AT HOME INJECTION KITS

Pharmaceutical Grade in the comfort of your own home

Regenics offers a range of vitamin and lipotropic injections that you can administer in the comfort of your own home. Whether your goal is losing weight, addressing nutritional deficiencies found on blood tests, or reversing the aging process….

Each At Home Injection Kits Includes:

1 Vial
10 injecting syringes
20 alcohol wipes
Dosing Instructions
Injecting Instructions

B12 Injection Kit

  • BOOSTS ENERGY
  • INCREASES METABOLISM
  • ENHANCES MOOD
  • HELPS REGULATE APPETITE
  • IMPROVES WEIGHT-LOSS

Compounded in USA
Pharmaceutical Grade

10ml of Vitamin B-12
5mg/mL
For IM Use Only

Also called hydroxocobalamin, B-12 is critical for metabolism and energy production for every cell in the body. It is also a cofactor in DNA synthesis. Deficiency in B-12 causes fatigue, weakness, nerve problems, and may lead to anemia.

$149.00

    Description

    This medication requires a prescription. Learn more about how Regenics uses free telehealth consults with our licensed medical providers to prescribe and fill this medication.

    Vitamin B12 is naturally found in animal foods. It can also be added to foods or supplements. Vitamin B12 is needed to form red blood cells and DNA. It is also a key player in the function and development of brain and nerve cells.

    Vitamin B12 binds to the protein in the foods we eat. In the stomach, hydrochloric acid and enzymes unbind vitamin B12 into its free form. From there, vitamin B12 combines with a protein called intrinsic factor so that it can be absorbed further down in the small intestine.

    Signs of deficiency may include:

    • Megaloblastic anemia—a condition of larger than normal sized red blood cells and a smaller than normal amount; this occurs because there is not enough vitamin B12 in the diet or poor absorption
    • Pernicious anemia—a type of megaloblastic anemia caused by a lack of intrinsic factor so that vitamin B12 is not absorbed
    • Fatigue, weakness
    • Nerve damage with numbness, tingling in the hands and legs
    • Memory loss, confusion
    • Dementia
    • Depression
    • Seizures

    Up to

    15%

    of the general population has a B12 deficiency

    Biotin (Vitamin B7) Injection Kit

    • IMPROVES HAIR GROWTH
    • STRENGTHENS NAILS
    • MAINTAINS HEALTHY SKIN
    • HELPS REGULATE CHOLESTEROL
    • PREVENTS GREY HAIR

    Compounded in USA
    Pharmaceutical Grade

    10ml Vial
    10mg/mL
    For IM Use Only

    $199.00 or subscribe and save up to 15%

    Choose a purchase plan:

      Description

      This medication requires a prescription. Learn more about how Regenics uses free telehealth consults with our licensed medical providers to prescribe and fill this medication.

      Biotin is a water-soluble B vitamin found naturally in some foods and also in supplements. It plays a vital role in assisting enzymes to break down fats, carbohydrates, and proteins in food. Biotin also helps to regulate signals sent by cells and the activity of genes.

      Biotin (vitamin H; coenzyme R; classified as a B vitamin) is a dietary component that is important for the metabolism of carbohydrates, fats, and amino acids. It is found primarily in liver, kidney, and muscle. Biotin functions as an essential cofactor for five carboxylases that catalyze steps in fatty acid, glucose, and amino acid metabolism. It is also an important factor in histone modifications, gene regulation, and cell signaling. Mammals must consume biotin to replenish stores. Sources of biotin include organ meats, eggs, fish, seeds, and nuts. As a dietary supplement, biotin has been promoted to be useful in the treatment of hair and nail problems, cradle cap (seborrheic dermatitis) in phenylketonuria patients, biotinidase deficiency, diabetes, peripheral neuropathy, candida infections, and high cholesterol. It has also been used in pregnancy, hemodialysis, and peritoneal dialysis, as biotin deficiency is more likely in these situations. Biotin is found in many cosmetics products. Radiolabeled biotin is used for pretargeted radioimmunotherapy of cancerous tumors.

      Biotin is found naturally in some foods and used as a dietary supplement. It is important for the metabolism of carbohydrates, fats, and amino acids. It is found primarily in liver, kidney, and muscle. Biotin functions as an essential cofactor for five carboxylases that catalyze steps in fatty acid, glucose, and amino acid metabolism. It is mostly protein-bound in foods such as organ meats, eggs, nuts, and soybeans. Gastrointestinal enzymes break down ingested biotin via proteolysis. This creates biocytin, which is then cleaved by biotinidase into free biotin and lysine. Free biotin is then absorbed in the small intestine. Biotin can be used for metabolism issues such as biotinidase, holocarboxylase synthetase, and isolated carboxylase enzyme deficiencies due to its essential role in the metabolism of fatty acids, glucose, and amino acids.

      DEFICIENCY

      Symptoms of biotin deficiency start gradually and can build up over time.

