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RAD-140 and Raloxifene Interaction: Avoid | Peptide Database

Compound Profiles RAD-140 Selective Androgen Receptor Modulator | Investigational SARM RAD-140 binds to the androgen receptor (AR) with high affinity and selectivity, functioning as a full agonist in muscle and bone tissue while exhibiting minimal agonist acti

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Compound Profiles

RAD-140

Selective Androgen Receptor Modulator | Investigational SARM

RAD-140 binds to the androgen receptor (AR) with high affinity and selectivity, functioning as a full agonist in muscle and bone tissue while exhibiting minimal agonist activity in the prostate and other androgen-sensitive tissues. This tissue selectivity is achieved through differential cofactor recruitment: upon binding to the AR, RAD-140 induces a conformational change that favors interaction with coactivators predominantly expressed in skeletal muscle and bone, rather than those prevalent in prostate or sebaceous glands.

Raloxifene

Selective Estrogen Receptor Modulator | Gynecomastia & Bone Health

Raloxifene binds to both estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta), producing tissue-dependent agonist or antagonist effects determined by the local complement of coactivator and corepressor proteins. In breast tissue, raloxifene functions as a potent estrogen antagonist, blocking estradiol-mediated proliferative signaling with high selectivity.

Combined Organ Load

Shared Safety Flags

Frequently Asked Questions

Can I take RAD-140 with Raloxifene?

Combining RAD-140 with Raloxifene is not recommended. Both RAD-140 and Raloxifene carry hepatotoxic risk. Combining hepatotoxic compounds significantly increases liver damage potential. If unavoidable, include liver support (TUDCA/NAC) and monitor ALT/AST frequently.

Is RAD-140 and Raloxifene safe together?

This combination carries significant risk. Both RAD-140 and Raloxifene carry hepatotoxic risk. Combining hepatotoxic compounds significantly increases liver damage potential. If unavoidable, include liver support (TUDCA/NAC) and monitor ALT/AST frequently. Consult a healthcare professional before combining.

What are the interactions between RAD-140 and Raloxifene?

Both RAD-140 and Raloxifene carry hepatotoxic risk. Combining hepatotoxic compounds significantly increases liver damage potential. If unavoidable, include liver support (TUDCA/NAC) and monitor ALT/AST frequently. This assessment has 53% confidence and is inferred from pharmacological mechanism analysis.

How should I time RAD-140 and Raloxifene?

RAD-140 has a half-life of ~60 hours and Raloxifene has a half-life of ~28 hours. No specific timing requirements identified for this combination, but separating administration can help monitor individual effects.

This interaction analysis is compiled from research literature and pharmacological mechanism data. This assessment is inferred from known mechanisms and may not reflect all real-world outcomes. Always consult a healthcare professional before combining compounds.

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Research context

Read sources and limitations before applying a claim.

Community Research

Join others researching Liothyronine (T3) — share findings, ask questions, and learn from real experiences Liothyronine (T3) is the biologically active form of thyroid hormone, responsible for regulating basal metabolic rate, thermogenesis, protein synthesis, and cellular energy metabolism throughout the body. Unlike levothyroxine (T4), which serves primarily as a prohormone requiring peripheral conversion by deiodinase enzymes, T3 acts directly on nuclear thyroid hormone receptors to exert its metabolic effects. It has been FDA-approved since the 1950s for the treatment of hypothyroidism, myxedema coma, and as a diagnostic agent in thyroid suppression tests. Pharmaceutical T3 is available as Cytomel (brand) and generic liothyronine sodium tablets. In performance and biohacking contexts, T3 is widely used during cutting phases to accelerate fat loss by directly upregulating metabolic rate, and by individuals seeking metabolic optimization when peripheral T4-to-T3 conversion is impaired due to caloric restriction, stress, or other factors. Liothyronine enters target cells via monocarboxylate transporter 8 (MCT8) and other thyroid hormone transporters, then binds to nuclear thyroid hormone receptors (primarily TR-beta in metabolic tissues and TR-alpha in cardiac tissue). The T3-receptor complex forms heterodimers with retinoid X receptors (RXR) and binds to thyroid hormone response elements (TREs) on DNA, directly modulating gene transcription. This increases expression of Na+/K+ ATPase (driving cellular energy expenditure), uncoupling proteins (UCP1 in brown adipose tissue, promoting thermogenesis), and enzymes involved in fatty acid oxidation, gluconeogenesis, and protein turnover. T3 also upregulates beta-adrenergic receptor density, which amplifies catecholamine sensitivity and contributes to increased heart rate, lipolysis, and thermogenesis. At physiological doses, T3 supports healthy metabolism; at supraphysiological doses, it shifts the body into a catabolic state where both fat and lean tissue can be catabolized for energy.

Source: peptide-db.com ↗

Community Research

Join others researching Dutasteride — share findings, ask questions, and learn from real experiences Dutasteride is a potent dual 5-alpha reductase inhibitor that blocks both Type I and Type II isoforms of the enzyme responsible for converting testosterone to dihydrotestosterone (DHT). FDA-approved at 0.5mg daily for benign prostatic hyperplasia (BPH) under the brand name Avodart, it is widely used off-label for the treatment of androgenetic alopecia (male pattern hair loss). By inhibiting both isoforms, dutasteride achieves approximately 90% suppression of serum DHT, compared to roughly 70% with finasteride, which blocks only the Type II isoform. This greater DHT suppression translates to potentially superior hair regrowth outcomes in head-to-head comparisons, though it also carries a somewhat higher risk of DHT-related side effects. Dutasteride has an exceptionally long half-life of approximately 5 weeks, meaning it takes several months to reach steady-state levels and equally long for effects to fully wash out after discontinuation. Dutasteride competitively inhibits both the Type I and Type II isoforms of the enzyme 5-alpha reductase. Type II is the predominant isoform in the prostate and hair follicles, while Type I is found primarily in the skin, sebaceous glands, and liver. By blocking both isoforms, dutasteride suppresses serum DHT levels by approximately 90% at the standard 0.5mg dose, compared to the roughly 70% suppression achieved by finasteride (which blocks only Type II). This near-complete DHT suppression more effectively reduces the androgenic stimulus driving follicular miniaturization in genetically susceptible individuals. The exceptionally long elimination half-life of approximately 5 weeks is due to extensive tissue binding and slow clearance. Serum testosterone may increase modestly (10-20%) as a compensatory response to the pronounced reduction in DHT, though this increase remains within the normal physiological range for most men.

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Practical and safety references

These excerpts are educational, not personalised medical instructions.

Dosage reference

Dosing Protocols

Primary administration route with well-established protocols for direct brain delivery via IV/IM. Small Volume IV Up to 10mL Once daily Undiluted IV slow push over 3 minutes Intramuscular Up to 5mL Undiluted IM injection over 3 minutes Acute Stroke 20-50mL Once daily for 10-21 days IV infusion (diluted to 100mL minimum) Traumatic Brain Injury Once daily for 7-30 days Alzheimer's Disease 10-30mL 5 days weekly for 4 weeks IV injection/infusion (2-4 cycles yearly) Vascular Dementia

Source: peptide-db.com ↗
Side effects

Common Side Effects

Minimal acute side effects reported Potential mild cardiovascular effects

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Peptide Therapy Guide Editorial Team

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