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10% minoxidil +60mg finasteride topical


hairIosssucks
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  • Senior Member

I've never tried it or heard any results from topical finasteride. Let us know how it works. I'm really hoping the next 3-5 year will be booming with FDA approved treatments.

My Hair Loss Website

 

Surgical Treatments:

 

Hair transplant 5-22-2013 with Dr. Paul Shapiro at Shapiro Medical Group

Total grafts transplanted: 3222

*536 singles *1651 doubles * 961 triples,

*74 quadruples.

Total hairs transplanted: 7017

 

 

Non-Surgical Treatments:

 

*1.25 mg finasteride daily

*Generic minoxidil foam 2x daily

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  • Regular Member

No, but I tried generic 5% minoxidil, 8% trichogen and another 5% minoxidil mixed with nutrients and blockers and I can honestly say that it worked 100%. I'd even say it worked perfect but I'll save perfect in case a cure comes out that does require daily applications haha!

 

I only tried finasteride as the pill and had too many negatives for far too few results. Topical finasteride hey? Let us know how it works! Also, be careful with 10% minoxidil, I have read several studies that suggest more than 5% can have many negative side effects.

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  • Senior Member

In theory, topical anti-androgens should be very effective. The problem, however, is appropriate absorption across the scalp. If the molecules are too large or the biochemistry of the medium is incorrect, the drug won't cross the scalp and reach the hair follicles.

 

Where did the topical finasteride come from?

"Doc" Blake Bloxham - formerly "Future_HT_Doc"

 

Forum Co-Moderator and Editorial Assistant for the Hair Transplant Network, the Hair Loss Learning Center, the Hair Loss Q&A Blog, and the Hair Restoration Forum

 

All opinions are my own and my advice does not constitute as medical advice. All medical questions and concerns should be addressed by a personal physician.

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  • Senior Member

I think CB-03-01 (Cortexolone 17alpha propionate) is the best topical Anti Androgen.

 

Here some interesting points about CB-03-01

 

- an impressive reduction of sebacious gland size, observed in about 85% of treated subjects.

- a decrease in dermal fibrosis, indicator of inflammatory process, after treatment mainly with CB-03-01

- a reduction of vessel diameter of peribulbar microvasculature

- a reduction of inflammatory cells after treatment with CB-03-01

 

Here is also an interesting article with more information:-

 

Cortexolone 17-alpha propionate (CB-03-01): Peripherally Selective Anti-Androgen

 

Cortexolone 17-alpha propionate, also called CB-03-01, is a derivative of 11-deoxycortisone with peripheral, selective anti-androgen activity. Published data demonstrate that cortexolone 17α-propionate possesses therapeutic potential as a topical anti-androgen for skin disorders such as acne, as well as androgenic alopecia (male pattern baldness). Cortexolone boasts equal or greater safety and potentially greater efficacy compared to retinoids used to treat acne, as well as a more localized and therefore potentially safer and more effective mechanism as compared to systemic 5-alpha reductase drugs such as finasteride and dutasteride. Though not currently FDA-approved, if FDA approval is granted cortexolone 17-alpha propionate will be the first commercially available topical anti-androgen.

 

Background and Timeline of Development

 

According to the manufacturer, Italian company Cosmo Pharmaceuticals, cortexolone “tightly mimics the profile of an ideal anti-androgen for topical use”. The stated objective of the manufacturer is “to create a product for topical application to treat acne, male pattern baldness, and seborrhoea that does not have the side effects of products currently being taken in tablet form” which presumably would include oral isotretinoin (Accutane) and antibiotics for acne, and 5-AR inhibitors such as dutasteride (Avodart) and finasteride (Propecia) for male pattern baldness.

 

Five clinical trials assessing the safety and efficacy of cortexolone 17-alpha propionate in European markets have been completed with favorable results, and non-clinical early data supporting the IND (investigational new drug) application was also deemed promising.

 

Per US FDA code, each individual disease or disorder claimed to be treated by a drug will require separate applications for the drug approval process. According to Cosmo, an IND application for acne was granted by FDA in the first quarter of 2012, with phase II escalating dose trials in process at the time of this writing[1]. While the future appears bright for cortexolone 17-alpha propionate as an alopecia drug, the IND process has not been initiated at this time; the manufacturer has stated their intent to apply for an IND for androgenic alopecia in 2014.

