This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within Human Libido Research and in reinforcing the significance of the 5-HT and dopaminergic systems in sexual desire thereby furthering the Promise of legitimate applications in treating hypoactive desire disorder.
Flibanserin - the powerful Approved female aphrodisiac compound is available in it's purest form AT...........
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A LITTLE OVERVIEW FOR A BIG PRODUCT
When news first came out (!) about the 'potential' drug in Clinical Trials that would, presumably; treat hypoactive sexual desire disorder (HSDD) in Women - the audience of course rose up ecstatically (well , figuratively speaking ). As time moved on - anticipation remained high...when the FDA approved the drug as "Addyi" (!) - a peak climactic excitement occurred in those individuals afflicted with lack of libido.... unfortunately; the Media also saw a chance to tag such an inseparable word with the news; dubbing the pill "Female Viagra"...which then prompted this article which thoroughly explains why it IS NOT or should not be called Female Viagra. At least from a scientific standpoint - well, by means of 'scientific correctness' - that is true. It does however improve sexual desire in pre-menopausal women and in women in general which then of course; leads to increased arousal. So in a way, it is female Viagra just that it doesn't operate specifically or exclusively on blood flow - but rather in the brain....Which makes it a much more appealing chemical overall...now some men would jump up at this statement or in the approval in general, namely those with low exposure to the concept of a 'tactical approach' to treating sexual dysfunction/s.
Some Men believe 'Viagra' is the only solution to erectile dysfunction or low libido but the reality is , men already have SEVERAL libido drugs...it's just that they aren't specifically approved or are only approved in certain countries....
Nevertheless, there are pharmaceutical drugs AND herbal remedies that can aid in male sexual dysfunction - but very little geared to aid sexual dysfunction in women..until now.
Even with so called 'female herbal aphrodisiacs' - the problem is many of these have estrogenic compounds; hastening an already estrogen-toxic biology that plagues women , today.
Overall, this pill - chemically named Flibanserin has an incredibly interesting and unique NON-HORMONAL pharmacology and mechanism of action. Making it incredibly diverse and having a fairly clean side-effect profile,..which we will go into on this next part.
Chemical name: 1,3-Dihydro-1-[2-[4-[3-(trifluoromethyl)phenyl]-1-piperazinyl]ethyl]-2H-benzimidazol-2-one
Flibanserin is a 5-HT1A receptor agonist and 5-HT2A receptor antagonist. Flibanserin has high affinity for human 5-HT1A receptors (Ki = 1 nM) and lower affinity for 5-HT2A (Ki = 49 nM) and D4 (Ki = 4–24 nM) receptors, and negligible affinity for a variety of other neurotransmitter receptors and ion channels.
Flibanserin has preferential affinity for serotonin 5-HT(1A), dopamine D(4k), and serotonin 5-HT(2A) receptors. In vitro and in microiontophoresis, flibanserin behaves as a 5-HT(1A) agonist, a very weak partial agonist on dopamine D(4) receptors, and a 5-HT(2A) antagonist. In vivo flibanserin binds equally to 5-HT(1A) and 5-HT(2A) receptors. However, under higher levels of brain 5-HT (i.e., under stress), flibanserin may occupy 5-HT(2A) receptors in higher proportion than 5-HT(1A) receptors. The effects of flibanserin on adenylyl cyclase are different from those of buspirone and 8-OH-DPAT, two other purported 5-HT(1A) receptor agonists. Flibanserin reduces neuronal firing rate in cells of the dorsal raphe, hippocampus, and cortex with the CA1 region being the most sensitive in the brain. Flibanserin-induced reduction in firing rate in the cortex seems to be mediated through stimulation of postsynaptic 5-HT(1A) receptors, whereas the reduction of the number of active cells seems to be mediated through dopamine D(4) receptor stimulation. Flibanserin quickly desensitizes somatic 5-HT autoreceptors in the dorsal raphe and enhances tonic activation of postsynaptic 5-HT(1A) receptors in the CA3 region. Flibanserin preferentially reduces synthesis and extracellular levels of 5-HT in the cortex, where it enhances extracellular levels of NE and DA. Flibanserin displays antidepressant-like activity in most animal models sensitive to antidepressants. Such activity, however, seems qualitatively different from that exerted by other antidepressants. Flibanserin seems to act via direct or indirect stimulation of 5-HT(1A), DA, and opioid receptors in those animal models. Flibanserin does not display consistent effects in animal models of anxiety and seems to exert potential antipsychotic effects. Flibanserin may induce some sedation but does not induce observable toxic effects at pharmacologically relevant doses.
