How to take Boladrol - AnabolicMinds.com

How to take Boladrol

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    How to take Boladrol


    On an empty stomach - with food - or doesn't matter?

    thanks -

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    doesn't seem to matter really. Try and take a dose right when you wake up. I take it with grapefruit juice first thing in the morning.
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    Its a pro hormone (will need to be converted in the body to bolasterone)so you may get better absorbtion on an empty stomach. The grapefruit juice could possibly help also.


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    If I want to take the recommended 4mg dosage, should I take all 4mg in the morning, or 2mg morning, and 2mg in the afternoon?

    Whats most effective?
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    2mg twice day. spaced in 8~12 hours.

    Absortion will be better with some fat. go with fish oil + bolasterone.
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    Quote Originally Posted by FelipeBR View Post
    2mg twice day. spaced in 8~12 hours.

    Absortion will be better with some fat. go with fish oil + bolasterone.
    What he said.


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    I hear taking methyls with carbs and EFAs makes it a little easier on the liver.
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    Quote Originally Posted by Chubbinmuffin View Post
    I hear taking methyls with carbs and EFAs makes it a little easier on the liver.

    I don't know if dimethyls are equally harsh on the liver at methyls. but i do know one thing for sure - three days in and this does seem as powerful as they advertise in comparison to other new substances after three days. i am not totally there - but getting same feeling as the old PH days. arm w/o tonight - my best w/o - so we'll see. i may start a separate thread on how this goes!

    double M - have you used this yet?
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    Quote Originally Posted by mmowry View Post
    Its a pro hormone (will need to be converted in the body to bolasterone)so you may get better absorbtion on an empty stomach. The grapefruit juice could possibly help also.
    this is perfects, also to keep in mind, boladrol is a diol compound, and does not need to convert in order to bind to the androgen receptor.
    whats this mean? it is already an active compound, but does have the potential to convert into a stronger one, but conversion can go both ways over and over, so I would put more weight in the diol binding to the ar & exerting its effects.

    Quote Originally Posted by FelipeBR View Post
    2mg twice day. spaced in 8~12 hours.
    this is right, or if you bought two bottles (does it come in bottles or packages?) you can run a higher dose after the first 2 weeks, (like 6-8mg)




    Quote Originally Posted by FelipeBR View Post
    Absortion will be better with some fat. go with fish oil + bolasterone.
    no, fats dont do much to help absorbtion of methylated compounds, best to take it on an empty stomach.

    if you have a non methylated pro hormone, like 4-androstenediol for example, a healthy amount of fats would aid in absorbtion.

    and the op could always go for maximum absorbtion by supository administration.
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    Quote Originally Posted by jbryand101b View Post
    boladrol is a diol compound, and does not need to convert in order to bind to the androgen receptor.
    whats this mean? it is already an active compound, but does have the potential to convert into a stronger one
    Wait a second, Boladrol doesn't become active unless the 3 Beta Hydroxy Steroid enzyme converts it upon ingestion..and it stays inactive if this converts into something different upon interference. I could've sworn this was the case. Enlighten me?
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    Quote Originally Posted by AnonyMoose View Post
    I don't know if dimethyls are equally harsh on the liver at methyls.
    Dimethyls are a lot worse. Superdrol and Dimethyzine for instance. But then again, single methyls are usually run at higher doses (besides a few) so it could be equally harsh.
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    Quote Originally Posted by Bry17 View Post
    Wait a second, Boladrol doesn't become active unless the 3 Beta Hydroxy Steroid enzyme converts it upon ingestion..and it stays inactive if this converts into something different upon interference. I could've sworn this was the case. Enlighten me?

    boladrol is a andro-diol pro hormone. diols are different than diones in that d/t their structure, they are already able to bind to the androgen receptor.

    the binding to the a.r. will not be as strong as say bolasterone, but still binds to the androgen receptor.

    another common one is cdma, commonly known as halodrol. this is an already active compound which converts into a more potent compound, but does not need to convert in order to bind to the ar.

    all diol compounds will have this ability.

    just because something can convert into another more potent compound, doesn't mean it isn't already able to have interaction.

    this is a common misconception.

    and because it is 7,17 dimethylated, it has oral availability, and does not need to convert.

    another thing people dont realize is that diol's are incapable of aromatization. meaning, some users of this compound (those who don't see alot of water retention) who have poor conversion, will see possibly leaner gains, and may also have to dose higher, d/t it not binding as strongly as bolasterone to the androgen receptor.