 

Anti-inflammatory and Anti-Androgenic Mechanism and Safety Profile and Rationale

 

Due to a common androgenic pathway between inflammatory acne and androgenic alopecia, cortexolone 17-alpha propionate is considered a promising drug for both disorders. What is unique about cortexolone 17-alpha propionate is the peripheral and selective mechanism.

 

Cortexolone has good penetrative properties, making it suitable for topical use, and while effective locally it is metabolized into a harmless, inactive parent compound prior to circulating systemically:

 

“CB-03-01’s mechanism of action is based on the competitive activity between testosterone and DHT for androgen-receptors in the skin. CB-03-01 is devoid of systemic anti-androgenic activity, in as far as it does not inhibit gonadotropins hypersecretion, and has a moderate anti-inflammatory effect. In preclinical studies, CB-03-01 was shown to be rapidly metabolized by the skin to the parent compound cortexolone, which is a physiological steroid lacking anti-androgen activity and is completely safe. CB-03-01 has also been shown to have good penetration through the skin, making it the first anti-androgen suitable for topical application.

 

The primary supporting study around which Cosmo bases their claims regarding safety and efficacy of topical anti-androgen therapy for acne was published in the British Journal of Dermatology in 2011.

 

There are effective anti-androgens currently available, but they are not suitable for topical use and act in a systemic manner which, due to the pervasiveness of androgen activity and androgen receptors in physiological function throughout the body, results in a poor safety profile. As Cosmo CEO Mauro Ajani states, “drugs available for the treatment of acne are either not very effective or have substantial negative side effects”.

 

The recent manufacturer-funded studies and internal data are abundant, but there is also early peer-reviewed data that is illustrative of the comparative potency, and safety rationale, of cortexolone (CB-03-01) compared to other drugs:

 

“The aim of this study was to investigate the antiandrogenic activity of a new monoester of cortexolone, cortexolone 17alpha-propionate (CAS 19608-29-8, CB-03-01). Although the compound displayed a strong local antiandrogenic activity… it did not exhibit antiandrogenic activity in rats after subcutaneous injection, nor did it affect gonadotropins hypersecretion… As topical antiandrogen, the steroid resulted about 4 times more active than progesterone (CAS 57-83-0) and, when compared to known antiandrogen standards, it was about 3 times more potent than flutamide (CAS 13311-84-7), about 2 times more effective than finasteride …Its pharmacological activity seemed to be primarily related to its ability to antagonistically compete at androgen receptor level.”

 

Comparative Efficacy

 

Cortexolone 17-alpha propionate, Androgen Receptors, and AR-Targeted Treatment of Alopecia

 

Compared to the recently-demonstrated PGD2 mechanism, knowledge of the effects of androgen receptor agonism is not cutting-edge; the mechanism was first mentioned in published literature in the late 1980s, and early off-label use of 5-alpha reductase (5AR) inhibitor drugs finasteride (then Proscar, now also Propecia) and Dutasteride (Avodart) existed in the 1990s prior to the approval of finasteride labeled for treatment of alopecia in 1997. 5AR inhibitors prevent the local enzymatic conversion of testosterone into dihydrotestosterone, which is 2.4-10 times more potent in its action at the androgen receptor than testosterone depending on tissue and action examined. However, they also reduce serum DHT levels, sometimes drastically, resulting in potentially undesirable effects.

 

5AR inhibitors are effective to prevent hair shedding when taken long-term by men with androgenic alopecia (AGA). However, lately there have been increasing concerns as to the short-term and long-term safety profiles of these drugs, both in civil courts and in the published literature:

 

“Men who suffered ongoing erectile dysfunction after taking prescription drugs to treat prostate problems and male pattern baldness will be able to pursue a class-action lawsuit against the drug maker, a B.C. judge has ruled.”

 

“The significant reduction in DFI within 3 months of finasteride cessation and continued improvement suggests a causal link between finasteride and sperm DNA damage. We hypothesize that low-dose finasteride may exert a negative influence on sperm DNA integrity, resulting in increased pregnancy losses. We suggest that in infertile men using finasteride, sperm DFI should be measured in addition to semen parameters, and a trial of discontinuation of finasteride may be warranted.”