      Symptoms can include thinning hair, progressing to loss of hair across the body, and a scaly, red rash around body openings, including the eyes, nose, mouth, and anus. Conjunctivitis can also develop. About a third of pregnant women show a mild biotin deficiency despite adequate intake, though the exact reason is not clear.

      Adults with biotin deficiency may suffer:

      • seizures
      • skin infections
      • brittle nails
      • neurological problems, such as depression, lethargy, hallucinations, and paresthesias (pins and needles) in the extremities

      Biotin is not stored in the body so deficiency is possible if there isn’t enough in your diet.

      MICC Amino Blend Injection Kit

      • HELPS BREAKDOWN FAT
      • IMPROVES MENTAL FUNCTION
      • ALLEVIATES FEELING OF DEPRESSION
      • REDUCES BLOOD CHOLESTEROL

      Compounded in USA
      Pharmaceutical Grade

      10ml Vial
      For IM Use Only

      Includes Methionine 25 mg, Inositol 50 mg, Choline 50 mg, and Cyanocobalamin 330 mcg which are ‘lipotropic nutrients’ or compounds that aid in the metabolism of fat for energy, AKA a fat burner.

      $199.00

        Description

        This medication requires a prescription. Learn more about how Regenics uses free telehealth consults with our licensed medical providers to prescribe and fill this medication.

        METHIONINE

        This important amino acid helps block fat storage and reverse weight gain through its various roles in the body.

        • Methionine supplement has a detoxifying effect on the body due to its sulfur component which helps to cleanse the liver and remove toxins efficiently.
        • L-Methionine is an essential amino acid that acts as an antioxidant promoter. The body is able to convert methionine to cysteine which acts as a precursor to the detoxifying antioxidant L-Glutathione.
        • Methionine stimulates the body to secrete the hormone somatotropin, an important fat-burning hormone, making methionine an important amino acid in one’s weight loss journey.
        • Methionine is also the primary methyl donor in the body through S- adenosyl methionine via the transmethylation pathway, which is involved in the synthesis of several key metabolites including creatine and phosphatidylcholine.
          • Creatine is a substance that is found naturally in muscle cells. It improves muscle development at the expense of fat and helps muscles produce energy during heavy lifting or high-intensity exercise.
          • Phosphatidylcholine helps prevent the accumulation of fat in the liver. It may also promote lipolysis or the breakdown of fats in the body.
          • These can help to increase your metabolic rate and aid in weight loss efforts.
        • Methionine supplement also aids in the process of making new cells, which is important news for any athletes out there to return them to premiere performance shape.
        • Methionine supplement has anti-inflammatory and pain-relieving properties to help muscles recover from damage after a rigorous training session.

        INOSITOL

        There is evidence to suggest inositol can correct many metabolic disorders that contribute to the development of high blood pressure, diabetes, and metabolic syndrome.

        A 2016 pilot study published in the International Journal of Endocrinology reported that people with type 2 diabetes given myo-inositol and d-chiro-inositol daily along with their anti-diabetes drugs had a significant drop in their fasting blood glucose (192.6 mg/dL down to 160.9 mg/dL) and A1C (8.6% down to 7.7%) after three months.

        Another small study published in the journal Menopause suggested that myo-inositol may aid in the treatment of metabolic syndrome in postmenopausal women. According to the research, women assigned to six months of myo-inositol supplements experienced significantly greater improvements in blood pressure and cholesterol levels than women provided a placebo.

        When treated with myo-inositol, women with metabolic syndrome experienced an 11% drop in diastolic blood pressure, a 20% drop in triglycerides, and a 22% increase in “good” high-density lipoprotein (HDL) cholesterol.

        All of these values translate to an improvement of metabolic syndrome as well as a decreased risk of cardiovascular disease.

        CHOLINE

        Choline plays an important role in controlling fat and cholesterol buildup in the body. It has even been suggested that choline helps the body burn fat, which may result in easier weight loss and better metabolic health.

        “Without an adequate supply of choline for phosphatidylcholine synthesis, triacylglycerides will accumulate, which leads to fatty liver condition,” according to the National Institutes of Health.

        Furthermore, there is credible evidence that sub-optimal choline levels in humans are associated with liver and muscular damage.

        “The importance of choline in the diet extends into adulthood and old age. In a study of healthy adult subjects deprived of dietary choline, 77% of the men and 80% of the postmenopausal women developed signs of subclinical organ dysfunction (fatty liver or muscle damage),” according to this report from the NIH.

        Basically, a choline deficiency can cause an abnormal deposition of fat in the liver, which may result in nonalcoholic fatty liver disease.