Flibanserin's 5-HT(1)A agonist properties make it suitable as an efficacious, neuronally based pain reliever and anti-nociceptive (1) (!*!) (decreasing perception of pain) . 5-HT1A activation promotes beta-endorphin release (2) and this mediates the anti-depressant effects of 5-HT1A ligands (3). Additionally, activating preferentially, the serotonin autoreceptors of the 1A class; which flibanserin does, is expected to increase oxytocin release (4) (5); which is a neuropeptide involved with mood, trust, love and anxiety (6). Increased oxytocin may improve social anxiety, decrease paranoia and have an empathogenic effect as well as improving sexual function and libido...(7)
Flibanserin's Pain-relieving and anti-nociceptive effects come from it's interaction with the 5-HT1A system; but in order to understand the HOW - we have to understand the WHY. As noted in the first reference; Flibanserin stimulates opioid receptors ; BUT NOT DIRECTLY. You see, whenever we STIMULATE the serotonin 5-HT1A receptors - beta-endorphin is released; this endogenous pain reliever and euphoriant then activates the opioid receptors to which it has predetermined affinity for. Additionally, activation of the 5-HT1A receptors may inhibit the NMDA-glutamate-nitric oxide pathway which leads to decreased pain perception (8) (9) By lessening over-active nerves, and by reducing calcium efflux/uptake into cells - the result is a lessened sensitivity to pain and reduction in neuropathic pain models.
In regards to it's aphrodisiac properties; it is more suitable for women than men. This is because a woman's brain generally responds favorably to 5-HT1A agonism whereas a man may have impaired sexual arousal from 1A agonists. (10) (11) (12). Specifically, 5-HT1A agonism; impairs erectile response in many cases while facilitating ejaculation(13). Though, in castrated subjects; 1A agonism appears to have a nearly opposite effect; facilitating coitus and thus acting as a partial aphrodisiac (14). 5-HT1A agonists block the testosterone boost caused by being around a female and thus lower sexual motivation even in the presence of female pheromones (15) (16) (17) .
On the up side however, it is also likely that those whom have excessive serotonergic activity and / or lower dopamine levels may derive overall sexual benefit from Flibanserin. Because 1A agonism is expected to reduce basal and stimulated serotonin release; and enhance diasylate levels of dopamine and noradrenaline - there is an overall trend to increased sexual motivation. Take note, that just because the compound may (theoretically) impair some aspects of arousal in males, in females it has no such adversity and thus is an aphrodisiac. Additionally, Flibanserin being also a 5-HT2A antagonist, and a partial dopaminergic agonist - may have advantages over 'simple' 1A agonists like Buspirone (18) (19); and thus, may over-ride the negatives of traditional 1A agonists by acting via multiple pathways to elicit sexual response and desire.
Flibanserin thus is likely to have a more profound positive sexual effect than say Buspirone in both men or women, but again, moreso in women(20).
Flibanserin has been shown to block/reduce drug-induced dyskinesia's and reduce side-effects of Parkinson's medications like L-DOPA (21)
FLIBANSERIN, BLOOD PRESSURE AND HEART RATE ; A not so pretty Combination - but not nearly as extreme as 'Viagra' either
Flibanserin is noted in some patients/trialers to induce hypotension (low blood pressure) (22) (23) and due to it's properties as a 5-HT1A agonist - it also lowers heart rate. This change however is not necessarily harmful and can be seen as statistically insignificant (24). With that being said, the FDA did have some hesitancy in approving the drug - in part because of speculation on long-term effects and risk-benefit assessments(25).
Despite all of this, from a neurophysiological perspective; 5-HT(2)A antagonism is expected to produce generally positive effects on mood, blood pressure and to counter-act stress hormone accumulation. This would explain why Flibanserin in particular is seen beneficial in stress-induced hyposexual states in women as well as in reversing distress-signals and depression that may stem from low libido(26) (27)..
FLIBANSERIN's SELECTIVITY - The Good Stuff ~ And the TRUE Reason why it could be a Strong Partition to the 'Dopaminergic Pot of Gold'.
Flibanserin demonstrates regional selectivity; that is, it impacts certian brain regions selectively. It decreases serotonin in the PFC (Prefrontal Cortex) and as well in the HYPOTHALAMUS - a key region involved in hormone production and sexual desire. This selectivity combined with direct effects on dopamine and noradrenaline are where the fascinating principles of neurobiology show their most glamorous points. The medicine industry just got even more heated up because this may be one of the first 'approved' medications where studies can ACTUALLY show in a straightforward way, that the compound can impact the regions involved in the target application favorably(28) (29) (30).
