• Trimix injection
  • Trimix injection

Overview Of TriMix Injection

Dosage Power Of TriMix Injection
Papaverine HCl 30 mg/mL, Phentolamine Mesylate 1 mg/mL Prostaglandin E1 10 mcg/mL. 5 mL Vial. Lyophilized.
Papaverine HCl 30 mg/mL, Phentolamine Mesylate 2 mg/mL Prostaglandin E1 20 mcg/mL. 5 mL Vial. Lyophilized.
Generic Details
Located in the front of the neck in the human body, the thyroiTriMix is administered as a penile self-injection, typically considered to be the most powerful class of anti-erectile dysfunction agents. While the components of TriMix injection (Papaverine, Phentolamine, Prostaglandin E1) are, on their own, indicated for a vast number of different conditions, the practice of bringing them together in concert to treat erectile dysfunction has become commonplace in sexual medicine and is now considered to be the go-to treatment if conventional PDE5 inhibitors are contraindicated or nonresponsive. and is now considered the go-to treatment if a patient is not responsive to conventional PDE5 inhibitors such as Viagra or Cialis.1 TriMix injection is indicated in the treatment of erectile dysfunction in males. TriMix injection contains three drugs from complimentary classes designed to act synergistically, mixed into a sterile injection. They are:


A drug that causes blood vessels to expand (vasodilator); it produces an erection by allowing for increased blood flow to the penis. Papaverine interacts with adenylate cyclase resulting in increased cyclic adenosine monophosphate (cAMP) production, ultimately resulting in increased erectile capacity by relaxation of penile smooth muscle. This drug was one of the first effective therapies for erectile dysfunction administered by penile injection. Papaverine works by inhibiting phosphodiesterase nonspecifically, there are also multiple other mechanisms by which this drug acts to improve erectile capacity. The current body of medical literature has not established the predominant mechanism by which papaverine works. The multi-mechanistic manner by which this drug acts may be concentration dependent. Experimental data, performed in-vitro, displays papaverine acting to relax the penile arteries, the cavernosal sinusoids, and the penile veins. Experiments carried out in dogs display papaverine’s ability to decrease the resistance to arterial inflow while also increasing the resistance to venous outflow. Papaverine’s ability to decrease resistance to venous outflow has been replicated in clinical studies. A veno-occlusive mechanism may be responsible for the aforementioned findings.

Biweekly intracavernous administration of papaverine for erectile dysfunction.

Participants: 50 patients age 40 to 70 years old
Administration: intracavernosal injection at base of the penis
Dosage: 60 mg papaverine in 5 ml saline every 2 weeks
Results: Erection of 80% or more of normal was achieved by all but one patient, improves sexual potency

Medical treatment of impotence with papaverine and phentolamine intracavernosal injection.

Participants: 20 patients age 32 to 72 years old
Administration: intracavernosal injection
Dosage: 30 mg papaverine and phentolamine 1 mg
Results: Response with erection in 20- 30 minutes, phentolamine and papaverine produced an erection sufficient for intercourse in 18 of the 20 subjects

Treatment of impotence by intrapenile injections of papaverine and phenoxybenzamine: a double blind, controlled trial.

Participants: 39 patients age 27 to 67 years old
Administration: intracavernosal injection
Dosage: 60 mg Papaverine in 10 ml saline
Results: 35% full restoration of erectile capacity 65% partial restoration of erectile capacity

Evaluating erectile dysfunction: oral sildenafil versus intracavernosal injection of papaverine.

Participants: 39 patients age 21 to 65 years old
Administration: intracavernosal injection
Dosage: 30 mg papaverine
Results: Papaverine improved length and circumference papaverine is effective as injection therapy for erectile dysfunction


When injected into the penis, it induces an erection by relaxing and dilating the blood vessels of the penis, as well as by elevating cardiac output.