        Lipo Mino Injection Kit

        • BURNS FAT
        • BOOSTS ENERGY
        • SUPPRESSES APPETITE
        • INCREASES METABOLISM

        Pryridoxine 2mg, Mythionine 12.4mg, Inositol 25mg, Choline 25mg, B12 1mg, Carnitine 125mg, Thiamine 50mg, Riboflavin 5mg

        Compounded in USA
        Pharmaceutical Grade

        10ml Vial
        For IM Use Only

        Paired with a healthy diet and exercise lipotropic injections could help you shed fat and boost energy levels.

        $249.00

          Description

          This medication requires a prescription. Learn more about how Regenics uses free telehealth consults with our licensed medical providers to prescribe and fill this medication.

          PRYRIDOXINE (VITAMIN B6)

          METABOLIZES FATS, CARBS, AND PROTEINS

          Vitamin B6 plays a crucial role in metabolizing fats, carbohydrates and proteins. By assisting in metabolizing fats, carbs and proteins, your metabolism speeds up and allows you to burn calories and lose weight quicker. This also aids in your body extracting nutrients from food. If you are trying to lose weight and are on a low calorie diet, Vitamin B assists in your maximizing the nutrients you get from the smaller portion of food you eat.

          INOSITOL

          There is evidence to suggest inositol can correct many metabolic disorders that contribute to the development of high blood pressure, diabetes, and metabolic syndrome.

          A 2016 pilot study published in the International Journal of Endocrinology reported that people with type 2 diabetes given myo-inositol and d-chiro-inositol daily along with their anti-diabetes drugs had a significant drop in their fasting blood glucose (192.6 mg/dL down to 160.9 mg/dL) and A1C (8.6% down to 7.7%) after three months.

          Another small study published in the journal Menopause suggested that myo-inositol may aid in the treatment of metabolic syndrome in postmenopausal women. According to the research, women assigned to six months of myo-inositol supplements experienced significantly greater improvements in blood pressure and cholesterol levels than women provided a placebo.

          When treated with myo-inositol, women with metabolic syndrome experienced an 11% drop in diastolic blood pressure, a 20% drop in triglycerides, and a 22% increase in “good” high-density lipoprotein (HDL) cholesterol.

          All of these values translate to an improvement of metabolic syndrome as well as a decreased risk of cardiovascular disease.

          CHOLINE

          Choline plays an important role in controlling fat and cholesterol buildup in the body. It has even been suggested that choline helps the body burn fat, which may result in easier weight loss and better metabolic health.

          “Without an adequate supply of choline for phosphatidylcholine synthesis, triacylglycerides will accumulate, which leads to fatty liver condition,” according to the National Institutes of Health.

          Furthermore, there is credible evidence that sub-optimal choline levels in humans are associated with liver and muscular damage.

          “The importance of choline in the diet extends into adulthood and old age. In a study of healthy adult subjects deprived of dietary choline, 77% of the men and 80% of the postmenopausal women developed signs of subclinical organ dysfunction (fatty liver or muscle damage),” according to this report from the NIH.

          Basically, a choline deficiency can cause an abnormal deposition of fat in the liver, which may result in nonalcoholic fatty liver disease.

          NAD+ Injections

          • PROMOTES DNA REPAIR
          • IMPROVES COGNITIVE ABILITIES
          • INCREASES ATHLETIC PERFORMANCE
          • SUPPORTS WEIGHT LOSS
          • DECREASES FATIGUE
          • COMPOUNDED IN USA
          • FOR IM OR SUBCUTANEOUS USE ONLY

          *NAD+ IV Infusions available in office

          $399.00$599.00

          Description

          This medication requires a prescription. Learn more about how Regenics uses free telehealth consults with our licensed medical providers to prescribe and fill this medication.

          Nicotinamide adenine dinucleotide (NAD) is one of the most essential molecules in your body. In fact, you’ll find it in every single cell working in more chemical reactions than any other vitamin-derived molecule. When the molecule has oxidized and becomes inactive, it is known as NADH, but in its active form, it is known as NAD+. NAD+ is a coenzyme of the Vitamin B3 that activates reactions after binding to protein molecules.

          At-Home Injection Kit Includes:

          1 1,000 or 500 mg NAD+ lyophilized vial
          1 10ml bacteriostatic water vial
          1 mixing syringe
          10 injecting syringes
          20 alcohol wipes
          Dosing Instructions
          Injecting Instructions

          Nicotinamide Adenine Dinucleotide (NAD+) is a prevalent cellular electron transporter, coenzyme, and signaling molecule found in all cells of the body and is vital for cell function and viability.12 Its reduced (NADH) and phosphorylated forms (NADP+ and NADPH) are as important as NAD+.12 Each step of cellular respiration—glycolysis in the cytoplasm, the Krebs cycle, and the electron transport chain in the mitochondria—requires the presence of NAD+ and NADH, their redox partner.