    I posted all of this information in the boladrol introduction thread way back.


    other more popular diol compounds include:

    halodrol
    pro magnon
    m14add

    none of these need to convert to be active, they are already active steroids in their own.
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    Quote Originally Posted by jbryand101b View Post
    boladrol is a andro-diol pro hormone. diols are different than diones in that d/t their structure, they are already able to bind to the androgen receptor.

    the binding to the a.r. will not be as strong as say bolasterone, but still binds to the androgen receptor.

    another common one is cdma, commonly known as halodrol. this is an already active compound which converts into a more potent compound, but does not need to convert in order to bind to the ar.

    all diol compounds will have this ability.

    just because something can convert into another more potent compound, doesn't mean it isn't already able to have interaction.

    this is a common misconception.

    and because it is 7,17 dimethylated, it has oral availability, and does not need to convert.
    Ok that was very clear and concise. This explains why diols have a higher potency than diones. Thankyou
    another thing people dont realize is that diol's are incapable of aromatization. meaning, some users of this compound (those who don't see alot of water retention) who have poor conversion, will see possibly leaner gains, and may also have to dose higher, d/t it not binding as strongly as bolasterone to the androgen receptor.
    Now this I don't agree with. If all diols are incapable of aromatization then why does Methyl 1, 4-Diol have considerable amounts of estrogen conversion? Because of the abscence of the 4-chloro. Diols/diones have little to do with aromatizing. 4-androstenediol is another perfect example, it's a diol with considerable aromatization.

    Sorry not trying to pick apart your post, my original question was answered. Thanks
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    Quote Originally Posted by Bry17 View Post
    Ok that was very clear and concise. This explains why diols have a higher potency than diones. Thankyou
    Now this I don't agree with. If all diols are incapable of aromatization then why does Methyl 1, 4-Diol have considerable amounts of estrogen conversion? Because of the abscence of the 4-chloro. Diols/diones have little to do with aromatizing. 4-androstenediol is another perfect example, it's a diol with considerable aromatization.

    Sorry not trying to pick apart your post, my original question was answered. Thanks
    because like bolasterone (converted boladrol) m14add converts into dianabol, which is also a compound which like bolasterone, converts into a more potent estrogen.

    4-androstenediol converts into testosterone, which aromatizes into estrogen.

    bolasterone + aromatase enzyme= di methyl estradiol

    dianabol + aromatase enzyme= methyl estradiol.

    testosterone + aromatase enzyme= estradiol & dione

    all of these compounds contain a 3-ketone, but the diol's do not have a 3 ketone until they convert via enzymes into these more potent compounds.

    but again, like I said, all this information I posted can be found in the original boladrol release thread.

    I also posted a good bit of this info in the thread asking me to come into and talk about the compound, from schwell:

    Quote Originally Posted by jbryand101b View Post
    A steroid needs a 3-ketone in order to aromatize, which this (diols) does not have. this compound is also a diol, and should have some binding ability to the androgen receptor itself, needing no conversion to begin working.

    I have a paper sent to me from henryv that I need to read that will give me more of an idea on the aromatization of bolasterone, which he says, looks like it will aromatize less than methyl testosterone.
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    Quote Originally Posted by jbryand101b View Post
    because like bolasterone (converted boladrol) m14add converts into dianabol, which is also a compound which like bolasterone, converts into a more potent estrogen.

    bolasterone + aromatase enzyme= di methyl estradiol

    dianabol + aromatase enzyme= methyl estradiol.

    but again, like I said, all this information I posted can be found in the original boladrol release thread.
    This would, theoretically, mean that boladrol doesn't convert to Bolasterone at a high rate because many users are experiencing, like myself, lean gains. So if bolasterone has a higher estrogen conversion than Dianabol and M14ADD has a higher estrogen conversion than Boladrol then something must be interfering with Boladrol's conversion because Boladrol should aromatize at a higher rate than M14ADD.. see what i'm saying?

