Tru-Genetics - Peptide & Hormone Safety Information Page

What Are Peptides?

Peptides are short chains of amino acids - the same building blocks that make up proteins in the human body. They are signaling molecules: they communicate information between cells, organs, and systems. Many peptides occur naturally in the body and are responsible for regulating fundamental biological processes including growth hormone secretion, metabolism, tissue repair, immune function, appetite, and reproductive health.

The peptides used in clinical medicine and medically supervised optimization are either identical to the peptides your body naturally produces, or are structurally modified analogs designed to be more stable, longer-acting, or more targeted in their activity. They are not anabolic steroids. They are not stimulants. They are biochemical messengers.

Because they mimic or modulate the body's own signaling pathways, they tend to work with physiology rather than overriding it - which is a meaningful distinction when evaluating safety profiles compared to synthetic pharmaceuticals that operate through more foreign mechanisms.

All compounds offered through Tru-Genetics are compounded at 503A-compliant pharmacies, meaning each preparation is made for a specific named patient under a valid prescription from a licensed practitioner - not mass manufactured. This framework exists to ensure pharmaceutical-grade purity, sterility, and patient-specific customization.

Metabolic & Weight Management Peptides

Semaglutide

Mechanism of Action

Semaglutide is a synthetic analog of glucagon-like peptide-1 (GLP-1), a hormone naturally produced in the small intestine in response to food intake. GLP-1 plays a central role in regulating blood sugar, appetite, and gastric emptying.

Semaglutide binds to GLP-1 receptors throughout the body - most critically in the brain's hypothalamus and brainstem, where it reduces hunger signals and increases the sensation of satiety. Simultaneously, it slows the rate at which food moves from the stomach into the small intestine (delayed gastric emptying), which extends the feeling of fullness after meals and blunts post-meal blood sugar spikes. In the pancreas, it stimulates insulin secretion in a glucose-dependent manner, meaning it only triggers insulin release when blood sugar is actually elevated - which significantly reduces the risk of hypoglycemia compared to older diabetes medications.

The cumulative effect is a meaningful reduction in caloric intake without requiring willpower-based restriction. Appetite is neurologically suppressed at the source.

Reported Benefits

• Significant body weight reduction (clinical trials show an average of 15–20% total body weight loss over 68 weeks)
• Improved insulin sensitivity and glycemic control
• Reduction in visceral and subcutaneous adipose tissue
• Demonstrated cardiovascular benefits including reduced risk of major cardiac events in diabetic populations
• Reduction in liver fat content
• Improvements in blood pressure and lipid profiles in some patients

Common Side Effects

• Nausea - the most commonly reported side effect, particularly during dose escalation. Typically improves as the body adapts over 4–8 weeks
• Vomiting
• Diarrhea or constipation
• Reduced appetite (expected; can be excessive at higher doses)
• Fatigue, particularly early in treatment
• Injection site reactions (mild redness, bruising)
• Potential for lean muscle mass loss alongside fat loss - particularly important to mitigate with adequate protein intake and resistance training
• Headache during early titration

Rare but Serious Risks

• Pancreatitis: Patients with a history of pancreatitis should not use this compound. Any severe abdominal pain should be evaluated immediately
• Thyroid C-cell tumors: Observed in rodent studies at doses significantly higher than therapeutic; human risk is considered theoretical but patients with personal or family history of medullary thyroid carcinoma or MEN 2 syndrome should not use GLP-1 agonists
• Gallbladder disease: Rapid weight loss and GLP-1 receptor activity may increase gallstone risk; patients with gallbladder history should be monitored
• Hypoglycemia risk: Low when used alone; increases if combined with insulin or sulfonylureas

Who Is a Candidate

• Adults with a BMI ≥ 27 (overweight) with at least one weight-related comorbidity (hypertension, dyslipidemia, metabolic syndrome, sleep apnea)
• Adults with a BMI ≥ 30 (obese)
• Men with clinically significant visceral adiposity impacting metabolic health markers
• Patients with type 2 diabetes or pre-diabetes seeking improved glycemic control
• Patients for whom weight loss would meaningfully improve hormone levels, cardiovascular risk, or inflammatory markers

Who Should Not Use This Compound

• Personal or family history of medullary thyroid carcinoma or MEN 2 syndrome
• Active or history of pancreatitis
• Severe gastrointestinal disease (gastroparesis, inflammatory bowel disease)
• Pregnancy or planning pregnancy
• Known hypersensitivity to semaglutide or any of its excipients
• Patients on insulin who are not being closely monitored for hypoglycemia

Monitoring Requirements

Baseline and periodic assessment of: HbA1c, fasting glucose, lipid panel, liver enzymes, kidney function, and body weight. Thyroid function in patients with thyroid history.

Tirzepatide

Mechanism of Action

Tirzepatide is a dual receptor agonist that simultaneously activates both GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) receptors. This dual-pathway activity is what distinguishes it mechanistically - and clinically - from semaglutide.

GIP receptors, found in fat tissue, the brain, bone, and pancreas, play a different role than GLP-1 receptors. When activated by GIP, the body becomes more responsive to insulin in fat cells and potentially preserves lean muscle mass more effectively during caloric restriction - a meaningful clinical advantage over pure GLP-1 agonists. The GIP pathway also appears to synergize with GLP-1's appetite-suppressing effects, producing a more pronounced reduction in food intake than either pathway alone.