          The manufacture of cholesterol and nucleic acids, elongation of fatty acids, and regeneration of glutathione, a vital antioxidant in the body, are just a few anabolic processes that frequently require NADP+ and NADPH.3 NAD+-dependent/-consuming enzymes modify proteins post-translationally in various cellular processes using NAD+ and its other forms as substrates.12 NAD+ also acts as a precursor for cyclic ADP ribose, an essential component of calcium signaling and a secondary messenger molecule.4

          The amino acid tryptophan and the vitamin precursors nicotinic acid and nicotinamide, often known as vitamin B3 or niacin, are used by the body to naturally produce NAD+. It can also be produced from biosynthetic intermediates including nicotinamide mononucleotide and nicotinamide riboside.23 NAD+ is continuously recycled within cells as it transitions between its many forms through salvage mechanisms.3 Mammalian cells may be able to take up extracellular NAD+, according to studies on cell culture.5

          The highest NAD+ levels are found in neonates, and they gradually decrease with increasing chronological age.6 They are around half of what they are in younger persons after age 50.6 Model organisms have been used to study the subject of why NAD+ levels fall with aging.78 However, during other metabolic activities, NAD+ is consumed by NAD+-dependent enzymes and may subsequently become depleted over time, contributing to increased DNA damage, age-related illnesses and diseases, and mitochondrial malfunction. During redox reactions, NAD+ and NADH are not consumed but rather continually regenerated.26 Views of aging and senescence frequently highlight a deterioration in mitochondrial health and function with age, and investigations of NAD+ depletion and the associated oxidative stress and damage corroborate these theories.12

          The age-related drop in NAD+ levels is caused by rising levels of CD38, a membrane-bound NADase that degrades both NAD+ and its precursor nicotinamide mononucleotide, according to a 2016 study in mice, which exhibit age-related declines in NAD+ levels similar to those seen in humans.7 The study also demonstrated that human adipose tissue from older adults (mean age, 61 years) expresses the CD38 gene at higher levels than that of younger adults (mean age, 34 years).7 Other research in mice, however, has shown that oxidative stress and inflammation brought on by aging lower NAD+ production.​​​​​​​8 Therefore, it is likely that a number of mechanisms work together to cause individuals to lose NAD+ as they age.

          When it was recognized that pellagra, a condition marked by diarrhea, dermatitis, dementia, and mortality, could be treated with foods containing NAD+ precursors, particularly vitamin B3, the clinical significance of maintaining NAD+ levels was established in the early 1900s.​​​​​​​9 Notably, the skin does not flush with NAD+ injection, in contrast to vitamin B3 (niacin) intake, which also causes this negative effect.​​​​​​​10 Low NAD+ levels have recently been associated with a variety of age-related ailments and diseases linked to increased oxidative/free radical damage, including diabetes,11 heart disease,812 vascular dysfunction,13 ischemic brain injury,14 Alzheimer’s disease,1516 and vision loss.17

          Since a 1961 report by Paul O’Hollaren, MD, of Shadel Hospital in Seattle, Washington, NAD+ IV infusion has been widely utilized for the treatment of addiction.181920 In more than 100 instances, Dr. O’Hollaren detailed the effective use of IV-infused NAD+ for the prevention, relief, or treatment of acute and chronic symptoms of addiction to a range of substances, including alcohol, heroin, opium extract, morphine, dihydromorphine, meperidine, codeine, cocaine, amphetamines, barbiturates, and tranquilizers.​​​​​​​18 The security and effectiveness of NAD+ treatment for addiction, however, have not yet been assessed in clinical trials.

          NAD+-replacement therapy may encourage optimal mitochondrial function and homeostasis, genomic stability, neuroprotection, long life, and may help with addiction treatment.12320 Clinical trials assessing these effects in humans receiving NAD+ injection have not yet been published; nevertheless, many clinical trials assessing the effectiveness and safety of NAD+-replacement therapy or augmentation in the context of human disease and aging have recently been completed, and many more are currently underway.

          Unknown are the precise mechanisms of NAD+ repair or enhancement for potential health benefits, such as supporting healthy aging and treating age-related illnesses, metabolic and mitochondrial diseases, and addiction12320

          In order to prevent mitochondrial malfunction and sustain metabolic function/energy generation (ATP), NAD+ supplementation may counterbalance the age-related degradation of NAD+ and its precursor nicotinamide mononucleotide by NADases, particularly CD38.7 NAD+ replenishment, however, appears to support a number of other metabolic pathways via NAD+-dependent enzymes in research involving human and animal models (as well as samples and cell lines).12320

          There are numerous well-known NAD+-dependent enzymes. Poly-ADP ribose polymerases (PARP 1–17) control nuclear stability and DNA repair.13 cADP-ribose, ADP-ribose, and nicotinic acid adenine dinucleotides are produced by NADases CD38 and CD157 in Ca2+ signaling and intercellular immunological communication.13 A family of histone deacetylases known as sirtuins (Sirt 1-7) controls a number of proteins involved in cellular metabolism, stress responses, circadian rhythms, and endocrine functions. Sirts have also been linked to longevity in model organisms and protective effects in cardiac and neuronal models.​​​​​​​13 A recently identified NAD+ hydrolase, Sterile Alpha and Toll/Interleukin-1 Receptor motif-containing 1 (SARM1), is implicated in the aging and regeneration of neurons.2122