    I've heard this information before so I know you're right.
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    well, it has been suggested in a paper that bolasterone's conversion into methyl estradiol is significantly less than that of methyl testosterone, which is just one less methyl (the 7a).

    7a methylation greatly changes the compound, in the same sense that adding a 17a methyl changes a compound.

    for example, boldenone has less aromatization than testosterone, but add a 17a methyl, and (now dianabol) has a higher rate or aromatization, also into a more potent estrogen.

    so it is most likely the 7a methylation that changes up the compound in this way, as well as many others.

    bolasterone's estrogen conversion would be more potent than dianabols, because of the extra 7a methylation, but this is also what is suggested to cause it's estrogen conversion to be so much less than that of methyl testosterone.

    remember "more potent" and "the rate of estrogen conversion" are two different things, which bolasterone seems to have lowered conversion into estrogen, but that the estrogen converted will just hang around longer.

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    Quote Originally Posted by jbryand101b View Post
    well, two things, it has been suggested in a paper that bolasterone's conversion into methyl estradiol is significantly less than that of methyl testosterone, which is just one less methyl (the 7a).

    7a methylation greatly changes the compound, in the same sense that adding a 17a methyl changes a compound.

    for example, boldenone has less aromatization than testosterone, but add a 17a methyl, and (now dianabol) has a higher rate or aromatization, also into a more potent estrogen.

    so it is most likely the 7a methylation that changes up the compound in this way, as well as many others.
    Well one would have to run Bolasterone to see if it does aromatize as high as Dianabol. So I guess the di-methyl estradiol has no merit in that sense. How could a methylation at the 7th position reduce a dimethyl estrogen to being less potent in aromatization than a methyl estrogen? Wish I could see that paper you read
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    Quote Originally Posted by Bry17 View Post
    Well one would have to run Bolasterone to see if it does aromatize as high as Dianabol. So I guess the di-methyl estradiol has no merit in that sense. How could a methylation at the 7th position reduce a dimethyl estrogen to being less potent in aromatization than a methyl estrogen? Wish I could see that paper you read
    I do have it, here is some of what it says:

    Thus it was suggested that structural
    modifications (7a methylation) of a compound can lead to changes in its biological
    activity based on binding affinity, differences in absorption,
    binding to plasma proteins and/or susceptibility to the action of
    metabolizing enzymes.
    [...]

    7-Alkyltestosterone derivatives show a progressive
    loss in activity, as competitive inhibitors of aromatase, as chain
    length increases. The change in binding affinity of these compounds
    seems too gradual to be the result of an absolute lack
    of bulk tolerance by the receptor.
    The similar affinities found for
    the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
    testosterone indicate that the reduction in affinity cannot arise
    solely as a consequence of a hydrophobic chain into a hydrophobic
    pocket.
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    Quote Originally Posted by jbryand101b View Post
    if I ever email mw, i'll send that paper to him for you to read.
    Cool that'd be great
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    Quote Originally Posted by jbryand101b View Post
    actually, i have to edit this, I just looked for the paper, looks like i deleted it, i'll have to get another copy from henry v.
    oh ok
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    Quote Originally Posted by jbryand101b View Post
    edit again, I think, im looking again.
    lol
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    Quote Originally Posted by jbryand101b View Post
    I do have it, here is some of what it says:

    Thus it was suggested that structural
    modifications (7a methylation) of a compound can lead to changes in its biological
    activity based on binding affinity, differences in absorption,
    binding to plasma proteins and/or susceptibility to the action of
    metabolizing enzymes.
    [...]