The net result is greater total weight loss, improved metabolic markers, and some evidence of better body composition outcomes compared to semaglutide.

Reported Benefits

• Superior weight reduction compared to semaglutide - clinical trials demonstrate average losses of 20–25% total body weight
• Better preserved lean muscle mass relative to fat loss (compared to pure GLP-1 agonists)
• Significant improvements in HbA1c and fasting glucose
• Improved liver health markers - meaningful reduction in hepatic fat content
• Improvements in blood pressure, triglycerides, and HDL
• Favorable effects on insulin resistance beyond weight loss alone

Common Side Effects

• Nausea (similar to semaglutide, dose-dependent, improves with time)
• Vomiting, diarrhea, constipation
• Reduced appetite
• Fatigue
• Injection site reactions
• Some patients report better GI tolerability than semaglutide; some report similar or worse

Rare but Serious Risks

• Same thyroid C-cell precautions as semaglutide (black box warning)
• Pancreatitis risk
• Hypoglycemia if combined with insulin or secretagogues
• Gallbladder disease
• Potential for rapid weight regain if discontinued without lifestyle behavior change

Who Is a Candidate

• All candidates qualifying for semaglutide
• Patients who require more aggressive metabolic intervention - higher BMI, more significant insulin resistance, or who have not achieved adequate response with semaglutide
• Men with substantial visceral fat, elevated triglycerides, and insulin resistance
• Patients where body composition preservation is a higher priority than with semaglutide alone

Who Should Not Use This Compound

• Same contraindications as semaglutide; additionally patients with known hypersensitivity to tirzepatide excipients

Monitoring Requirements

Same as semaglutide; additional monitoring of lean mass recommended given the body composition implications of significant weight loss.

Retatrutide (RETA / TrueTide)

Mechanism of Action

Retatrutide adds a third mechanism to the dual-agonist framework: glucagon receptor activation. Glucagon is the hormone responsible for stimulating the liver to release stored glucose and for driving fat oxidation. At therapeutic doses in a receptor agonist format, glucagon receptor activation increases the rate at which the body burns fat for fuel, contributes to reduced appetite, and enhances metabolic rate.

The triple-agonist mechanism creates a compounding effect across three complementary pathways: GLP-1 reduces appetite centrally and slows gastric emptying; GIP improves insulin sensitivity and potentially preserves lean mass; glucagon directly accelerates fat burning and raises metabolic expenditure. No other class of metabolic compound currently active in clinical development addresses all three pathways simultaneously.

Phase 2 clinical trial data demonstrated average body weight reductions of 24%+ - the largest ever recorded in a single metabolic compound trial. Some patients showed losses exceeding 30%.

Reported Benefits

• Most potent weight reduction of any compound in its class currently in clinical development
• Significant visceral fat reduction
• Improvements in liver fat (NAFLD/NASH markers)
• Favorable effects on triglycerides, blood pressure, and inflammatory markers
• Emerging data on cardiovascular risk reduction
• Elevated metabolic rate relative to other GLP-1 class compounds due to glucagon activity

Common Side Effects

• Nausea, vomiting, diarrhea - consistent with the class; severity may be higher at aggressive titration
• Fatigue
• Reduced appetite (potentially more pronounced)
• Injection site reactions

Additional Considerations for Retatrutide

Because retatrutide activates the glucagon receptor, it carries slightly different metabolic considerations than semaglutide or tirzepatide. The glucagon pathway can elevate fasting glucose in some patients, which is typically offset by the GLP-1-driven insulin sensitization but warrants monitoring - particularly in patients with existing glucose dysregulation. Blood glucose, liver enzymes, and lipid panels should be monitored more closely during titration.

Who Is a Candidate

• Patients with significant metabolic dysfunction, high visceral fat burden, or significant BMI elevation who require more aggressive intervention
• Patients who have reached a plateau with semaglutide or tirzepatide
• Patients with concurrent metabolic liver disease
• Men in whom metabolic rate elevation (via glucagon) is a desirable mechanism

Who Should Not Use This Compound

• Same contraindications as semaglutide and tirzepatide
• Patients with significant glucose dysregulation who are not being closely monitored
• Patients with history of severe hypoglycemic episodes

Monitoring Requirements

Comprehensive metabolic panel, HbA1c, fasting glucose, fasting insulin, lipid panel, liver enzymes (ALT/AST), body weight and composition tracking. More frequent monitoring recommended during initial titration compared to other GLP-1 class compounds.

GH Axis Optimization - Pituitary Stimulators

Overview of the GH Axis

Before examining individual compounds, it's important to understand how growth hormone (GH) is regulated in the human body.

The hypothalamus produces Growth Hormone Releasing Hormone (GHRH), which travels to the pituitary gland and stimulates it to release pulses of GH into circulation. GH then acts on the liver and other tissues to produce IGF-1 (Insulin-like Growth Factor 1), which drives most of GH's anabolic and metabolic effects.

GHRH analogs work by mimicking the body's own GHRH signal - they tell the pituitary to release more GH in its natural pulsatile pattern rather than flooding the system with exogenous GH directly. This is a meaningfully safer and more physiologically appropriate approach than exogenous HGH administration, because the pituitary retains control over total GH output and the natural feedback loop remains intact.