          The mechanism of action of NAD+ replenishment has been somewhat clarified by research on progeroid (premature aging) disorders, which resemble the clinical and molecular aspects of aging. It is believed that the Werner syndrome (WS), which is characterized by severe metabolic dysfunction, dyslipidemia, early atherosclerosis, and insulin resistance diabetes, most closely resembles the aging process.23 The source of WS is the Werner (WRN) DNA helicase gene24, which regulates the transcription of the essential NAD+ 25biosynthetic enzyme Nicotinamide Nucleotide Adenylyltransferase 1.​​​​​​​

          NAD+ depletion through disruption of mitochondrial homeostasis is a substantial contributor to the metabolic dysfunction in WS, according to a 2019 study.25 WS patient samples and WS animal models’ NAD+-deficient cells showed impaired mitophagy (selective degradation of defective mitochondria).25 NAD+ repletion restored NAD+ metabolic profiles, improved fat metabolism, lowered mitochondrial oxidative stress, and improved mitochondrial integrity in human cells with mutant WRN via restoring normal mitophagy.25 In animal models, NAD+ repletion significantly increased lifespan, delayed the beginning of accelerated aging, and increased the number of proliferating stem cells in the germ line.​​​​​​​25 Several NAD+ precursor molecules were released to replace NAD+, demonstrating that NAD+ replacement is what generates the beneficial effects.25

          More evidence of NAD+’s significance in promoting mitochondrial and metabolic health may be seen in murine cells overexpressing the NADase CD38, which also had greater lactate levels, aberrant mitochondria, including missing or enlarged cristae, and lower oxygen consumption.7 Isolated mitochondria from these cells showed a substantial reduction in NAD+ and NADH compared to controls. In CD38-deficient animals, NAD+ levels, mitochondrial respiratory rates, and metabolic activities remained constant with age.7

          A set of 11 healthy male individuals (n=8 for NAD+ and n=3 for controls) participated in a pharmacokinetic study to examine how changes in NAD+ and its metabolite concentrations during NAD+ IV infusion affected the subjects’ overall health. Over the course of six hours, participants received a 750 mg dosage of NAD+ through an IV infusion at a rate of three moles per minute. NAD+, nicotinamide, and adenosine phosphoribose (ADPR) plasma levels were all substantially greater than those in the control group (p<.001, p<.001, and p<.0001, respectively) as a result of this, relative to baseline (p<.0001).10 After 8 hours, there was no difference in nicotinamide or ADPR levels across the groups, although there was a difference in NAD+ levels.​​​​​​​10 Over the course of the 8-hour period, levels of these two NAD+ byproducts were substantially correlated in both groups (=1.0, p<.001), suggesting that NADases like CD38 may be in charge of cleaving NAD+ to nicotinamide and ADPR.10

          Plasma levels of nicotinamide’s metabolites, methylnicotinamide (350%) and nicotinamide mononucleotide (NMN; 472%), also significantly increased at the end of the NAD+ infusion compared to baseline and the control group (p<.0001 and p<.05, respectively), which is consistent with increased nicotinamide.10

          NAD+ levels excreted in the urine of the NAD+ group were significantly higher (538%) after infusion (at 6 h) compared to those tested at 30 minutes (p<.001); they were also significantly different from the controls (p<.05).10 This level decreased by 43% at the 8-hour time point relative to the peak at 6 hours (p <.05).10

          Urine contains more NAD+ and its metabolites.10 The NAD+ group’s nicotinamide urine excretion levels remained stable during an 8-hour period, but those of methylnicotinamide significantly increased (403 percent) following infusion (at 6 h) compared to that assessed at 30 minutes (p<.01).​​​​​​​10 In comparison to the high at 6 hours, this level likewise dropped by 43% at the 8-hour mark (p <.05).10

          Notably, no significant increases in plasma or urine levels of NAD+ or its metabolites were observed within the first 2 hours of infusion, indicating rapid and complete tissue uptake and/or metabolism (at least for the first 2 hours).10

          Notably, within the first two hours after infusion, no discernible increases in plasma or urine levels of NAD+ or its metabolites were seen, indicating quick and thorough tissue absorption and/or metabolism (at least for the first 2 hours).​​​​​​​1 NAD+ injections’ impact on intracellular and compartmental NAD+ pools, however, is not yet known.1

          At the time of writing, there were no other reported contraindications/precautions for NAD+ injection. Individuals with known allergy to NAD+ injection should not use this product.

          The safety of NAD+ injection has not been evaluated in pregnant women. Due to this lack of safety data, pregnant women should avoid NAD+ injection.