    7-Alkyltestosterone derivatives show a progressive
    loss in activity, as competitive inhibitors of aromatase, as chain
    length increases. The change in binding affinity of these compounds
    seems too gradual to be the result of an absolute lack
    of bulk tolerance by the receptor.
    The similar affinities found for
    the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
    testosterone indicate that the reduction in affinity cannot arise
    solely as a consequence of a hydrophobic chain into a hydrophobic
    pocket.
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    Quote Originally Posted by jbryand101b View Post
    I do have it, here is some of what it says:

    Thus it was suggested that structural
    modifications (7a methylation) of a compound can lead to changes in its biological
    activity based on binding affinity, differences in absorption,
    binding to plasma proteins and/or susceptibility to the action of
    metabolizing enzymes.
    [...]

    7-Alkyltestosterone derivatives show a progressive
    loss in activity, as competitive inhibitors of aromatase, as chain
    length increases. The change in binding affinity of these compounds
    seems too gradual to be the result of an absolute lack
    of bulk tolerance by the receptor.
    The similar affinities found for
    the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
    testosterone indicate that the reduction in affinity cannot arise
    solely as a consequence of a hydrophobic chain into a hydrophobic
    pocket.
    This is talking about estrogen receptor affinity right? Is this the conclusion as to why it reduces affinity or just one of the reasons?

    The point of 7 alkylation is to reduce the 5a-reductase enzyme, but it seems this change has effected potency of the compound and aromatization.
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    the section talks about various changes 7a methylation causes in the structure of the compound, i'll post the whole thing.