Sermorelin

Mechanism of Action

Sermorelin is a synthetic analog of the first 29 amino acids of naturally occurring GHRH. It binds to GHRH receptors in the pituitary and stimulates GH release in the natural pulsatile pattern - specifically during sleep, which is when the majority of natural GH secretion occurs. Because it stimulates rather than replaces GH secretion, IGF-1 levels rise gradually and physiologically rather than sharply.

Reported Benefits

• Improved body composition: gradual reduction in body fat, particularly visceral fat
• Enhanced lean muscle mass over extended protocols (3–6+ months)
• Improved sleep quality and recovery
• Enhanced skin elasticity and collagen synthesis
• Improved energy and reduced fatigue
• Support for joint health

Common Side Effects

• Injection site redness, itching, or mild swelling
• Flushing - typically brief and mild
• Water retention, particularly early in the protocol
• Headache
• Dizziness (rare, typically with rapid injection)

Who Is a Candidate

• Adults with clinically low IGF-1 or documented GH insufficiency
• Men over 35 experiencing age-related declines in body composition, recovery, or energy attributable to declining GH axis function
• Patients seeking gradual, sustainable improvements in body composition without the risks of exogenous HGH

Who Should Not Use This Compound

• Active malignancy or recent history of cancer (GH stimulation is contraindicated)
• Hypothyroidism (untreated) - GH secretagogues may be less effective without adequate thyroid function
• Active head injury or intracranial lesion
• Known hypersensitivity

CJC-1295

Mechanism of Action

CJC-1295 is a modified GHRH analog with a significantly extended half-life compared to sermorelin. The most commonly used form - CJC-1295 with DAC (Drug Affinity Complex) - binds to albumin in the blood, extending its activity to 6–8 days per injection, which creates a sustained elevation in baseline GH and IGF-1 levels rather than a sharp single pulse.

The non-DAC form (CJC-1295 without DAC, also called Modified GRF 1-29) acts over 30 minutes and is typically paired with a GHRP to create a synergistic combined pulse.

Reported Benefits

• More sustained IGF-1 elevation compared to sermorelin
• Progressive improvements in lean body mass and fat reduction over 3–6 months
• Enhanced recovery and tissue repair
• Improved sleep architecture
• Anti-aging effects on skin and connective tissue

Common Side Effects

• Water retention (more pronounced than sermorelin due to sustained GH elevation)
• Injection site reactions
• Flushing
• Tingling in hands or feet (carpal-tunnel-like symptoms, particularly at higher doses)
• Potential for IGF-1 over-elevation at aggressive doses - requires monitoring

Stacking Note

CJC-1295 without DAC is most commonly paired with Ipamorelin in a nightly combination. This creates a powerful synergistic GH pulse that mimics - and amplifies - the natural nightly GH release pattern.

Tesamorelin

Mechanism of Action

Tesamorelin is a stabilized synthetic analog of GHRH that is specifically optimized for visceral fat reduction. It stimulates GH release via GHRH receptor binding, and the resulting GH pulse directly drives lipolysis (fat breakdown) in visceral adipose tissue.

What distinguishes tesamorelin from other GHRH analogs is the specificity of its effect: clinical data consistently shows significant reduction in visceral fat - the metabolically active, dangerous fat stored around the abdominal organs - with minimal effect on subcutaneous fat. It does not significantly affect blood glucose or increase IGF-1 to supraphysiological levels at standard doses.

Tesamorelin is one of the few peptides with robust long-term human clinical trial data, including randomized controlled trials and multi-year safety follow-up data from the FDA approval process.

Reported Benefits

• Clinically documented 10–18% reduction in visceral adipose tissue
• Improvements in liver health markers and triglycerides
• No adverse effects on glucose metabolism at therapeutic doses
• Improvements in cognitive function and mental clarity (emerging data from dementia-related research)
• GH-axis support with low risk of IGF-1 overshoot

Common Side Effects

• Injection site reactions (redness, itching)
• Fluid retention
• Joint pain (arthralgias)
• Peripheral edema at higher doses
• Nausea (uncommon)

Who Is a Candidate

• Men with significant visceral adiposity and documented metabolic risk
• Patients where visceral fat reduction is the primary objective (rather than systemic GH optimization)
• Older men with declining GH axis function and abdominal fat accumulation
• Patients where other compounds require avoidance

Who Should Not Use This Compound

• Active malignancy
• Pituitary tumor or history thereof
• Known hypersensitivity to GHRH or tesamorelin
• Pregnancy

Ghrelin Receptor Agonists - GH Pulse Amplifiers

Overview of GHRPs

Growth Hormone Releasing Peptides (GHRPs) are a distinct class from GHRH analogs. Rather than mimicking GHRH, GHRPs act on the ghrelin receptor (GHSR-1a) in the pituitary and hypothalamus to stimulate GH release through a complementary - and synergistic - pathway.

When a GHRP is combined with a GHRH analog (such as CJC-1295 + Ipamorelin), the two compounds work on separate but converging pathways to produce a GH pulse that is significantly larger than either compound alone. This combination approach is the standard of care in GH axis optimization protocols.

Ipamorelin

Mechanism of Action

Ipamorelin is a selective ghrelin receptor agonist. It binds to the GHSR-1a receptor in the pituitary, stimulating GH release while having minimal to no effect on cortisol, prolactin, or ACTH - which is the key distinction that makes it the preferred GHRP in clinical protocols. Earlier GHRPs (GHRP-2, GHRP-6) stimulate these stress hormones and appetite-related hormones significantly, creating side effects ipamorelin avoids.