A LITTLE OVERVIEW FOR A BIG PRODUCT
When news first came out (!) about the 'potential' drug in Clinical Trials that would, presumably; treat hypoactive sexual desire disorder (HSDD) in Women - the audience of course rose up ecstatically (well , figuratively speaking ). As time moved on - anticipation remained high...when the FDA approved the drug as "Addyi" (!) - a peak climactic excitement occurred in those individuals afflicted with lack of libido.... unfortunately; the Media also saw a chance to tag such an inseparable word with the news; dubbing the pill "Female Viagra"...which then prompted this article which thoroughly explains why it IS NOT or should not be called Female Viagra. At least from a scientific standpoint - well, by means of 'scientific correctness' - that is true. It does however improve sexual desire in pre-menopausal women and in women in general which then of course; leads to increased arousal. So in a way, it is female Viagra just that it doesn't operate specifically or exclusively on blood flow - but rather in the brain....Which makes it a much more appealing chemical overall...now some men would jump up at this statement or in the approval in general, namely those with low exposure to the concept of a 'tactical approach' to treating sexual dysfunction/s.
Some Men believe 'Viagra' is the only solution to erectile dysfunction or low libido but the reality is , men already have SEVERAL libido drugs...it's just that they aren't specifically approved or are only approved in certain countries....
Nevertheless, there are pharmaceutical drugs AND herbal remedies that can aid in male sexual dysfunction - but very little geared to aid sexual dysfunction in women..until now.
Even with so called 'female herbal aphrodisiacs' - the problem is many of these have estrogenic compounds; hastening an already estrogen-toxic biology that plagues women , today.
Overall, this pill - chemically named Flibanserin has an incredibly interesting and unique NON-HORMONAL pharmacology and mechanism of action. Making it incredibly diverse and having a fairly clean side-effect profile,..which we will go into on this next part.
Chemical name: 1,3-Dihydro-1-[2-[4-[3-(trifluoromethyl)phenyl]-1-piperazinyl]ethyl]-2H-benzimidazol-2-one
Flibanserin is a 5-HT1A receptor agonist and 5-HT2A receptor antagonist. Flibanserin has high affinity for human 5-HT1A receptors (Ki = 1 nM) and lower affinity for 5-HT2A (Ki = 49 nM) and D4 (Ki = 4–24 nM) receptors, and negligible affinity for a variety of other neurotransmitter receptors and ion channels.
Flibanserin has preferential affinity for serotonin 5-HT(1A), dopamine D(4k), and serotonin 5-HT(2A) receptors. In vitro and in microiontophoresis, flibanserin behaves as a 5-HT(1A) agonist, a very weak partial agonist on dopamine D(4) receptors, and a 5-HT(2A) antagonist. In vivo flibanserin binds equally to 5-HT(1A) and 5-HT(2A) receptors. However, under higher levels of brain 5-HT (i.e., under stress), flibanserin may occupy 5-HT(2A) receptors in higher proportion than 5-HT(1A) receptors. The effects of flibanserin on adenylyl cyclase are different from those of buspirone and 8-OH-DPAT, two other purported 5-HT(1A) receptor agonists. Flibanserin reduces neuronal firing rate in cells of the dorsal raphe, hippocampus, and cortex with the CA1 region being the most sensitive in the brain. Flibanserin-induced reduction in firing rate in the cortex seems to be mediated through stimulation of postsynaptic 5-HT(1A) receptors, whereas the reduction of the number of active cells seems to be mediated through dopamine D(4) receptor stimulation. Flibanserin quickly desensitizes somatic 5-HT autoreceptors in the dorsal raphe and enhances tonic activation of postsynaptic 5-HT(1A) receptors in the CA3 region. Flibanserin preferentially reduces synthesis and extracellular levels of 5-HT in the cortex, where it enhances extracellular levels of NE and DA. Flibanserin displays antidepressant-like activity in most animal models sensitive to antidepressants. Such activity, however, seems qualitatively different from that exerted by other antidepressants. Flibanserin seems to act via direct or indirect stimulation of 5-HT(1A), DA, and opioid receptors in those animal models. Flibanserin does not display consistent effects in animal models of anxiety and seems to exert potential antipsychotic effects. Flibanserin may induce some sedation but does not induce observable toxic effects at pharmacologically relevant doses.
FLIBANSERIN As a Novel Pain Reliever & Aphrodisiac
Flibanserin's 5-HT(1)A agonist properties make it suitable as an efficacious, neuronally based pain reliever and anti-nociceptive (1) (!*!) (decreasing perception of pain) . 5-HT1A activation promotes beta-endorphin release (2) and this mediates the anti-depressant effects of 5-HT1A ligands (3). Additionally, activating preferentially, the serotonin autoreceptors of the 1A class; which flibanserin does, is expected to increase oxytocin release (4) (5); which is a neuropeptide involved with mood, trust, love and anxiety (6). Increased oxytocin may improve social anxiety, decrease paranoia and have an empathogenic effect as well as improving sexual function and libido...(7)
Flibanserin's Pain-relieving and anti-nociceptive effects come from it's interaction with the 5-HT1A system; but in order to understand the HOW - we have to understand the WHY. As noted in the first reference; Flibanserin stimulates opioid receptors ; BUT NOT DIRECTLY. You see, whenever we STIMULATE the serotonin 5-HT1A receptors - beta-endorphin is released; this endogenous pain reliever and euphoriant then activates the opioid receptors to which it has predetermined affinity for. Additionally, activation of the 5-HT1A receptors may inhibit the NMDA-glutamate-nitric oxide pathway which leads to decreased pain perception (8) (9) By lessening over-active nerves, and by reducing calcium efflux/uptake into cells - the result is a lessened sensitivity to pain and reduction in neuropathic pain models.