Phentolamine is classified as an Alpha-Adrenoceptor Antagonists. Noradrenaline effects the smooth muscle tone of the penile tissues by keeping the corpora cavernosa in a contracted state. By blocking the functional noradrenaline receptors, the Alpha-Adrenoceptor, erectile response can be achieved. Phentolamine competes with endogenous norepinephrine for the Alpha1-Adrenoceptor and Alpha2-Adrenoceptor. Phentolamine has similar binding capacities to both receptors. The current literature suggests that this is the main mechanism by which phentolamine exerts its physiological effects. Phentolamine also blocks 5-HT receptors, inducing the release of histamine from mast cells. Some studies also show that NOS activation could possibly be involved in another mechanism, inducing increased vasodilation.
The Alpha-Adrenoceptor Antagonist of phentolamine is considered to be complex. The non-selective receptor blocking action interacts with adrenergic nerves in a complex fashion. Phentolamine action on adrenergic nerves has not been fully established. It is thought that there might be counteracting regulation on pre-and post-junctional nerves. It is not known how the counteracting regulation might affect the efficacy of phentolamine for the treatment of erectile dysfunction.
In animal studies, penile arterial inflow resistance was decreased. This proves in vivo that the physiological response to phentolamine acts in a manner to achieve erectile response. However, phentolamine has not displayed a significant effect on the venous outflow from penile tissues in humans. The current body of literature has not established pharmacokinetics for phentolamine.
First pass metabolism effectively reduces the efficacy in the treatment of erectile dysfunction. Therefore, this drug has to be administered by TriMix injection. The half-life of phentolamine is 30 minutes, with an effect duration of 2.5 to 4 hours. After penile injection the concentration of phentolamine in serum reaches a maximum within 20 to 30 minutes. After this amount of time has passed the drug rapidly is metabolized.
Side effects of phentolamine are rare. However, it has been reported that orthostatic hypotension, tachycardia, arrhythmias and myocardial infarction, have occurred after penile injection. The mechanism to which this set of side effects occur has not been rationally deduced through scientific study.
Phentolamine is usually added in combination with papaverine or vasoactive intestinal peptide to increase erectile response.
Medical treatment of impotence with papaverine and phentolamine intracavernosal injection.

Participants: 20 patients age 32 to 72 years old
Administration: intracavernosal injection
Dosage: 30 mg papaverine and phentolamine 1 mg
Results: Response with erection in 20- 30 minutes, phentolamine and papaverine produced an erection sufficient for intercourse in 18 of the 20 subjects