The selectivity of ipamorelin means that almost all of its physiological effect is GH release - clean, predictable, and without the cortisol-related side effects that blunt the benefits of GH secretagogues.

Reported Benefits

• Significant GH pulse amplification when combined with GHRH analogs
• Improved body composition: lean mass gains, fat reduction
• Enhanced sleep quality (deep sleep/REM)
• Improved recovery from training and injury
• Elevated collagen synthesis and skin quality
• Increased bone density over extended protocols
• No significant appetite stimulation (unlike GHRP-6)

Common Side Effects

• Mild water retention
• Injection site reactions
• Flushing (brief)
• Very mild, transient hunger in some patients (significantly less than GHRP-6)

Who Is a Candidate

• Any patient pursuing GH axis optimization who is not contraindicated for GH stimulation
• Preferred first-line GHRP due to its favorable side effect profile

Who Should Not Use This Compound

• Active malignancy
• History of pituitary tumor
• Untreated hypothyroidism (reduces GH secretagogue response)

GHRP-2 and GHRP-6

Mechanism of Action

GHRP-2 and GHRP-6 are first and second-generation GHRPs that also act on the ghrelin receptor to stimulate GH release. Both produce potent GH pulses - often more powerful than ipamorelin - but with less receptor selectivity, which produces additional hormonal effects beyond GH secretion.

GHRP-2 stimulates GH release strongly but also increases cortisol and prolactin, particularly at higher doses. The cortisol elevation can blunt some of the anabolic and fat-loss benefits of elevated GH, though its GH output is robust.

GHRP-6 produces strong GH release and also strongly activates hunger signals via ghrelin pathways. The appetite stimulation is significant - patients often report substantial increases in hunger within 30–60 minutes of injection, which can be an asset (patients needing to increase caloric intake) or a liability (patients focused on fat loss or caloric restriction).

Clinical Use

GHRP-6 and GHRP-2 are typically reserved for specific protocols where their additional effects are useful - particularly GHRP-6 in patients who need to support caloric intake, or in specialized recovery stacks. Ipamorelin has largely replaced them as the default GHRP in optimization protocols due to its cleaner profile.

Common Side Effects

• Significant appetite stimulation (GHRP-6 more than GHRP-2)
• Cortisol and prolactin elevation (GHRP-2 more than GHRP-6)
• Water retention
• Fatigue (associated with cortisol dysregulation at high doses)
• Injection site reactions

Hexarelin

Mechanism of Action

Hexarelin is among the most potent GHRPs in terms of raw GH output. It binds to both the ghrelin receptor and a separate cardiac receptor, which is the source of both its notable cardiovascular properties and an important limitation: the ghrelin receptor downregulates relatively quickly with continuous hexarelin use, making cycling necessary to maintain efficacy.

Hexarelin's cardiac receptor binding has generated research interest for its potential cardioprotective properties, including improvements in myocardial contractility. This is an active area of investigation.

Reported Benefits

• Strong GH pulse stimulation
• Potential cardioprotective effects (research ongoing)
• Increased lean mass and reduced fat when combined with GHRH analog

Common Side Effects

• Water retention
• Cortisol increase
• Tachyphylaxis (receptor desensitization) with continuous use - cycling required
• Injection site reactions

Cellular Energy, Repair, and Anti-Aging

Overview of Mitochondrial Peptides

Mitochondrial-derived peptides (MDPs) are a recently discovered class of endogenous peptides encoded within the mitochondrial genome - the small, separate genetic library that exists inside every mitochondrion. These peptides were only identified in the last 15–20 years and represent one of the most active and exciting frontiers in longevity medicine.

Their shared mechanism is the optimization of mitochondrial function: improving how efficiently cells produce energy (ATP), reducing the accumulation of reactive oxygen species (free radicals), protecting mitochondrial membranes from oxidative damage, and enhancing the body's intrinsic repair and stress-response capacity. Because mitochondrial dysfunction underlies the vast majority of age-related diseases - including cardiovascular disease, metabolic syndrome, neurodegeneration, and cancer - compounds that restore mitochondrial function have broad potential implications across medicine.

SS-31 (Elamipretide)

Mechanism of Action

SS-31 is a tetrapeptide (four amino acids) that selectively concentrates inside mitochondria - specifically on the inner mitochondrial membrane - at a concentration that is several hundred times higher than the surrounding cell. This targeting is not random: SS-31 contains alternating aromatic and basic amino acid residues that give it a strong positive charge, allowing it to be drawn to the negatively charged inner mitochondrial membrane by the electrochemical gradient.

Once localized, SS-31 binds to cardiolipin - a phospholipid unique to the inner mitochondrial membrane that is essential for the structure and function of the mitochondrial electron transport chain (ETC). Cardiolipin oxidizes during periods of stress, age, or disease, and this oxidation disrupts ETC function, slows ATP production, and increases reactive oxygen species (ROS) generation - a self-amplifying cycle of damage.

SS-31 stabilizes cardiolipin in its reduced (non-oxidized) form, restoring ETC efficiency, dramatically reducing ROS production, and protecting the mitochondria's structural integrity. The downstream effects are extensive: improved cellular energy production, reduced inflammation, protection of cells under ischemic or oxidative stress, and potential reversal of mitochondria-driven aging phenotypes.

