Download Product:

Product: P6 EXTREME
Raw Ingredients:
Ovine Placental Powder (Equine Chorionic Gonadotropin, eCG)
Tribulus terrestris (Protodioscin)
Βeta-sitosterol
Cimicifuga racemosa (Triterpene Glycosides)
Agaricus bisporus
Eurycoma longifolia
3,4-divanillyltetrahydrofuran
Dihydroxy Diosgenin
Sclareolide
Analysis of Compounds:
Ovine Placental Powder:
Key Action:
Ovine Placental Powder increases the release of luteinizing hormone (LH) from
the pituitary gland. It activates Leydig cell steroidogenesis via LH.
Physiological Mechanism:
Equine Chorionic Gonadotropin (eCG), produced by the trophoblastic cells of
the placenta, functions the same way in the human body as Human Chorionic
Gonadotropin (hCG). This hormone directly activates the secretion of LH from
the pituitary gland. LH then signals for Leydig cell steroidogenesis in the testes
and causes a noticeable increase in serum testosterone levels.
Tribulus terrestris (Protodioscin):
Key Action:
Protodioscin increases testosterone levels via multiple pathways.
Physiological Mechanism:
Protodioscin is an active steroidal saponin of the plant T. terrestris and has
been shown to be a potent, sexually stimulating chemical; it has also been
shown to increase body weight as well as testosterone, dihydrotestosterone
(DHT), and dehydroepiandrosterone (DHEA) levels. It has certain androgenic
activity, but its mechanism of action is poorly understood. One possible
mechanism is that the saponin is converted directly into DHEA due to its
structural similarity to male sex steroids. Protodioscin could possibly undergo
many biotransformations via enzymatic activity.
Βeta-sitosterol:
Key Action:
Beta-sitosterol is an inhibitor of 5-alpha reductase. It decreases the conversion
of androgens into DHT and aids in the avoidance of the undesirable side effects
of excessive DHT levels.
Physiological Mechanism:
The 5-alpha reductase enzyme is responsible for the conversion of most
androgens into DHT. Beta-sitosterol is a phytosterol (plant steroid) that closely
resembles the portion of androgens that binds to the 5-alpha reductase
enzyme. The Beta-sitosterol molecule itself also has a high affinity for the 5alpha reductase enzyme, which allows Beta-sitosterol to sequester and inhibit
5-alpha reductase from converting androgens into DHT.
C. racemosa (Triterpene Glycosides):
Key Action:
Triterpene Glycosides inhibit cytochrome P450 3A enzymes. They enhance the
absorption of drug-like compounds and prevent their breakdown in the liver.
Physiological Mechanism:
During the inhibition of the cytochrome P450 3A4 (CYP3A4) enzymes, triterpene
glycosides lose their glycoside portion due to cleavage, then the remaining
triterpene moiety, which is structurally similar to certain fatty acids, folds in
upon itself to form a tetracyclic ring that resembles the structure of a steroid.
This newly formed compound is then able to act as a decoy for the CYP3A4
enzymes, enabling the enhanced absorption of drug-like substances.
Agaricus bisporus:
Key Action:
A. bisporus is comprised of a non-competitive aromatase inhibitor that elicits a
mutagenic effect on the aromatase enzyme and prevents it from functioning.
Physiological Mechanism:
The combination of the active components of A. bisporus has a mutagenic
effect on the aromatase enzyme. Upon binding with the enzyme, these
components cause the cleavage of certain amino acids that make up the
aromatase protein, disabling it from converting androgens into estradiol.
Eurycoma longifolia (Eurypeptides):
Key Action:
Eurypeptides increase testosterone, male virility, and frequency of arousal.
Physiological Mechanism:
Although the mechanism of action of the Eurypeptides is still unknown and is a
current focus of study, some authors have demonstrated that supplementation
with E. longifolia slightly increased testosterone levels. This finding is likely
due to a proportional decrease in the activity of sex hormone-binding globulin
(SHBG) that binds testosterone. In addition, DHEA levels were markedly
increased. The results of these experiments definitely show a correlation
between the activity of eurypeptides and testosterone levels, although the
exact mechanism is not yet known.
3,4-divanillyltetrahydrofuran (3,4-divanillyl THF):
Key Action:
3,4-divanillyl THF inhibits SHBG.
Physiological Mechanism:
SHBG is a protein that is responsible for the rate-limiting transport of
androgens into the cell. Inhibition of this protein causes an increase in the
frequency of androgens that enter the cell. Although SHBG aids the transport
of androgens into the cell, androgens can enter the cell independently, due to
their small molecular size and lypophilic nature that helps them permeate the
cell membrane. 3,4-divanillyl THF actively inhibits SHBG, therefore increasing
the rate at which androgens enter the cell and activate metabolic transcription
factors.
Dihydroxy Diosgenin:
Key Action:
Dihydroxy Diosgenin is a phytosterol that regulates cholesterol levels.
Physiological Mechanism:
Dihydroxy Diosgenin acts by inhibiting the absorption of cholesterol into the
liver. It also decreases cholesterol synthesis in both the liver and intestines.
As the absorption of cholesterol is compromised in the presence of Dihydroxy
Diosgenin, there is a subsequent, significant decrease in the levels of both HDL
and LDL. This decrease in cholesterol absorption also leads to an increase in
the excretion of cholesterol in the feces.
Sclareolide:
Key Action:
Sclareolide increases cyclic AMP levels and increases ATP synthesis.
Physiological Mechanism:
Sclareolide activates cell membrane-bound G proteins that lead to the
activation of adenylyl cyclase, converting cellular ATP into cyclic adenosine
monophosphate (cAMP). This immediate, high concentration of cAMP causes a
sudden surge in cellular ATP levels, causing a dramatic increase in energy.