 

The likely primary mechanism of most or all reported side-effects not due to nocebo-type effect is systemic action of 5-alpha reductase. When taken orally, 5AR drugs have systemic action and are in no way confined in their action to the peripheral (local) area of effect, namely the scalps of balding men. Topical applications of finasteride preparations may reduce systemic circulation, but will not prevent this issue, since, unlike cortexolone, the finasteride gel that absorbs into the dermal layer can still be circulated systemically in its active form.

 

The androgen-receptor-mediated mechanism is upstream of PGD2, meaning that it is hypothetically possible to reduce PGD2 levels to treat baldness without interfering with androgen levels. On the other hand, since PGD2 is likely associated in a general sense with inflammation, modulation of the androgen pathway may be an insufficient way to address baldness in some men if PGD2 elevation is caused by a pathway other than androgen receptor binding by DHT. Without more published PGD2 data, though, it is impossible to predict how future PGD2 inhibitor drugs may change the treatment landscape for AGA patients.

 

It is reasonable to state that the androgen receptor pathway of baldness is well-demonstrated, well-studied, and is an effective target for drug development in the interest of treating androgenic alopecia. Cortexolone, with a distinct yet similar mechanism (competitive inhibition/receptor inactivation, preventing DHT-binding) is a major step forward in addressing the major downside to 5AR inhibition as a baldness treatment because, if approved, it may be as effective as systemic, orally-dosed 5AR inhibitors, and would almost certainly be safer.

Plug removal + Strip scar revision - Dr. Ali Karadeniz (AEK)- May 23, 2015

Plug removal + 250 FUE temple points- Dr. Hakan Doganay (AHD)- July 3, 2013

Scar Tricopigmentation- Dr. Koray Erdogan (ASMED)- May 3, 2013

2500 FUT (Hairline Repair)- Dr. Rahal- July 26, 2011

 

My Hair Treatments:

1- Alpecin Double Effect Shampoo (Daily)

2- Regaine Solution Minoxidil 5% (2 ml once a day)

3- GNC Ultra NourishHair™ (Once a day)

4- GNC Herbal Plus Standardized Saw Palmetto (Once a day)

 

My Rahal HT thread http://www.hairrestorationnetwork.com/eve/164456-2500-fut-dr-rahal-hairline-repair.html[/size]

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  • Regular Member
I think CB-03-01 (Cortexolone 17alpha propionate) is the best topical Anti Androgen.

 

Here some interesting points about CB-03-01

 

- an impressive reduction of sebacious gland size, observed in about 85% of treated subjects.

- a decrease in dermal fibrosis, indicator of inflammatory process, after treatment mainly with CB-03-01

- a reduction of vessel diameter of peribulbar microvasculature

- a reduction of inflammatory cells after treatment with CB-03-01

 

Here is also an interesting article with more information:-

 

Cortexolone 17-alpha propionate (CB-03-01): Peripherally Selective Anti-Androgen

 

Cortexolone 17-alpha propionate, also called CB-03-01, is a derivative of 11-deoxycortisone with peripheral, selective anti-androgen activity. Published data demonstrate that cortexolone 17α-propionate possesses therapeutic potential as a topical anti-androgen for skin disorders such as acne, as well as androgenic alopecia (male pattern baldness). Cortexolone boasts equal or greater safety and potentially greater efficacy compared to retinoids used to treat acne, as well as a more localized and therefore potentially safer and more effective mechanism as compared to systemic 5-alpha reductase drugs such as finasteride and dutasteride. Though not currently FDA-approved, if FDA approval is granted cortexolone 17-alpha propionate will be the first commercially available topical anti-androgen.

 

Background and Timeline of Development

 

According to the manufacturer, Italian company Cosmo Pharmaceuticals, cortexolone “tightly mimics the profile of an ideal anti-androgen for topical use”. The stated objective of the manufacturer is “to create a product for topical application to treat acne, male pattern baldness, and seborrhoea that does not have the side effects of products currently being taken in tablet form” which presumably would include oral isotretinoin (Accutane) and antibiotics for acne, and 5-AR inhibitors such as dutasteride (Avodart) and finasteride (Propecia) for male pattern baldness.

 

Five clinical trials assessing the safety and efficacy of cortexolone 17-alpha propionate in European markets have been completed with favorable results, and non-clinical early data supporting the IND (investigational new drug) application was also deemed promising.