Reported Benefits in Research

• Significant improvement in cardiac function in heart failure patients (Phase 2 trials)
• Restoration of mitochondrial function in aged muscle tissue
• Reduction in systemic oxidative stress markers
• Improvement in exercise capacity and fatigue resistance
• Potential neuroprotective effects (ongoing research)
• Renal protection during ischemia-reperfusion injury
• Anti-inflammatory effects downstream of mitochondrial ROS reduction

Common Side Effects

• Injection site reactions (the most consistently reported adverse event in trials)
• Mild flu-like symptoms in some patients early in treatment
• Generally well-tolerated in human trials at therapeutic doses

Important Clinical Note

SS-31 is primarily an investigational compound. While human trial data exists and is promising - particularly for cardiac applications - it should be understood as an emerging therapy with a strong mechanistic basis and encouraging early clinical signals rather than a fully validated treatment. Patients should discuss the research landscape candidly with their provider.

Who Is a Candidate

• Men with evidence of mitochondrial dysfunction: chronic fatigue, reduced exercise tolerance, early cardiovascular risk
• Patients with significant oxidative stress burden
• Men focused on longevity and cellular health optimization as core protocol goals
• Patients with cardiovascular risk markers or early cardiac compromise

MOTS-c

Mechanism of Action

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-C) is a peptide encoded by the mitochondrial genome that functions as a metabolic regulator. Unlike SS-31, which primarily operates at the mitochondrial membrane, MOTS-c travels from mitochondria to the cell nucleus, where it directly influences gene expression - specifically genes involved in glucose and fat metabolism.

Its primary metabolic action is the activation of AMPK (AMP-activated protein kinase), often called the body's "metabolic master switch." AMPK activation shifts cellular metabolism away from energy storage and toward energy expenditure: it increases glucose uptake, enhances fat oxidation, improves insulin sensitivity, and mimics many of the metabolic effects of exercise at the cellular level.

MOTS-c also modulates the folate cycle and regulates the production of a metabolite called AICAR, which itself is a potent AMPK activator. This makes MOTS-c a multi-layered metabolic regulator operating through converging pathways.

Research in animal models shows that MOTS-c injections improve metabolic function, reduce obesity, reverse insulin resistance, and extend lifespan markers. Human trials are in early stages but directionally consistent.

Reported Benefits

• Improvement in insulin sensitivity and glucose metabolism
• Support for fat oxidation and weight management
• Potential improvement in physical exercise capacity
• Anti-aging effects at the cellular metabolic level
• Reduction in age-related metabolic decline
• Potential benefits for skeletal muscle function and preservation

Common Side Effects

• Injection site reactions
• Mild fatigue in some patients early in treatment
• Limited long-term human safety data; generally well-tolerated in short-term studies

Who Is a Candidate

• Men with insulin resistance, metabolic syndrome, or elevated fasting glucose
• Patients focused on longevity who want to address the cellular mechanisms of metabolic aging
• Men with declining exercise capacity or metabolic efficiency
• Patients seeking complementary metabolic support alongside GLP-1 therapy or GH axis optimization

NAD+ (Nicotinamide Adenine Dinucleotide)

Mechanism of Action

NAD+ is not a peptide, but it is a foundational molecule in cellular energy metabolism and longevity biology and is frequently integrated into comprehensive optimization protocols. NAD+ is a coenzyme found in every cell of the body and is essential for hundreds of enzymatic reactions - most critically, the electron transport chain reactions that produce ATP (cellular energy) in mitochondria.

NAD+ also serves as a substrate for sirtuins (SIRT1–SIRT7), a family of enzymes that regulate gene expression, DNA repair, inflammation, and cellular stress responses. Sirtuin activity - and therefore the broad biological processes they regulate - is directly dependent on cellular NAD+ availability.

NAD+ levels decline significantly with age. By the time a man is in his 50s, cellular NAD+ may be 40–50% lower than at age 20. This decline is believed to be a central driver of mitochondrial dysfunction, cellular aging, reduced DNA repair fidelity, and increased inflammatory signaling. Replenishing NAD+ restores sirtuin activity, supports mitochondrial health, and improves cellular repair mechanisms.

Reported Benefits

• Improved cellular energy production and mitochondrial function
• Enhanced DNA repair capacity
• Reduced systemic inflammation (through sirtuin pathway activation)
• Improvement in cognitive function and mental clarity
• Improved insulin sensitivity and metabolic function
• Potential improvement in muscle function and exercise recovery
• Support for liver health
• Broad anti-aging effects through sirtuin activation

Common Side Effects (IV Administration)

• Flushing, warmth, chest tightness - classic IV NAD+ reactions; dose-rate dependent and typically resolve quickly when infusion rate is slowed
• Nausea during infusion
• Fatigue or "energy crash" in some patients shortly after infusion
• Headache

Common Side Effects (Subcutaneous / Oral Precursors)

• Generally well-tolerated
• Mild GI discomfort with oral precursors (NMN, NR)
• Occasional injection site reactions with subcutaneous preparations

HPG Axis Modulators, Fertility Preservation, and Estrogen Management

Overview of the HPG Axis

The Hypothalamic-Pituitary-Gonadal (HPG) axis is the hormonal cascade that regulates testosterone production and reproductive function in men. The hypothalamus releases GnRH (gonadotropin-releasing hormone), which signals the pituitary to release LH (luteinizing hormone) and FSH (follicle-stimulating hormone). LH signals the Leydig cells in the testes to produce testosterone; FSH supports sperm production (spermatogenesis).