    4.6. C-7 substitution of steroids
    Methylation is a common substitution at C-7 position of the
    steroidal structure. A representative example of a 7-methylated
    synthetic anabolic steroid is bolasterone (Fig. 1, 36). Bolasterone
    synthesis was reported in 1959 and is the 7,17-dimethyl
    analogue of testosterone, causing increased protein synthesis,
    amino acid consumption and catabolism. It is used for relief and
    recovery from common injuries, rehabilitation, weight control,
    anti-insomnia, and regulation of sexuality, aggression, and cognition.
    The activity by oral administration of the compound found to
    be over 13 times as active as 17-methyltestosterone in the levator
    ani assay for myotrophic activity, while having only 3 times
    the androgenic activity, as indicated by the seminal vesicles assay.
    The 19-nor analogue of bolasterone is mibolerone (Fig. 1, 16)which
    was found to have about 18 times the androgenic activity of 17-
    methyltestosterone when assayed orally in the rat, and 41 times its
    myotrophic activity (Table 2, row19) [79].
    However, 7-methylation of 19-nortestosterone (MENT, Fig. 1,
    37) reduces the androgenic effect and amplifies the anabolic
    potency compared to testosterone. This probably happens since
    MENT does not undergo 5-reduction in a large extent, probably
    because the 7-methyl group hinders the action of 5-reductase
    and, thus, a reduction in the androgenic potency is caused. The 5-
    reduced MENT is slightly stimulatory to both prostate and muscle
    in agreement with its low binding affinity to the AR [108111,116].
    Like MENT, other nor-androgens were tested for their resistance to
    5-reduction due to 7-methylation. Results indicated that they
    were, also, more anabolic relative to testosterone [109]. The high
    potency of 7-methylated androgens was shown to correlate with
    their higher binding affinity to androgen receptors. The substitution
    at the 7-position with a methyl group is important for increased
    binding affinity and increased biological activity.
    In comparison, the effects of 7-methyl substitution on testosterone,
    5-DHT or 19-nor-5-DHT (Fig. 1, 38) were surprisingly
    small [83]. The substitution at the 7-position with a cyano or
    acetylthio moiety resulted in lower binding affinity and decreased
    biological activity compared to the 7-methyl substitution. The
    importance of the -configuration of the methyl groupwas further
    confirmed since a -configuration led to a decrease in its androgenic
    potency. This suggested that the conformational changes for
    increased receptor binding are specific for 7-methylated derivatives
    [116]. Studies on the conformation of the 7-methyl group of
    MENT also showed that methyl substitution at the 7-position
    resulted in 8-fold decrease in binding affinity compared to 7-
    methyl derivative.
    The 7-methyl analogue of 5-DHT (Table 2, row20)was tested
    and found to be weakly androgenic [112]. The 7-methyl substitution
    may also be important in connection with antitumor activity,
    since the introduction of this group into methyltestosterone (e.g.
    calusterone, Fig. 1, 39) enhanced the antitumor efficacy in the
    treatment of advanced female breast cancer while decreasing the
    androgenic activity.
    More recently, several 7-fluoro and 7-iodo analogues of 5-
    DHT and 19-nor-5-DHT have been synthesized and tested for
    binding to theARand for their biological activity in vitro [113].Some
    of these analogues designed to have a 17-methyl group in order
    to protect from oxidation of the 17-hydroxyl group. The syntheses
    of the mentioned analogues was based on the assumption that C-7
    is sufficiently distant from C-3 and C-17 in order the halogen substitution
    to have minimal steric or stereoelectronic effects which
    might interfere with the important interactions between the receptor
    and the carbonyl and hydroxyl groups of the steroid. Fromall the
    compounds tested, 7-fluoro-17-methyl-5-DHT had the highest
    receptor affinity as well as androgenic potency (Table 2, row 21).
    Previous studies indicate the 7-methylation of 19-nor androgens
    with a 17-methyl group (17-methyl-19-nortestosterone,
    Fig. 1, 40) causes a many fold increase in androgenicity due to a
    sufficient protection of the 17-methyl group that permits delivery
    of the highly active 19-nor steroid to the end organ [114].
    When the 7-methyl group is added to the 19-nor compounds,
    there is a many-fold increase in androgenicity which is least for
    19-nor-androst-4-ene-3,17-dione and greatest for 17-methyl-19-
    nortestosterone (Table 2, rows 22-23). This shows the additional
    protective activity of the 17-methyl group. The synergistic effect
    of the three changes (19-nor, 7-methyl and 17-methyl) is indicative
    of sufficient protection to permit delivery of the highly active
    19-nor steroid to the end organ [114,115]. Substitution with a
    methyl group in 7- and/or 17-positions results inflattening of the
    steroid molecule which leads to conformation that is less hindered
    for receptor binding. However, other reports showed no correlation
    between the receptor binding affinity and bioactivity of some
    7-methylated androgens. Thus it was suggested that structural
    modifications of a compound can lead to changes in its biological
    activity based on binding affinity, differences in absorption,
    binding to plasma proteins and/or susceptibility to the action of
    metabolizing enzymes [116].
    The synthesis of some 7- and 7-methyl derivatives
    of testosterone, methyl-testosterone and 11-hydroxy-17-
    methyltestosterone (Table 2, row 24) has been reported since
    1958, but no data about the androgenic and/or the anabolic activity
    of these compounds accompanied these studies [117,118].
    Two modifications in the molecule of 19-nortestosterone; the
    7-methylation and a C-14,15 double bond, revealed that the modified
    molecule (7-methyl-14-dehydro-19-nortestosterone, Fig. 1,
    41)was 1000 times as active as testosterone in the chick comb assay
    and 100 times as active as testosterone in either the rat ventral
    prostate or levator ani assay (Table 2, row 25) [119].
    Many 7-alkyltestosterone derivatives were tested (Table 2,
    row 26) [120] and were found to lose androgenic and anabolic
    activity rapidly as the size of the group at the C-7 position
    increased. 7-Alkyltestosterone derivatives show a progressive
    loss in activity, as competitive inhibitors of aromatase, as chain
    length increases. The change in binding affinity of these compounds
    seems too gradual to be the result of an absolute lack
    of bulk tolerance by the receptor. The similar affinities found for
    the 7-hydroxypropyl and the isosteric 7-butyl derivatives of
    testosterone indicate that the reduction in affinity cannot arise
    solely as a consequence of a hydrophobic chain into a hydrophobic
    pocket.
    A steroid incorporating a 7-chroro-4,6-dien-3-one system represents
    a series of steroids with interesting biological activity, but
    C-7 chloro substitution revealed no antigonadotropic, anabolic or
    androgenic activity (Table 2, row27) [121].
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    ^wow I think i'm actually gonna try and break that up tonight, but I'll make my own assumptions and observations outside of this thread or any thread. Thanks jbry pm coming your way
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    if you guys don't start talking english here i am going to post in Italian!
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    im looking into some info of methyl 1,4-androstenediol (m14add) possibly being able to convert into estrogen via a non enzymatic reaction. (according to pa, this may be possible)

    not sure if this would also pertain to all diols, like boladrol. 1,4ad seems to be different in how it would need to be converted. I think.