          The safety of NAD+ injection has not been evaluated in women who are breastfeeding or children. Due to this lack of safety data, women who are breastfeeding and children should avoid NAD+ injection.

          At the time of writing, there were no reported interactions for NAD+ injection. It is possible that unknown interactions exist.

          Injection of NAD+ seems to be secure and well-tolerated.10 The injection of NAD+ may cause adverse reactions and side effects, such as headache, shortness of breath, constipation,18 increased plasma bilirubin, and decreased levels of gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransferase.10

          Case studies of the use of NAD+ to treat drug addiction offered early information on side effects and safety.​​​​​​​1819 According to a 1961 study, patients with addiction who got NAD+ at a moderate IV drip rate (no more than 35 drops per minute) reported “no distress” but those who received it at a quicker drip rate complained of headache and shortness of breath.​​​​​​​18 In this study, the dosage was 500–1000 mg per day for 4 days, then two injections every week for a month, and then one injection every two months as a maintenance dose. One of the two patients who had therapy reported experiencing constipation.18

          In a 2019 study, a cohort of healthy male participants (n=11; NAD+ n = 8 and Control n = 3) aged 30-55 years had their safety of IV infusion of NAD+ evaluated using liver function tests (serum, total bilirubin, alkaline phosphatase, alanine aminotransferase, gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransfer.10 Neither the NAD+ cohort nor the placebo (saline) cohort experienced any negative side effects throughout the 6 hour infusion.​​​​​​​10 At 8 hours following the start of the NAD+ infusion, it was shown that the NAD+ group had significant declines in the liver function enzymes gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransferase as well as a large increase in plasma bilirubin.​​​​​​​10 The modifications, however, were not regarded as clinically important. Because of the limited sample sizes, notably for the control group, which are acknowledged by the authors, these results should be evaluated with care.​​​​​​​10

          Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

          Additional information

          Potency

          500mg, 1000mg

          This At-Home Injection Kit Includes:

          1 1,000 or 500 mg NAD+ lyophilized vial
          1 10ml bacteriostatic water vial
          1 mixing syringe
          10 injecting syringes
          20 alcohol wipes
          Dosing Instructions
          Injecting Instructions

          Nicotinamide adenine dinucleotide (NAD) is one of the most essential molecules in your body. In fact, you’ll find it in every single cell working in more chemical reactions than any other vitamin-derived molecule. When the molecule has oxidized and becomes inactive, it is known as NADH, but in its active form, it is known as NAD+. NAD+ is a coenzyme of the Vitamin B3 that activates reactions after binding to protein molecules.

          Nicotinamide Adenine Dinucleotide (NAD+) is a prevalent cellular electron transporter, coenzyme, and signaling molecule found in all cells of the body and is vital for cell function and viability. Its reduced (NADH) and phosphorylated forms (NADP+ and NADPH) are as important as NAD+. Each step of cellular respiration—glycolysis in the cytoplasm, the Krebs cycle, and the electron transport chain in the mitochondria—requires the presence of NAD+ and NADH, their redox partner.

          The manufacture of cholesterol and nucleic acids, elongation of fatty acids, and regeneration of glutathione, a vital antioxidant in the body, are just a few anabolic processes that frequently require NADP+ and NADPH. NAD+-dependent/-consuming enzymes modify proteins post-translationally in various cellular processes using NAD+ and its other forms as substrates. NAD+ also acts as a precursor for cyclic ADP ribose, an essential component of calcium signaling and a secondary messenger molecule.

          The amino acid tryptophan and the vitamin precursors nicotinic acid and nicotinamide, often known as vitamin B3 or niacin, are used by the body to naturally produce NAD+. It can also be produced from biosynthetic intermediates including nicotinamide mononucleotide and nicotinamide riboside. NAD+ is continuously recycled within cells as it transitions between its many forms through salvage mechanisms. Mammalian cells may be able to take up extracellular NAD+, according to studies on cell culture.

          The highest NAD+ levels are found in neonates, and they gradually decrease with increasing chronological age. They are around half of what they are in younger persons after age 50. Model organisms have been used to study the subject of why NAD+ levels fall with aging. However, during other metabolic activities, NAD+ is consumed by NAD+-dependent enzymes and may subsequently become depleted over time, contributing to increased DNA damage, age-related illnesses and diseases, and mitochondrial malfunction. During redox reactions, NAD+ and NADH are not consumed but rather continually regenerated. Views of aging and senescence frequently highlight a deterioration in mitochondrial health and function with age, and investigations of NAD+ depletion and the associated oxidative stress and damage corroborate these theories.