Prostaglandin E1

A potent hormone-like substance that induces erection by relaxing the penis’s blood vessels and dilating cavernosal arteries-dilation of the cavernosal arteries is accompanied by increased arterial inflow velocity and increased venous outflow resistance allowing for more blood into the penis and less blood out.
Prostaglandin E1 is administered intracavernosally. This drug is prescribed as a second-line treatment, after oral PDE5 inhibitors have been ineffective for treatment of erectile dysfunction. Several aspects of its effects and clinical use have been reviewed previously. Currently the body of medical literature demonstrates that 40 to 70% of erectile dysfunction patients respond to treatment with prostaglandin E1. The failure to respond to prostaglandin E1 has not been established. The demonstration that prostaglandin E1 with S-nitrosoglutathione in combination is more effective than prostaglandin E1 alone may shed light on the lack of efficacy in some patients.
Medications to activate alternative relaxant pathways in addition to by prostaglandin E1 may be necessary in patients who fail to respond to prostaglandin E1. Relaxation of smooth muscle is a critical component of erectile capacity. Additional agents to work in combination with prostaglandin E1 might have significant therapeutic benefits. Prostaglandin E1 with S-nitrosoglutathione or other erectile dysfunction medications, might have advantages in the treatment of male erectile dysfunction. Empower Pharmacy strives to compound medications that take advantage of multi-compound synergy. When injected into penile tissue prostaglandin E1 is readily metabolized into other erectile promoting molecules. These molecules potentiate the efficacy of prostaglandin E1. Prostaglandin E1 has been demonstrated to alter the concentrations of noradrenalin, adding a secondary mechanism of action. However, it is still believed prostaglandin E1 primarily acts directly by increasing cAMP synthesis via EP receptor interaction, increasing muscular relaxation.
Prostaglandin E1 has ubiquitous actions in controlling processes in many tissues. Known effects of prostaglandin E1 include systemic vasodilation, prevention of platelet aggregation, and ask to stimulate intestinal activity. Thus, prostaglandin E1 has very rarely been administered in a fashion to elicit a systemic response. Pharmacokinetics data is currently lacking on prostaglandin E1, the current data suggest short action duration and high rate of metabolic breakdown. After the first pass through the lungs 70% is metabolized. Because prostaglandin E1 is readily metabolized throughout the body, penile injection effects mainly penile tissues. Furthermore, this further explains the rare circulatory side effects.
d gland is an endocrine gland responsible for the production of the thyroid hormones triiodothyronine (T3) and tetraiodothyronine, also known as thyroxine (T4). The thyroid hormone exerts its effects throughout the entire body; it plays an essential role in metabolism, bone growth, as well as many other processes and functions within the body. Most of the regulatory and metabolic actions of thyroid hormones are carried out by T3, which is the active form. T4 is mostly inactive and has to be converted in to active T3 before it can exert it effects in the body. Unlike most other hormones, the effects of the thyroid hormone are widespread throughout the entire body and not limited to a single organ or body system. Some effects of thyroid hormone include:

  • Cardiovascular system: Thyroid hormones causes and increase in the expression of beta-receptors in the body. This increased expression has positive chronotropic and inotropic effects of the cardiac muscles resulting in an increased cardiac output, stroke volume, and resting heart rate. There is also an increased inotropic effect as thyroid hormone causes an increase in intracellular calcium within the myocardium. Additionally, thyroid hormones cause a decrease in peripheral vascular resistance through the dilatation of the cardiac, skin, and muscle vessels. Furthermore, thyroid hormones activate the renin-angiotensin-aldosterone system which results in an increased blood volume due to an increase in fluid reabsorption.