In regards to it's aphrodisiac properties; it is more suitable for women than men. This is because a woman's brain generally responds favorably to 5-HT1A agonism whereas a man may have impaired sexual arousal from 1A agonists. (10) (11) (12). Specifically, 5-HT1A agonism; impairs erectile response in many cases while facilitating ejaculation(13). Though, in castrated subjects; 1A agonism appears to have a nearly opposite effect; facilitating coitus and thus acting as a partial aphrodisiac (14). 5-HT1A agonists block the testosterone boost caused by being around a female and thus lower sexual motivation even in the presence of female pheromones (15) (16) (17) .
On the up side however, it is also likely that those whom have excessive serotonergic activity and / or lower dopamine levels may derive overall sexual benefit from Flibanserin. Because 1A agonism is expected to reduce basal and stimulated serotonin release; and enhance diasylate levels of dopamine and noradrenaline - there is an overall trend to increased sexual motivation. Take note, that just because the compound may (theoretically) impair some aspects of arousal in males, in females it has no such adversity and thus is an aphrodisiac. Additionally, Flibanserin being also a 5-HT2A antagonist, and a partial dopaminergic agonist - may have advantages over 'simple' 1A agonists like Buspirone (18) (19); and thus, may over-ride the negatives of traditional 1A agonists by acting via multiple pathways to elicit sexual response and desire.
Flibanserin thus is likely to have a more profound positive sexual effect than say Buspirone in both men or women, but again, moreso in women(20).
Flibanserin has been shown to block/reduce drug-induced dyskinesia's and reduce side-effects of Parkinson's medications like L-DOPA (21)
FLIBANSERIN, BLOOD PRESSURE AND HEART RATE ; A not so pretty Combination - but not nearly as extreme as 'Viagra' either
Flibanserin is noted in some patients/trialers to induce hypotension (low blood pressure) (22) (23) and due to it's properties as a 5-HT1A agonist - it also lowers heart rate. This change however is not necessarily harmful and can be seen as statistically insignificant (24). With that being said, the FDA did have some hesitancy in approving the drug - in part because of speculation on long-term effects and risk-benefit assessments(25).
Despite all of this, from a neurophysiological perspective; 5-HT(2)A antagonism is expected to produce generally positive effects on mood, blood pressure and to counter-act stress hormone accumulation. This would explain why Flibanserin in particular is seen beneficial in stress-induced hyposexual states in women as well as in reversing distress-signals and depression that may stem from low libido(26) (27)..
Finally....
FLIBANSERIN's SELECTIVITY - The Good Stuff ~ And the TRUE Reason why it could be a Strong Partition to the 'Dopaminergic Pot of Gold'. Flibanserin demonstrates regional selectivity; that is, it impacts certian brain regions selectively. It decreases serotonin in the PFC (Prefrontal Cortex) and as well in the HYPOTHALAMUS - a key region involved in hormone production and sexual desire. This selectivity combined with direct effects on dopamine and noradrenaline are where the fascinating principles of neurobiology show their most glamorous points. The medicine industry just got even more heated up because this may be one of the first 'approved' medications where studies can ACTUALLY show in a straightforward way, that the compound can impact the regions involved in the target application favorably(28) (29) (30).
The implications of this for the NOW in medical research; specifically neurology and endocrinology are not in just reaffirming past Insights into monoaminergic systems in human sexual behavior but as a WHOLE - in casting aside contemplations and conjecture that may otherwise further the divide between the simplistic hormonal experts and Psychiatrists hoping to achieve an even balance in their study/application of knowledge. Essentially the development and evidence associated with Flibanserin proves the predominant area of research in terms of human sexuality can lie within the concepts of these monoamine systems and as more research is conducted - the remainder of the unexplained 'pieces' can be mapped out and elucidated - finally evolving the constants in brain research to a level seen as much 'clearer'. In Summary, A more coherent message can be received with more solid examples to be placed such as that of FLIBANSERIN...
Hello, flibanserin certainly good pills for the treatment of sexual disorders in women, but their price is too high, there are many more affordable drugs such as lovegra or ledy era and of course generic female viagra https://edpstock.com/buy-female-viagra-uk.html is my choice
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