Exogenous testosterone (TRT) suppresses this axis: when the body detects adequate testosterone levels circulating from an external source, it stops producing GnRH, which stops LH and FSH secretion, which stops natural testosterone production and significantly impairs sperm production. Managing this suppression - particularly for men who wish to preserve fertility or maintain testicular function on TRT - requires specific pharmacological interventions.

HCG (Human Chorionic Gonadotropin)

Mechanism of Action

HCG is a naturally occurring hormone produced in large quantities during pregnancy. Structurally, it closely mimics LH (luteinizing hormone) and binds to the same LH receptors on Leydig cells in the testes.

When exogenous testosterone suppresses LH production by the pituitary, the testes lose their primary stimulation signal and begin to atrophy. HCG bypasses the suppressed pituitary by delivering an LH-equivalent signal directly to the testes, maintaining intratesticular testosterone production, testicular volume, and the local hormonal environment necessary for sperm maturation.

This is a critical distinction: even when systemic testosterone is adequate from exogenous sources, intratesticular testosterone - which is 50–100 times higher than blood testosterone and is essential for spermatogenesis - becomes depleted without LH stimulation. HCG is the primary tool for preserving this intratesticular testosterone.

Reported Benefits

• Prevention and reversal of testicular atrophy during TRT
• Maintenance of intratesticular testosterone and spermatogenesis
• Significantly faster HPG axis recovery if/when TRT is discontinued
• Improved libido and sexual function in some patients (possibly due to intratesticular testosterone effects)
• Maintained fertility potential during testosterone therapy

Common Side Effects

• Acne (due to increased androgen activity within the testes)
• Water retention
• Increased estrogen - HCG stimulates testicular testosterone production, some of which aromatizes to estrogen; may require adjustment of aromatase inhibitor dosing
• Injection site reactions
• Mild mood changes in some patients

Who Is a Candidate

• Any man on TRT who wishes to preserve fertility
• Men on TRT concerned about testicular atrophy
• Men planning to discontinue TRT who want to facilitate recovery
• Men with primary hypogonadism where LH stimulation of the testes is appropriate

Anastrozole

Mechanism of Action

Testosterone naturally converts to estradiol (the primary estrogen in men) through a process called aromatization, catalyzed by the enzyme aromatase. Aromatase is found throughout the body - in fat tissue, the liver, the brain, and elsewhere. On TRT - particularly at higher testosterone levels - aromatization can become excessive, leading to elevated estradiol, which causes fluid retention, gynecomastia, mood disturbances, and suppressed libido despite adequate testosterone levels.

Anastrozole competitively inhibits the aromatase enzyme, reducing the rate of testosterone-to-estradiol conversion and lowering circulating estradiol levels. It is prescribed when a patient's estradiol levels - particularly estradiol sensitive (E2 sensitive, LC/MS) - rise above the optimal range during testosterone therapy.

Important Nuance: The Estrogen Balance Problem

Estrogen is not simply a harmful byproduct of testosterone conversion in men. Estradiol is essential for bone density, cardiovascular health, cognitive function, libido, mood, and joint health. Excessive suppression of estradiol is as clinically problematic as excessive elevation. Anastrozole should be dosed conservatively and guided by laboratory values, not symptoms alone. Crashed estradiol is a documented and debilitating clinical state.

Common Side Effects

• Joint pain and stiffness (particularly at higher doses or with overly suppressed estradiol)
• Fatigue and mood disturbances (associated with low estradiol)
• Reduced libido (paradoxically, from estrogen being too low)
• Bone density reduction over long-term use at high doses
• Cognitive impairment in some patients with very low estradiol

Who Is a Candidate

• Men on TRT with confirmed elevated estradiol on sensitive assay
• Men experiencing symptoms of high estrogen: water retention, breast tenderness/sensitivity, mood lability, reduced libido despite adequate testosterone levels
• Men using HCG (which increases aromatization) who require estrogen management

Who Should Not Use This Compound

• Men with normal or low estradiol levels
• Men with documented osteoporosis or significant bone density loss
• Men with cardiovascular disease history where estrogen's cardioprotective effects are important

Enclomiphene

Mechanism of Action

Enclomiphene is the trans-isomer of clomiphene citrate (Clomid), isolated from its less desirable cis-isomer (zuclomiphene). This is an important distinction.

At the hypothalamus and pituitary, estrogen receptors provide negative feedback - when estrogen binds these receptors, the brain reduces GnRH and LH/FSH output. Enclomiphene blocks these estrogen receptors, fooling the hypothalamic-pituitary system into believing estrogen levels are low. The system responds by increasing GnRH, LH, and FSH secretion - which then drives increased natural testosterone production and supports spermatogenesis.

This mechanism makes enclomiphene fundamentally different from TRT: rather than replacing testosterone from an external source (which suppresses the HPG axis), enclomiphene stimulates the HPG axis to produce more testosterone naturally. The testes remain active. Fertility is preserved and often improved.

By isolating the enclomiphene isomer, most of the side effects associated with clomiphene (particularly visual disturbances and emotional instability linked to zuclomiphene's CNS estrogenic activity) are significantly reduced.

