A fish embryo screen and a toxicology package are not the same kind of object, and the gap between them is where every unpleasant surprise in drug development has historically lived.

Y-134 — its own safety story, not its class's

The first safety fact is a classification error waiting to happen. Y-134 is a SERM, not a SARM — one letter apart, different receptor entirely — and not an aromatase inhibitor either. Mistaking it for an AI is the most likely way it hurts somebody: an AI lowers estradiol, so a falling estradiol says the drug is working, while Y-134 leaves estradiol circulating and blocks the receptor. Estradiol reads normal or high while the receptor is antagonized, so anyone titrating against that number reads “no effect” and applies more.

The class liability, predicted from where the receptor is expressed rather than from a warning label. Hepatocyte estrogen receptors regulate transcription of coagulation factors and of the anticoagulant proteins opposing them, and shifting that balance is the mechanism behind the venous thromboembolic signal running through the whole SERM class. No Y-134 human data exists, so for this molecule that is a mechanistic prediction rather than an observation — and it is the one to take most seriously, because it has no early marker. D-dimer does not screen asymptomatic people. The mitigation is a decision made before the first application, not a test afterwards: a personal or family history of clotting, immobilization, recent surgery, pregnancy, an estrogen-containing contraceptive, or a long-haul flight in the same window all put someone in the group this mechanism has hurt even under medical supervision.

Predicted, from central estrogen-receptor antagonism: vasomotor symptoms. Hot flashes and night sweats are the class's most common complaint precisely because the mechanism is working — estrogen signaling blocked in hypothalamic thermoregulatory circuits. Mitigation: they reverse on discontinuation, and their appearance is the earliest subjective evidence that systemic exposure is real, which makes them information rather than a nuisance.

Predicted, for reproductive tissue, and the paper is specific about the direction. Ning 2007 measured uterine wet weight and BrdU incorporation in ovariectomized rats and found Y-134's inhibitory effect on the uterus comparable to raloxifene's. So the uterus is suppressed, not spared. In humans the endometrial consequences of SERMs are the part of the class that diverges most sharply by molecule — which is exactly why an uncharacterized member should not be assumed to behave like the best-behaved one. Mitigation: any unexpected vaginal bleeding is a stop-and-be-examined event, and the assessment is transvaginal ultrasound rather than a blood test. No bloodwork reports on the endometrium.

Predicted, for bone, in both directions. If the series' bone agonism holds Yang 2005, the skeletal effect is protective and should show as CTX falling by 3 months. If it does not hold for this member — and it has never been tested in this member — then what remains is estrogen-receptor antagonism without the bone-sparing half, which in a male user or a postmenopausal woman is a mechanism for losing bone. Mitigation: CTX and P1NP at baseline and 3 months as the early readout, DEXA only on a 12-month-plus horizon, and vitamin D and calcium adequacy checked at the start because a bone intervention on a deficient substrate is wasted either way.

The interaction question with a named receptor. Y-134 activates the aryl hydrocarbon receptor, and AhR is required for its apoptotic effect in ER-negative cells Jang 2017. AhR is the xenobiotic sensor whose job is inducing the CYP1A drug-metabolizing enzymes. That paper measured apoptosis, not drug clearance, so what exists is a mechanistic route rather than an observed interaction — but anybody on a narrow-therapeutic-index medicine, or on anything cleared by CYP1A2, should want that answered rather than assumed. Mitigation: a CMP with ALT and GGT at baseline and 12 weeks is the cheap surrogate, covering both the conjugation load a bis-phenol implies and the hepatocyte apoptosis seen in hepatoma cells in that same paper.

You cannot verify what you bought. DA's page carries a concentration, a volume and a total content, and as read on 29 September 2026 no CAS number, no formula, no molecular weight and no purity figure. The real compound has a CAS (849662-80-2) and a public reagent datasheet, so this is one of the few pages where a buyer could check the identity claim against an outside reference — if the vendor printed the identifier.

The honest summary of the risk shape. This is not a molecule with a frightening published toxicology; its only comparative safety datum found it gentler than raloxifene in fish embryos Jang 2017. It is a molecule with sub-nanomolar potency at a receptor governing clotting proteins, bone turnover, lipids and endometrial tissue, supplied as 600 mg in a bottle, with no human exposure and no pharmacokinetics in any species. The risk is not that something is known to go wrong — it is that the mechanism is powerful, slow, poorly self-reported and completely uncalibrated.

Sources read for this page

• Ning M, Zhou C, Weng J, Zhang S, Chen D, Yang C, Wang H, Ren J, Zhou L, Jin C, Wang MW. Biological activities of a novel selective oestrogen receptor modulator derived from raloxifene (Y134). British Journal of Pharmacology 2007;150(1):19-28 · PMID 17115070
• Jang HS, Pearce M, O'Donnell EF, Nguyen BD, Truong L, Mueller MJ, Bisson WH, Kerkvliet NI, Tanguay RL, Kolluri SK. Identification of a Raloxifene Analog That Promotes AhR-Mediated Apoptosis in Cancer Cells. Biology (Basel) 2017;6(4):41 · PMID 29194351
• Zhang D, Yang S, Yang C, Jin G, Zhen X. Estrogen regulates responses of dopamine neurons in the ventral tegmental area to cocaine. Psychopharmacology (Berlin) 2008;199(4):625-35 · PMID 18516717
• Yang C, Xu G, Li J, Wu X, Liu B, Yan X, Wang M, Xie Y. Benzothiophenes containing a piperazine side chain as selective ligands for the estrogen receptor alpha and their bioactivities in vivo. Bioorganic & Medicinal Chemistry Letters 2005;15(5):1505-7 · PMID 15713417
• Khan SA, Mi X, Xu Y, Blanco LZ Jr, Akasha AM, Pilewskie M, Degnim AC, AlHilli Z, Amin AL, Hwang ES, Guenther JM, Kocherginsky M, Benante K, Zhang S, Helland T, Hustad SS, Gursel DB, Mellgren G, Dimond E, Perloff M, Heckman-Stoddard BM, Lee O. Presurgical Oral Tamoxifen vs Transdermal 4-Hydroxytamoxifen in Women With Ductal Carcinoma In Situ: A Randomized Clinical Trial. JAMA Surgery 2023 (published online 23 October 2023) · PMID 37870954

Y-134 — interference & stacking

Bloodwork to run alongside Y-134

Baseline first, then again at 8–12 weeks.

The “Low T? Rule Out the Reversible Causes First” panel covers these in one order — 11 markers, $211.50 with the discount applied.

Check results you already have → · All 103 markers A–Z

Y-134 — frequently asked questions

What Y-134 is used for

Y-134 appears under 3 goals in the goal router.

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