          The age-related drop in NAD+ levels is caused by rising levels of CD38, a membrane-bound NADase that degrades both NAD+ and its precursor nicotinamide mononucleotide, according to a 2016 study in mice, which exhibit age-related declines in NAD+ levels similar to those seen in humans. The study also demonstrated that human adipose tissue from older adults (mean age, 61 years) expresses the CD38 gene at higher levels than that of younger adults (mean age, 34 years). Other research in mice, however, has shown that oxidative stress and inflammation brought on by aging lower NAD+ production.​​​​​​​ Therefore, it is likely that a number of mechanisms work together to cause individuals to lose NAD+ as they age.

          When it was recognized that pellagra, a condition marked by diarrhea, dermatitis, dementia, and mortality, could be treated with foods containing NAD+ precursors, particularly vitamin B3, the clinical significance of maintaining NAD+ levels was established in the early 1900s.​​​​​​​ Notably, the skin does not flush with NAD+ injection, in contrast to vitamin B3 (niacin) intake, which also causes this negative effect.​​​​​​​ Low NAD+ levels have recently been associated with a variety of age-related ailments and diseases linked to increased oxidative/free radical damage, including diabetes, heart disease, vascular dysfunction, ischemic brain injury, Alzheimer’s disease, and vision loss.

          Since a 1961 report by Paul O’Hollaren, MD, of Shadel Hospital in Seattle, Washington, NAD+ IV infusion has been widely utilized for the treatment of addiction. In more than 100 instances, Dr. O’Hollaren detailed the effective use of IV-infused NAD+ for the prevention, relief, or treatment of acute and chronic symptoms of addiction to a range of substances, including alcohol, heroin, opium extract, morphine, dihydromorphine, meperidine, codeine, cocaine, amphetamines, barbiturates, and tranquilizers.​​​​​​​ The security and effectiveness of NAD+ treatment for addiction, however, have not yet been assessed in clinical trials.

          NAD+-replacement therapy may encourage optimal mitochondrial function and homeostasis, genomic stability, neuroprotection, long life, and may help with addiction treatment. Clinical trials assessing these effects in humans receiving NAD+ injection have not yet been published; nevertheless, many clinical trials assessing the effectiveness and safety of NAD+-replacement therapy or augmentation in the context of human disease and aging have recently been completed, and many more are currently underway.

          Unknown are the precise mechanisms of NAD+ repair or enhancement for potential health benefits, such as supporting healthy aging and treating age-related illnesses, metabolic and mitochondrial diseases, and addiction

          In order to prevent mitochondrial malfunction and sustain metabolic function/energy generation (ATP), NAD+ supplementation may counterbalance the age-related degradation of NAD+ and its precursor nicotinamide mononucleotide by NADases, particularly CD38. NAD+ replenishment, however, appears to support a number of other metabolic pathways via NAD+-dependent enzymes in research involving human and animal models (as well as samples and cell lines).

          There are numerous well-known NAD+-dependent enzymes. Poly-ADP ribose polymerases (PARP 1–17) control nuclear stability and DNA repair. cADP-ribose, ADP-ribose, and nicotinic acid adenine dinucleotides are produced by NADases CD38 and CD157 in Ca2+ signaling and intercellular immunological communication. A family of histone deacetylases known as sirtuins (Sirt 1-7) controls a number of proteins involved in cellular metabolism, stress responses, circadian rhythms, and endocrine functions. Sirts have also been linked to longevity in model organisms and protective effects in cardiac and neuronal models.​​​​​​​ A recently identified NAD+ hydrolase, Sterile Alpha and Toll/Interleukin-1 Receptor motif-containing 1 (SARM1), is implicated in the aging and regeneration of neurons.

          The mechanism of action of NAD+ replenishment has been somewhat clarified by research on progeroid (premature aging) disorders, which resemble the clinical and molecular aspects of aging. It is believed that the Werner syndrome (WS), which is characterized by severe metabolic dysfunction, dyslipidemia, early atherosclerosis, and insulin resistance diabetes, most closely resembles the aging process The source of WS is the Werner (WRN) DNA helicase gene, which regulates the transcription of the essential NAD+ biosynthetic enzyme Nicotinamide Nucleotide Adenylyltransferase 1.​​​​​​​

          NAD+ depletion through disruption of mitochondrial homeostasis is a substantial contributor to the metabolic dysfunction in WS, according to a 2019 study. WS patient samples and WS animal models’ NAD+-deficient cells showed impaired mitophagy (selective degradation of defective mitochondria). NAD+ repletion restored NAD+ metabolic profiles, improved fat metabolism, lowered mitochondrial oxidative stress, and improved mitochondrial integrity in human cells with mutant WRN via restoring normal mitophagy. In animal models, NAD+ repletion significantly increased lifespan, delayed the beginning of accelerated aging, and increased the number of proliferating stem cells in the germ line.​​​​​​​ Several NAD+ precursor molecules were released to replace NAD+, demonstrating that NAD+ replacement is what generates the beneficial effects.

