QSC supplies Tadalafil (50mg) and Vardenafil (35mg) as research-grade tablets. PDE5 inhibitors prevent cGMP degradation in smooth muscle — extending NO-mediated vasodilation. Research applications: erectile dysfunction pharmacology, pulmonary arterial hypertension, cardiovascular NO/cGMP biology, and melanocortin-PDE5 interaction studies (pairing with PT-141/Bremelanotide research).
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NO/cGMP/PDE5 Mechanism
Nitric oxide (NO) activates guanylyl cyclase, which produces cGMP from GTP. cGMP activates PKG, causing smooth muscle relaxation and vasodilation. PDE5 degrades cGMP, terminating the vasodilatory signal. PDE5 inhibitors block cGMP degradation, sustaining smooth muscle relaxation. Primary tissue targets: penile corpus cavernosum, pulmonary arterial smooth muscle, systemic vasculature.
PDE5 inhibitors and PT-141 — central vs peripheral
PT-141 acts centrally via MC3R/MC4R in the hypothalamic mPOA, initiating the psychogenic erectile response upstream of NO/cGMP. PDE5 inhibitors act peripherally, extending the vascular response once initiated. Combining both compounds allows dissection of central vs peripheral erectile physiology components. See the PT-141 research hub for the MC4R mechanism.
Tadalafil vs Vardenafil
Property
Tadalafil (Cialis)
Vardenafil (Levitra)
CAS
171596-29-5
224785-90-4
QSC format
50mg tablets
35mg tablets
Half-life
~17.5 hr
~4-5 hr
PDE5 selectivity
PDE5 > PDE6, PDE11
PDE5 > PDE6 (higher PDE6 vs tadalafil)
Onset
30-60 min
15-30 min (faster)
Duration
Up to 36 hr
4-6 hr
Research advantage
Long half-life — sustained PDE5 inhibition for chronic models