Reported Benefits

• Significant increase in natural LH, FSH, and testosterone production
• Preserved testicular function and fertility
• Can be used as standalone therapy for men with secondary hypogonadism who do not want to suppress their HPG axis
• Effective for HPG axis restart after TRT discontinuation
• Preserved - and sometimes improved - sperm parameters

Common Side Effects

• Mild visual symptoms (significantly less than Clomid due to absence of zuclomiphene)
• Mood changes (reported less frequently than with Clomid)
• Transient estrogen elevation as testosterone rises (requires monitoring)
• Headache in some patients

Who Is a Candidate

• Men with secondary hypogonadism (normal testes, insufficient pituitary signaling) who want to raise testosterone without suppressing the HPG axis
• Men on TRT who want to preserve or restore fertility as part of a comprehensive protocol
• Men transitioning off TRT who need HPG axis recovery support
• Younger men who want testosterone optimization without the permanence of committing to exogenous TRT

Who Should Not Use This Compound

• Men with primary hypogonadism (non-functional testes - the pituitary signal can be amplified, but if the testes cannot respond, enclomiphene has no effect)
• Men with estrogen-sensitive conditions
• Men with liver disease

Clomiphene Citrate (Clomid)

Mechanism of Action

Clomiphene citrate is the parent compound containing both enclomiphene (trans) and zuclomiphene (cis) isomers. The enclomiphene component drives HPG axis stimulation; the zuclomiphene component has a longer half-life, accumulates with daily use, and has partial estrogenic activity in certain tissues - including the CNS, which is responsible for the mood and visual side effects more commonly associated with clomiphene than enclomiphene.

Clomiphene is prescribed in similar contexts to enclomiphene but carries a somewhat less favorable side effect profile due to the zuclomiphene component. Many providers now prefer enclomiphene where available for this reason.

Note on "Caspeptin"

The compound referred to as "caspeptin" in some clinical contexts may refer to specific compounded formulations or combinations; if you have been prescribed a compound under this name, your provider will review the specific compound, mechanism, and monitoring requirements with you directly.

BPC-157 (Body Protection Compound)

Mechanism of Action

BPC-157 is a pentadecapeptide (15 amino acids) derived from a protective protein found in gastric juice. It appears to work through multiple mechanisms involving angiogenesis (formation of new blood vessels), nitric oxide pathway modulation, growth factor upregulation (including VEGF, EGF, and FGF), and regulation of the dopaminergic and serotonergic neurotransmitter systems.

Its dominant clinically relevant mechanism is acceleration of tissue healing through enhanced angiogenesis and fibroblast activity - it increases blood supply to damaged tissue and accelerates the deposition of repair proteins. This applies across tissue types: tendons, ligaments, muscle, gut mucosa, and neural tissue.

Reported Benefits

• Accelerated healing of tendon, ligament, and muscle injuries
• Gut health improvement: significant evidence for healing of gastrointestinal mucosa, reduction in gut permeability, improvement in inflammatory bowel conditions
• Anti-inflammatory effects across multiple pathways
• Neurological support: evidence for protection against neurotoxic damage and support of dopamine/serotonin system function
• Joint health and protection from articular cartilage damage
• Potential benefit for post-surgery recovery
• Systemic anti-inflammatory effects relevant to autoimmune and inflammatory conditions

Common Side Effects

BPC-157 is notable for its remarkably clean safety profile in animal studies spanning multiple decades. In human use (primarily anecdotal and clinical observation), side effects are uncommon and generally mild:

• Dizziness (rare)
• Nausea (uncommon)
• Injection site reactions
• No documented serious adverse events in the published literature

Who Is a Candidate

• Men with active musculoskeletal injuries - tendinopathies, ligament damage, muscle tears
• Patients with GI issues: IBS, Crohn's, leaky gut, GERD, or post-surgical gut recovery
• Men with chronic joint pain or inflammatory conditions
• Patients seeking enhanced recovery from surgery or tissue damage
• Men with neurological symptoms or seeking neuroprotective support

TB-500 (Thymosin Beta-4 Fragment)

Mechanism of Action

TB-500 is a synthetic fragment of Thymosin Beta-4, an endogenous peptide involved in actin regulation, cell migration, blood vessel formation, and wound healing. Its primary mechanism is the upregulation of actin, the protein that forms the cytoskeleton of cells and is essential for cell migration to sites of injury, tissue regeneration, and angiogenesis.

TB-500 enhances the movement of repair cells (endothelial cells, fibroblasts, keratinocytes) into damaged tissue, stimulates new blood vessel growth, and reduces inflammation in damaged areas - accelerating repair from the cellular level up.

Reported Benefits

• Improved healing of soft tissue injuries: muscle, tendon, fascia
• Enhanced flexibility and range of motion as a result of tissue repair
• Reduction of fibrous scar tissue formation
• Complementary to BPC-157 in combined injury recovery stacks
• Anti-inflammatory effects in damaged tissue

Common Side Effects

• Generally well-tolerated
• Injection site reactions
• Mild fatigue in some patients
• Headache (uncommon)

IGF-1 LR3

Mechanism of Action

IGF-1 LR3 is a modified form of Insulin-like Growth Factor 1 with an extended half-life (compared to native IGF-1). It acts downstream of GH in the GH/IGF-1 axis, binding to IGF-1 receptors throughout the body to drive anabolic and fat-mobilizing effects without requiring GH secretion to mediate them.

IGF-1 receptors are found in muscle, fat, bone, brain, liver, and virtually every other tissue - which explains both its broad physiological effects and the need for careful dosing and monitoring.