  • Respiratory system:T3 enhances the production of erythropoietin and hemoglobin which thereby increases the amount of oxygen delivered to the body tissues. It enhances the production of erythrocytes by improving folate and cobalamin absorption from the gastrointestinal tract; this allows for an increased capacity in oxygen delivery to tissues. The active thyroid hormone also stimulates resting respiratory rate as well as minute ventilation in instances of increased oxidation to ensure that blood oxygen levels remain within its normal range.
    Metabolism: T3 is directly responsible for the basal metabolic rate (BMR) and heat production (thermogenesis) in the body. Increased T3 levels results in an increased BMR as well as thermogenesis which is the pathogenesis behind the excessive sweating associated with hyperthyroidism. It also stimulates carbohydrate catabolism, protein anabolism, as well as lipid synthesis.
    Neurological system: Within the peripheral nervous system, T3 promotes an increase in peripheral reflexes and gastrointestinal motility; the increased reflexes is also due to the effect of T3 on increasing the production of Type II (fast twitch) muscle fibers. Additionally, T3 helps in increased alertness and responsiveness to the external environment. Furthermore, T3 is important in brain development because it stimulates the growth of axons within the neuron and myelin sheath formation.
  • Skeletal system: Within the maternal uterus, T3 is key in the developing fetal growth centers. In children, T3 is needed for linear bone growth, endochondral ossification and maturation of the epiphyseal bone centers. T3 deficiency in childhood may result in stunting of bone growth and development; this may become permanent even after the administration of supplemental thyroid hormone.
  • Reproductive system: T3 plays an essential role in the reproductive health in both men and women the regulation of the regulatory cycle and spermatogenesis respectively.
    Given the wide-ranging roles of thyroid hormone in the human body, it is essential that its levels are well-maintained within the recommended range. Generally, normal levels of T3 should fall between 100 – 200 ng/dL, depending on the age and gender of the individual. When serum T3 levels fall below the recommended range, a condition known as hypothyroidism, oral thyroid supplementation may be warranted to prevent the disruption of systems and processes dependent on this hormone.
Drug Caution
Do not take TriMix injection with any of the following medications: hypersensitivity or allergy to any component of this formulation; conditions predisposing you to priapism (painful erection lasting 4 hours or more): sickle cell anemia, multiple myeloma or leukemia; anatomical deformation of the penis or penile implants; direction by your physician that sexual activity is inadvisable or contraindicated. Tell your doctor if you have a condition or are taking a medicine that interferes with blood clotting.
Ideally, the TriMix injection should be administered just prior to foreplay. It is administered via intravavernosal injection and should produce an erection in 5 to 20 minutes and can be expected to last up to one hour. To prevent bruising, apply firm pressure to the injection site for 5 minutes after injecting. Do not use TriMix Injection more than two times a week; use at least 24 hours apart. There is a possibility of needle breakage with use of TriMix Injection: you should pay careful attention to your doctor’s instructions and handle syringe and needle properly.
TriMix Side Effects
Mild to moderate pain during injection; painful sensation with erection; small amount of bleeding at the injection site. Call your healthcare provider if you notice any redness, lumps, swelling, tenderness or curvature of the erect penis. If you experience an erection lasting more than 2 hours, you may take 2 – 4 pseudoephedrine 30 mg by mouth once and apply an ice pack. If your erection does not go away within the next hour, seek professional help immediately. Erections that last more than 6 hours can cause serious damage to the penile tissue.
How to Store?
Store dry powder at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Once reconstituted keep the TriMix injection in a refrigerator between 36°F to 46°F (2°C to 8°C). 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.
Where to Buy TriMix Injections in Florida?
You can order Super TriMix Injection from MediLab’s Compounding Pharmacy in the following Florida regions:

North Florida South Florida
Jacksonville Miami West Palm Beach Weston
Pensacola Hialeah Pompano Beach Delray Beach
Tallahassee Fort Lauderdale Davie Homestead
Ocala Port St. Lucie Miami Beach Tamarac
Gainesville Pembroke Pines Plantation Sarasota
Fort Walton Beach Hollywood Sunrise Wellington
Panama City Miramar Boca Raton Jupiter
Palm Coast Coral Springs Deerfield Beach Margate
Dunnellon Miami Gardens Boynton Beach Coconut Creek
Naples Lauderhill Broward
Spring hill Orlando
References [Click to open/close]
  • Montague DK, Jarow JP, Broderick GA, et al. Chapter 1: The management of erectile dysfunction: an AUA update. J Urol 2005;174:230-9.
  • Leungwattanakij S, Flynn V, Hellstrom WJG. Intracavernosal injection and intraurethral therapy for erectile dysfunction. Urol Clin North Am 2001;28:343-354.
  • Andersson, K.E., Pharmacology of penile erection. Pharmacol Rev, 2001. 53(3): p. 417-50.
  • Montague DK, Jarow JP, Broderick GA, et al. Chapter 1: The management of erectile dysfunction: an AUA update. J Urol 2005;174:230-9.
  • Leungwattanakij S, Flynn V, Hellstrom WJG. Intracavernosal injection and intraurethral therapy for erectile dysfunction. Urol Clin North Am 2001;28:343-354.
  • Andersson, K.E., Pharmacology of penile erection. Pharmacol Rev, 2001. 53(3): p. 417-50.
  • Virag, R., et al., Vasoactive intestinal polypeptide release during penile erection in man. Lancet, 1982. 2(8308): p. 1166.
  • K.E., A., Pharmacology of erection: agents which initiate and terminate erection. Sex Disabil 1994. 12: p. 53–79.
  • Kirkeby, H.J., et al., [Infusion cavernosography and erectile dysfunction]. Ugeskr Laeger, 1990. 152(24): p. 1724-6.
  • Juenemann, K.P., et al., Hemodynamics of papaverine- and phentolamine-induced penile erection. J Urol, 1986. 136(1): p. 158-61.
  • Delcour, C., et al., The effect of papaverine on arterial and venous hemodynamics of erection. J Urol, 1987. 138(1): p. 187-9.
  • Mooradian, A.D., et al., Biweekly intracavernous administration of papaverine for erectile dysfunction. West J Med, 1989. 151(5): p. 515-7.
  • Dinsmore, W.W., Medical treatment of impotence with papaverine and phentolamine intracavernosal injection. Ulster Med J, 1990. 59(2): p. 174-6.
  • Keogh, E.J., et al., Treatment of impotence by intrapenile injections of papaverine and phenoxybenzamine: a double blind, controlled trial. Aust N Z J Med, 1989. 19(2): p. 108-12.
  • Viswaroop, B., A. B, and G. Gopalakrishnan, Evaluating erectile dysfunction: oral sildenafil versus intracavernosal injection of papaverine. Natl Med J India, 2005. 18(6): p. 299-301.
  • Traish, A.M., et al., Expression of functional alpha2-adrenergic receptor subtypes in human corpus cavernosum and in cultured trabecular smooth muscle cells. Recept Signal Transduct, 1997. 7(1): p. 55-67.
  • Traish, A., et al., Phentolamine mesylate relaxes penile corpus cavernosum tissue by adrenergic and non-adrenergic mechanisms. Int J Impot Res, 1998. 10(4): p. 215-23.
  • Wespes, E., C. Rondeux, and C.C. Schulman, Effect of phentolamine on venous return in human erection. Br J Urol, 1989. 63(1): p. 95-7.
  • P.R., I., G. B., and B.L. . Human pharmacology of orally administered phentolamine, in Phentolamine in Heart Failure and Other Cardiac Disorders., in Proceedings of an International Workshop London, November 1975 T. S.H. and G. L.A., Editors. 1975, Hans Huber Publishers: Bern, Switzerland.
  • O, H., W. U, and K. U, Systemic pharmacokinetics of papaverine and phentolamine: comparison of intravenous and intracavernous application. Int J Impot Res, 1990. 2 (Suppl 2): p. 247–248.
  • Eardley, I., et al., Pharmacotherapy for erectile dysfunction. J Sex Med, 2010. 7(1 Pt 2): p. 524-40.
  • Dinsmore, W.W. and M.G. Wyllie, Vasoactive intestinal polypeptide/phentolamine for intracavernosal injection in erectile dysfunction. BJU Int, 2008. 102(8): p. 933-7.
  • Albersen, M., et al., Evaluation and treatment of erectile dysfunction. Med Clin North Am, 2011. 95(1): p. 201-12.
  • Linet, O.I. and F.G. Ogrinc, Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. The Alprostadil Study Group. N Engl J Med, 1996. 334(14): p. 873-7.
  • Porst, H., The rationale for prostaglandin E1 in erectile failure: a survey of worldwide experience. J Urol, 1996. 155(3): p. 802-15.
  • Angulo, J., et al., Rationale for the combination of PGE(1) and S-nitroso-glutathione to induce relaxation of human penile smooth muscle. J Pharmacol Exp Ther, 2000. 295(2): p. 586-93.
  • Molderings, G.J., et al., Inhibition of noradrenaline release from the sympathetic nerves of the human saphenous vein by presynaptic histamine H3 receptors. Naunyn Schmiedebergs Arch Pharmacol, 1992. 346(1): p. 46-50.
  • Palmer, L.S., et al., Characterization of cyclic AMP accumulation in cultured human corpus cavernosum smooth muscle cells. J Urol, 1994. 152(4): p. 1308-14.
  • Golub, M., et al., Metabolism of prostaglandins A1 and E1 in man. J Clin Invest, 1975. 56(6): p. 1404-10.