    It's so complex, and I can access the paper pa told me to read.
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    Quote Originally Posted by jbryand101b View Post
    im looking into some info of methyl 1,4-androstenediol (m14add) possibly being able to convert into estrogen via a non enzymatic reaction. (according to pa, this may be possible)

    not sure if this would also pertain to all diols, like boladrol. 1,4ad seems to be different in how it would need to be converted. I think.

    It's so complex, and I can access the paper pa told me to read.
    I saw he posted that. M14ADD looks like it would have trouble making the conversion to Dianabol. It has to gain a hydroxylation somehow and then dehydrate before it can make that conversion right? Is that via the 3b-HSD pathway or another enzyme pa is talking about because I always thought 17a-methyl-1,4-androstadiene-3b,17b-diol + 3b-HSD = 17a-methyl-1,4-androstadiene-3-one-17b-ol
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    Quote Originally Posted by Bry17 View Post
    This would, theoretically, mean that boladrol doesn't convert to Bolasterone at a high rate because many users are experiencing, like myself, lean gains. So if bolasterone has a higher estrogen conversion than Dianabol and M14ADD has a higher estrogen conversion than Boladrol then something must be interfering with Boladrol's conversion because Boladrol should aromatize at a higher rate than M14ADD.. see what i'm saying?

    I've heard this information before so I know you're right.
    No-one's said that bolasterone has a higher estrogen conversion than dianabol.

    Quote Originally Posted by jbryand101b View Post
    well, it has been suggested in a paper that bolasterone's conversion into methyl estradiol is significantly less than that of methyl testosterone, which is just one less methyl (the 7a).

    7a methylation greatly changes the compound, in the same sense that adding a 17a methyl changes a compound.

    for example, boldenone has less aromatization than testosterone, but add a 17a methyl, and (now dianabol) has a higher rate or aromatization, also into a more potent estrogen.

    so it is most likely the 7a methylation that changes up the compound in this way, as well as many others.

    bolasterone's estrogen conversion would be more potent than dianabols, because of the extra 7a methylation, but this is also what is suggested to cause it's estrogen conversion to be so much less than that of methyl testosterone.

    remember "more potent" and "the rate of estrogen conversion" are two different things, which bolasterone seems to have lowered conversion into estrogen, but that the estrogen converted will just hang around longer.

    Do you have any evidence that dianabol aromatises more readily than boldenone?

    Quote Originally Posted by Bry17 View Post
    This is talking about estrogen receptor affinity right? Is this the conclusion as to why it reduces affinity or just one of the reasons?

    The point of 7 alkylation is to reduce the 5a-reductase enzyme, but it seems this change has effected potency of the compound and aromatization.
    It's not talking about ER affinity. It's talking about the affinity of the compound for binding to the aromatase enzyme.

    7a-alkylation doesn't "reduce the 5a-reductase enzyme". 7a-alkylation prevents 5a-reduction (but not 5b-reduction), as well as having other effects such as flattening the molecule, increasing AR affinity, and may also reduce aromatisation.

    Quote Originally Posted by Bry17 View Post
    I always thought 17a-methyl-1,4-androstadiene-3b,17b-diol + 3b-HSD = 17a-methyl-1,4-androstadiene-3-one-17b-ol
    That's always been the assumption.
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    Quote Originally Posted by henryv View Post
    Do you have any evidence that dianabol aromatises more readily than boldenone?
    Of course not, I am probably committing the same error I accuse people of doing, in mixing up the potency of methyl estrogen vs estrogen & rate of aromatization.

    I can always count on you to correct me an open my eyes.
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    Two excerpts from the text jbry posted that really stuck out at me..

