UK Registered DoctorsAlprostadil vs. Invicorp
Erectile dysfunction (ED), defined as difficulty getting or keeping an erection firm enough for sex, can affect far more than a man’s sex life—it can undermine confidence, strain relationships and diminish quality of life. According to NHS Inform, around half of men aged 40–70 experience it to some degree. This widely quoted estimate is consistent with the Massachusetts Male Aging Study, conducted in the United States between 1987 and 1989, rather than a recent UK survey.1
When Viagra arrived in the late 1990s, debate over whether it was a “lifestyle drug” raised questions about whether treatment should be funded by the NHS, with Pfizer challenging restrictions on access. Today, several treatments are available, but no single approach works for everyone. When tablets are ineffective or unsuitable, injectable treatments such as alprostadil and Invicorp offer alternatives. Understanding how they differ can help patients know what to expect and discuss their options with a clinician.
For many men, the first—and often simplest—treatment is a pill. The arrival of sildenafil (Viagra) in 1998, followed by alternatives such as tadalafil (Cialis), vardenafil (Levitra) and avanafil (Spedra), transformed the treatment of ED. Viagra also became a cultural phenomenon, inspiring jokes, anecdotes and headlines, and bringing a previously private subject into public discussion.
These drugs all work in a similar way: they slow the breakdown of a chemical messenger involved in an erection. During arousal, nitric oxide is released in the penis. This triggers production of cyclic GMP (cGMP), which relaxes smooth muscle in the erectile tissue and blood vessels, allowing more blood to enter.
An enzyme called phosphodiesterase type 5 (PDE5) breaks down cGMP. Drugs such as sildenafil inhibit this enzyme, allowing cGMP to remain active for longer and helping an erection develop and last. Sexual stimulation is still needed to initiate the process; the tablet does not automatically produce an erection.2
PDE5 inhibitors depend on the body producing erection signals and the erectile tissue responding to them. Nerve or blood vessel damage, hormonal problems and psychological factors can reduce their effectiveness. Some men initially experience an inadequate response but improve after a clinician reviews the dose, timing and how the medicine is taken. Others may benefit from a treatment that works through a different mechanism.2
This brings us to our two injectable ED treatments: alprostadil and Invicorp. A somewhat unconventional demonstration of what injectable medicines could do gave a medical audience an unforgettable evening in 1983. During a lecture in Las Vegas, British physiologist Professor Giles Brindley lowered his trousers to reveal an erection produced by an injection he had given himself beforehand. His demonstration made a serious scientific point: drugs acting directly on erectile tissue could produce an erection without sexual arousal.3
Brindley’s demonstration involved an earlier injectable drug, but it helps set the scene for alprostadil, an ED treatment that also predates Viagra. Alprostadil is a synthetic version of prostaglandin E1 (PGE1), a substance naturally produced in the body.
Prostaglandins are a family of short-lived chemical messengers made from fatty acids. They are produced where they are needed and generally act nearby, helping regulate the surrounding tissue. Different prostaglandins have different—and sometimes opposing—effects, depending on the tissue and receptors involved. Their roles include controlling blood flow, influencing clotting, coordinating inflammation and stimulating uterine contractions during labour.
PGE1 is made from dihomo-gamma-linolenic acid (DGLA), an omega-6 fatty acid derived from dietary linoleic acid. DGLA is released from cell membranes and converted by cyclooxygenase, or COX, enzymes into an intermediate, which is then converted into PGE1. Alprostadil is the synthetically manufactured version of the same molecule.
The scientific groundwork stretches back further, to Swedish researchers Sune Bergström and Jan Sjövall, who isolated and characterised prostaglandins in the late 1950s and early 1960s. Upjohn played an important role in turning prostaglandin research into medicines and later developed the injectable ED treatment Caverject, subsequently supplied by Pfizer.
Alprostadil binds to prostaglandin receptors and activates an enzyme called adenylate cyclase. This increases cyclic AMP (cAMP), a chemical messenger that helps smooth muscle relax. As the muscle relaxes, blood flows into the penis and fills its expandable erectile spaces. These spaces enlarge, compressing the small veins that normally carry blood away. Increased blood flow in, combined with reduced drainage out, produces an erection. Notice the different messenger: cAMP here, rather than the cGMP supported by PDE5 inhibitors.
Alprostadil has been developed in several forms for ED. It is rapidly metabolised, so local administration allows it to act on the erectile tissue before it is cleared from the body. With an intracavernosal injection, a fine needle delivers the medicine through the side of the penis into that tissue. The dose is adjusted under medical supervision. Caverject is a familiar brand name, although some UK presentations have been replaced by generic alprostadil.
Another formulation was the intraurethral treatment MUSE (Medicated Urethral System for Erection). An applicator placed a small medicated pellet inside the urethra—the tube that carries urine from the bladder through the penis. MUSE has since been listed as discontinued in UK NHS formularies. For those who would rather avoid a needle, alprostadil is also formulated as a topical cream, Vitaros, applied to the opening of the urethra at the tip of the penis. These formulations are not equally effective: non-injected alprostadil generally produces a less reliable response than injections.2
The second injectable treatment, Invicorp, combines two active ingredients: aviptadil and phentolamine. It contains no prostaglandin. Instead, aviptadil is a synthetic version of vasoactive intestinal peptide, usually shortened to VIP, another chemical messenger naturally produced in the body.