          More evidence of NAD+’s significance in promoting mitochondrial and metabolic health may be seen in murine cells overexpressing the NADase CD38, which also had greater lactate levels, aberrant mitochondria, including missing or enlarged cristae, and lower oxygen consumption. Isolated mitochondria from these cells showed a substantial reduction in NAD+ and NADH compared to controls. In CD38-deficient animals, NAD+ levels, mitochondrial respiratory rates, and metabolic activities remained constant with age.

          A set of 11 healthy male individuals (n=8 for NAD+ and n=3 for controls) participated in a pharmacokinetic study to examine how changes in NAD+ and its metabolite concentrations during NAD+ IV infusion affected the subjects’ overall health. Over the course of six hours, participants received a 750 mg dosage of NAD+ through an IV infusion at a rate of three moles per minute. NAD+, nicotinamide, and adenosine phosphoribose (ADPR) plasma levels were all substantially greater than those in the control group (p<.001, p<.001, and p<.0001, respectively) as a result of this, relative to baseline (p<.0001). After 8 hours, there was no difference in nicotinamide or ADPR levels across the groups, although there was a difference in NAD+ levels.​​​​​​​ Over the course of the 8-hour period, levels of these two NAD+ byproducts were substantially correlated in both groups (=1.0, p<.001), suggesting that NADases like CD38 may be in charge of cleaving NAD+ to nicotinamide and ADPR.

          Plasma levels of nicotinamide’s metabolites, methylnicotinamide (350%) and nicotinamide mononucleotide (NMN; 472%), also significantly increased at the end of the NAD+ infusion compared to baseline and the control group (p<.0001 and p<.05, respectively), which is consistent with increased nicotinamide.

          NAD+ levels excreted in the urine of the NAD+ group were significantly higher (538%) after infusion (at 6 h) compared to those tested at 30 minutes (p<.001); they were also significantly different from the controls (p<.05). This level decreased by 43% at the 8-hour time point relative to the peak at 6 hours (p <.05).

          Urine contains more NAD+ and its metabolites. The NAD+ group’s nicotinamide urine excretion levels remained stable during an 8-hour period, but those of methylnicotinamide significantly increased (403 percent) following infusion (at 6 h) compared to that assessed at 30 minutes (p<.01).​​​​​​​ In comparison to the high at 6 hours, this level likewise dropped by 43% at the 8-hour mark (p <.05).

          Notably, no significant increases in plasma or urine levels of NAD+ or its metabolites were observed within the first 2 hours of infusion, indicating rapid and complete tissue uptake and/or metabolism (at least for the first 2 hours).

          Notably, within the first two hours after infusion, no discernible increases in plasma or urine levels of NAD+ or its metabolites were seen, indicating quick and thorough tissue absorption and/or metabolism (at least for the first 2 hours).​​​​​​​ NAD+ injections’ impact on intracellular and compartmental NAD+ pools, however, is not yet known.

          At the time of writing, there were no other reported contraindications/precautions for NAD+ injection. Individuals with known allergy to NAD+ injection should not use this product.

          The safety of NAD+ injection has not been evaluated in pregnant women. Due to this lack of safety data, pregnant women should avoid NAD+ injection.

          The safety of NAD+ injection has not been evaluated in women who are breastfeeding or children. Due to this lack of safety data, women who are breastfeeding and children should avoid NAD+ injection.

          At the time of writing, there were no reported interactions for NAD+ injection. It is possible that unknown interactions exist.

          Injection of NAD+ seems to be secure and well-tolerated. The injection of NAD+ may cause adverse reactions and side effects, such as headache, shortness of breath, constipation, increased plasma bilirubin, and decreased levels of gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransferase.

          Case studies of the use of NAD+ to treat drug addiction offered early information on side effects and safety.​​​​​​​ According to a 1961 study, patients with addiction who got NAD+ at a moderate IV drip rate (no more than 35 drops per minute) reported “no distress” but those who received it at a quicker drip rate complained of headache and shortness of breath.​​​​​​​ In this study, the dosage was 500–1000 mg per day for 4 days, then two injections every week for a month, and then one injection every two months as a maintenance dose. One of the two patients who had therapy reported experiencing constipation.

          In a 2019 study, a cohort of healthy male participants (n=11; NAD+ n = 8 and Control n = 3) aged 30-55 years had their safety of IV infusion of NAD+ evaluated using liver function tests (serum, total bilirubin, alkaline phosphatase, alanine aminotransferase, gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransfer. Neither the NAD+ cohort nor the placebo (saline) cohort experienced any negative side effects throughout the 6 hour infusion.​​​​​​​ At 8 hours following the start of the NAD+ infusion, it was shown that the NAD+ group had significant declines in the liver function enzymes gamma glutamyl transferase, lactate dehydrogenase, and aspartate aminotransferase as well as a large increase in plasma bilirubin.​​​​​​​ The modifications, however, were not regarded as clinically important. Because of the limited sample sizes, notably for the control group, which are acknowledged by the authors, these results should be evaluated with care.​​​​​​​

          Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.