    7-alkyltestosterone derivatives were tested and were found to lose androgenic and anabolic activity rapidly as the size of the group at the C-7 position increased.
    What does it mean by "as the size of group at C-7 position increased?" What causes this size increase? ; as this excerpt makes it sound like this "size increase" of the carbon molecule at the 7th position is what's responsible for Bolasterone's and Calusterone's A/A ratio (or any 7a for that matter)
    7-methylation of 19-nor androgens with a 17-methyl group causes a many fold increase in androgenicity due to a sufficient protection of the 17-methyl group that permits delivery of the highly active 19-nor steroid to the end organ
    ^One can only imagine how suppressive ment-dione will be. Good lord. 7a methylation, according to this text, only increases androgenicity in a 19 nor derivative like ment-dione.. ~ EDIT: NVM, it says only if it has a 17a methylation, so disregard this one
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    Quote Originally Posted by Bry17 View Post
    Two excerpts from the text jbry posted that really stuck out at me..

    What does it mean by "as the size of group at C-7 position increased?" What causes this size increase? ; as this excerpt makes it sound like this "size increase" of the carbon molecule at the 7th position is what's responsible for Bolasterone's and Calusterone's A/A ratio (or any 7a for that matter)
    They tested a number of 7a-alkylated testosterone derivatives with different 7a-substituents. They found that smaller functional groups (like a methyl group) caused a significant increase in anabolic and androgenic activity, but the larger the substituent, the less anabolic and androgenic activity was seen.
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    Quote Originally Posted by henryv View Post
    They tested a number of 7a-alkylated testosterone derivatives with different 7a-substituents. They found that smaller functional groups (like a methyl group) caused a significant increase in anabolic and androgenic activity, but the larger the substituent, the less anabolic and androgenic activity was seen.


    The substitution at the 7-position with a cyano or
    acetylthio moiety resulted in lower binding affinity and decreased
    biological activity compared to the 7-methyl substitution
    Oh duh, somehow I missed this part of the paper. So basically that means methyl substitution was the most prudent in comparison to a cyano group and the others that were tested (does not surprise me, it's always a methyl lmao). But how would that relate to size? Is a cyano larger than a methyl group or something?
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    Quote Originally Posted by Bry17 View Post
    Oh duh, somehow I missed this part of the paper. So basically that means methyl substitution was the most prudent in comparison to a cyano group and the others that were tested (does not surprise me, it's always a methyl lmao). But how would that relate to size? Is a cyano larger than a methyl group or something?
    A methyl group is a small functional group. This is why it is used at 17a. Its existence prevents the 17b-ol from becoming a 17-one, but it is small enough not to impair receptor binding. The same is true of the 7a position - a methyl group here imparts a number of positive receptor binding effects that larger substituents do not.

    The paper it is referring to does not study bolasterone specifically, or a testosterone derivative with a 7a cyano group.
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    so far it is looking like boladrol dosage should be dosed between 8-10mg
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    Quote Originally Posted by henryv View Post
    A methyl group is a small functional group. This is why it is used at 17a. Its existence prevents the 17b-ol from becoming a 17-one, but it is small enough not to impair receptor binding. The same is true of the 7a position - a methyl group here imparts a number of positive receptor binding effects that larger substituents do not.

    The paper it is referring to does not study bolasterone specifically, or a testosterone derivative with a 7a cyano group.
    Ok thanks henry, yeah I knew it wasn't talking about anything specific I just drew conclusions from its context.
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    Quote Originally Posted by IBE View Post
    so far it is looking like boladrol dosage should be dosed between 8-10mg
    It would seem that way. It would've been more consumer friendly to make the tablets 3-4mg, At 8 mg I could feel it in full swing and leaned out nicely
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    the next run will be 3 or 4mg per tablet we still did not make out minds up yet..lol
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    hmmm........... ree-hee-hee-heelyyyy.....
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    Quote Originally Posted by IBE View Post
    so far it is looking like boladrol dosage should be dosed between 8-10mg
    Split into 2 equal AM and PM doses?
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