VIP was isolated from pig intestine in 1970 by Sami Said and Viktor Mutt. It is a peptide—a chain of 28 amino acids—that acts as a messenger in nerves throughout the body. Its functions include relaxing smooth muscle, widening blood vessels, regulating intestinal fluid secretion and influencing immune responses. It is also present in nerves supplying the erectile tissue.
In erectile tissue, aviptadil activates VIP receptors, increasing cAMP and helping the muscle relax so blood can enter. It therefore reaches the same intracellular messenger as alprostadil, but through different receptors.
The second component, phentolamine, reduces an opposing signal. Noradrenaline is a chemical messenger released by nerves. It attaches to alpha receptors on smooth muscle cells in the penis, telling them to contract—a process that helps keep the penis flaccid. Phentolamine blocks these receptors, weakening the contraction signal and allowing the muscle to relax more easily. Together, the two ingredients help the erectile tissue fill with blood.6
Invicorp’s early commercial development was undertaken by Senetek. The current product’s marketing authorisation holder is Evolan Pharma. Invicorp is given by intracavernosal injection: a fine needle delivers a solution of the two drugs through the side of the penis into the erectile tissue. It is not supplied as a cream or urethral pellet. As with alprostadil injections, professional instruction is essential before home use.6
Both alprostadil and Invicorp can produce an erection when tablets have failed, but effectiveness is only part of the story—comfort matters too. In a comparative study of 187 men, more initially responded to alprostadil than to the VIP/phentolamine combination used in Invicorp: 83% versus 73%. Among those who responded to both, subsequent injections were similarly effective.4
The clearest difference was pain, reported after 28% of alprostadil injections compared with 3% of VIP/phentolamine injections. Facial flushing was more common with VIP/phentolamine, but more patients preferred it. The study used several doses and delivery devices, and its later phase included only men who responded to both medicines, so these figures should not be treated as a precise prediction for every patient.4
Facial flushing occurs when the medicines’ blood-vessel-relaxing effects extend beyond the penis. Increased blood flow near the skin’s surface causes temporary redness and warmth—an extension of their pharmacological action, rather than necessarily an allergic reaction.
Failure with one does not necessarily mean failure with the other. A 2025 study of 308 men found that Invicorp helped 59% resume penetrative sex after alprostadil had proved ineffective or too painful. The distinction matters: it helped 76% of those who stopped alprostadil because of pain, compared with 36% of those who had not responded to its maximum dose. Encouraging results, although this was a retrospective study from one centre rather than a randomised trial.5
Neither is universally better. The choice depends on individual response, side effects and confidence using the treatment. Both require professional instruction and can cause bruising or prolonged erections; repeated injections can also be associated with scarring. An erection lasting four hours needs urgent medical attention.2,6
If tablets or injections are not your thing—or their side effects outweigh the benefits—there are still options. CBT (cognitive behavioural therapy) and psychosexual therapy can help address performance anxiety, confidence and relationship difficulties, either alone or alongside other treatments. They cannot reverse damaged nerves or blood vessels, but they can address factors that compound a physical problem. Vacuum erection devices offer a drug-free alternative, while penile implants remain an option when other approaches prove unsuccessful.2
Research continues into low-intensity shockwave therapy and treatments using platelet-rich plasma (PRP) or stem cells, with the aim of improving the underlying tissue rather than temporarily supporting an erection. Shockwave results remain variable, and PRP and stem-cell treatments are still experimental—not established cures.2
The encouraging news is that treatment can usually improve ED, even if finding the right approach takes time. The best treatment is one that works for you, feels manageable and helps restore enjoyment rather than adding pressure.
References
- NHS Inform. Erectile dysfunction (impotence). Patient information and prevalence estimate.
https://www.nhsinform.scot/illnesses-and-conditions/sexual-and-reproductive/erectile-dysfunction-impotence/ - European Association of Urology. Guidelines on Sexual and Reproductive Health: Management of Erectile Dysfunction. Treatment options, counselling, safety and emerging therapies.
https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/management-of-erectile-dysfunction - A comprehensive history of injection therapy for erectile dysfunction, 1982–2023. Sexual Medicine Reviews. 2024. doi:10.1093/sxmrev/qeae020.
https://doi.org/10.1093/sxmrev/qeae020 - Shah PJR, Dinsmore W, Oakes RA, Hackett G. Injection therapy for the treatment of erectile dysfunction: a comparison between alprostadil and a combination of vasoactive intestinal polypeptide and phentolamine mesilate. Current Medical Research and Opinion. 2007;23(10):2577–2583. doi:10.1185/030079907X233232.
https://pubmed.ncbi.nlm.nih.gov/17875241/ - Al-Mitwalli A, Holden F, et al. Intracavernosal injection of aviptadil and phentolamine for refractory erectile dysfunction. Journal of Sexual Medicine. 2025. doi:10.1093/jsxmed/qdaf067.
https://doi.org/10.1093/jsxmed/qdaf067 - Dinsmore WW, Wyllie MG. Vasoactive intestinal polypeptide/phentolamine for intracavernosal injection in erectile dysfunction. BJU International. 2008;102(8):933–937. doi:10.1111/j.1464-410X.2008.07764.x.
https://doi.org/10.1111/j.1464-410X.2008.07764.x