Reported Benefits

• Anabolic stimulation: muscle protein synthesis and satellite cell activation
• Fat oxidation
• Improved recovery and tissue repair
• Improved insulin sensitivity at lower doses
• Neurological support (IGF-1 has well-established neuroprotective effects)

Safety Considerations

IGF-1 LR3 carries more significant safety considerations than peptides that work upstream in the GH axis:

• Hypoglycemia risk - IGF-1 has insulin-like activity and can significantly lower blood sugar; proper dosing, timing, and food intake management are critical
• Long-term IGF-1 elevation has theoretical cancer-promotion implications (IGF-1 receptors are upregulated in many cancers); this is an important monitoring consideration
• Not appropriate for patients with any active malignancy or significant family history
• Requires experienced clinical supervision and monitoring of IGF-1 levels

PT-141 (Bremelanotide)

Mechanism of Action

PT-141 works through a fundamentally different mechanism than PDE5 inhibitors (Viagra, Cialis). Rather than acting peripherally on blood flow, it acts centrally in the brain - specifically on MC3R and MC4R (melanocortin receptors) in the hypothalamus - to directly increase sexual desire and arousal at the neurological level.

This means PT-141 addresses the psychological and neurological components of sexual function, not just the mechanical/vascular components. It initiates desire rather than simply facilitating the physical response to desire that is already present.

Reported Benefits

• Increased sexual desire and spontaneous arousal
• Improved erectile quality (particularly in men with psychological or neurogenic components of erectile dysfunction)
• Enhanced sexual satisfaction
• Efficacy in men who do not respond adequately to PDE5 inhibitors

Common Side Effects

• Nausea - the most significant side effect; dose-dependent; can be mitigated with anti-nausea medication and appropriate dosing
• Facial flushing and warmth
• Transient blood pressure elevation - patients with cardiovascular disease or hypertension require careful evaluation
• Headache

Who Should Not Use This Compound

• Men with uncontrolled hypertension or significant cardiovascular disease
• Men with history of hypersensitivity to melanocortin agonists

GHK-Cu (Copper Peptide)

Mechanism of Action

GHK-Cu is a naturally occurring copper-binding peptide found in human plasma, saliva, and urine. Plasma concentrations decline significantly with age (from ~200 ng/mL at age 20 to ~80 ng/mL by age 60). It has broad biological activity - particularly in tissue remodeling - through regulation of matrix metalloproteinases (enzymes that break down old collagen and extracellular matrix) and stimulation of collagen, elastin, and glycosaminoglycan synthesis.

Reported Benefits

• Improved skin elasticity and collagen synthesis
• Wound healing acceleration
• Anti-inflammatory effects in skin and tissue
• Hair follicle stimulation
• Systemic anti-inflammatory and antioxidant effects with injectable use
• Nerve regeneration support (emerging data)

General Safety Framework

Understanding "Prescription Compounded" vs. Research Chemicals

All compounds dispensed through Tru-Genetics protocols are prescribed by licensed U.S. medical providers and filled through 503A-compliant compounding pharmacies. This is a meaningful legal and quality distinction.

503A Compounding Pharmacies:

• Fill patient-specific prescriptions for individual named patients
• Must comply with USP standards for sterility, purity, and potency
• Subject to state board of pharmacy oversight
• Require a valid prescriber-patient relationship
• Are not the same as overseas or "research chemical" peptide suppliers

Patients should understand that obtaining the same compounds outside of a licensed medical framework - from grey-market suppliers, overseas vendors, or unregulated sources - removes all quality controls, medical oversight, and legal protections. Purity, sterility, actual peptide content, and contamination risk are unverifiable in such products.

The FDA & Human Trials: Where Each Compound Stands

Universal Contraindications Across All GH-Stimulating Compounds

Any compound that stimulates growth hormone, IGF-1, or cellular growth signaling is contraindicated in:

• Active malignancy of any kind - GH and IGF-1 signaling can promote tumor growth
• History of pituitary tumors or pituitary disease
• Active diabetic retinopathy
• Severe carpal tunnel syndrome (GH elevation can worsen it)

Monitoring Standards at Tru-Genetics

All patients on active protocols undergo routine laboratory monitoring that at minimum includes:

• Complete Metabolic Panel (kidney and liver function, electrolytes, glucose)
• Lipid Panel (total cholesterol, LDL, HDL, triglycerides)
• Complete Blood Count
• Testosterone (total and free), Estradiol (sensitive LC/MS)
• LH, FSH (as appropriate to protocol)
• IGF-1 (for all GH-axis protocols)
• HbA1c and fasting insulin (for metabolic protocols)
• PSA (for men on TRT)
• Thyroid panel (baseline and periodic)

Protocol-specific monitoring is layered on top of this baseline depending on the compounds prescribed.

Talking to Your Medical Provider

Every compound described on this page is dispensed through a licensed medical framework. If you have questions about a specific compound, its inclusion in your protocol, its interactions with existing medications, or its monitoring requirements - these conversations belong with your assigned medical provider, not with self-research alone.

This page exists to ensure you are informed, not to replace the clinical relationship at the center of your care.

All information on this page reflects the current state of clinical research and standard of care as of the date of publication. The field of peptide therapy and hormone optimization is evolving rapidly. Protocols, indications, and regulatory statuses may change. Your medical provider will advise you of any changes material to your specific protocol.