 

Per US FDA code, each individual disease or disorder claimed to be treated by a drug will require separate applications for the drug approval process. According to Cosmo, an IND application for acne was granted by FDA in the first quarter of 2012, with phase II escalating dose trials in process at the time of this writing[1]. While the future appears bright for cortexolone 17-alpha propionate as an alopecia drug, the IND process has not been initiated at this time; the manufacturer has stated their intent to apply for an IND for androgenic alopecia in 2014.

 

Anti-inflammatory and Anti-Androgenic Mechanism and Safety Profile and Rationale

 

Due to a common androgenic pathway between inflammatory acne and androgenic alopecia, cortexolone 17-alpha propionate is considered a promising drug for both disorders. What is unique about cortexolone 17-alpha propionate is the peripheral and selective mechanism.

 

Cortexolone has good penetrative properties, making it suitable for topical use, and while effective locally it is metabolized into a harmless, inactive parent compound prior to circulating systemically:

 

“CB-03-01’s mechanism of action is based on the competitive activity between testosterone and DHT for androgen-receptors in the skin. CB-03-01 is devoid of systemic anti-androgenic activity, in as far as it does not inhibit gonadotropins hypersecretion, and has a moderate anti-inflammatory effect. In preclinical studies, CB-03-01 was shown to be rapidly metabolized by the skin to the parent compound cortexolone, which is a physiological steroid lacking anti-androgen activity and is completely safe. CB-03-01 has also been shown to have good penetration through the skin, making it the first anti-androgen suitable for topical application.

 

The primary supporting study around which Cosmo bases their claims regarding safety and efficacy of topical anti-androgen therapy for acne was published in the British Journal of Dermatology in 2011.

 

There are effective anti-androgens currently available, but they are not suitable for topical use and act in a systemic manner which, due to the pervasiveness of androgen activity and androgen receptors in physiological function throughout the body, results in a poor safety profile. As Cosmo CEO Mauro Ajani states, “drugs available for the treatment of acne are either not very effective or have substantial negative side effects”.

 

The recent manufacturer-funded studies and internal data are abundant, but there is also early peer-reviewed data that is illustrative of the comparative potency, and safety rationale, of cortexolone (CB-03-01) compared to other drugs:

 

“The aim of this study was to investigate the antiandrogenic activity of a new monoester of cortexolone, cortexolone 17alpha-propionate (CAS 19608-29-8, CB-03-01). Although the compound displayed a strong local antiandrogenic activity… it did not exhibit antiandrogenic activity in rats after subcutaneous injection, nor did it affect gonadotropins hypersecretion… As topical antiandrogen, the steroid resulted about 4 times more active than progesterone (CAS 57-83-0) and, when compared to known antiandrogen standards, it was about 3 times more potent than flutamide (CAS 13311-84-7), about 2 times more effective than finasteride …Its pharmacological activity seemed to be primarily related to its ability to antagonistically compete at androgen receptor level.”

 

Comparative Efficacy

 

Cortexolone 17-alpha propionate, Androgen Receptors, and AR-Targeted Treatment of Alopecia

 

Compared to the recently-demonstrated PGD2 mechanism, knowledge of the effects of androgen receptor agonism is not cutting-edge; the mechanism was first mentioned in published literature in the late 1980s, and early off-label use of 5-alpha reductase (5AR) inhibitor drugs finasteride (then Proscar, now also Propecia) and Dutasteride (Avodart) existed in the 1990s prior to the approval of finasteride labeled for treatment of alopecia in 1997. 5AR inhibitors prevent the local enzymatic conversion of testosterone into dihydrotestosterone, which is 2.4-10 times more potent in its action at the androgen receptor than testosterone depending on tissue and action examined. However, they also reduce serum DHT levels, sometimes drastically, resulting in potentially undesirable effects.

 

5AR inhibitors are effective to prevent hair shedding when taken long-term by men with androgenic alopecia (AGA). However, lately there have been increasing concerns as to the short-term and long-term safety profiles of these drugs, both in civil courts and in the published literature:

 

“Men who suffered ongoing erectile dysfunction after taking prescription drugs to treat prostate problems and male pattern baldness will be able to pursue a class-action lawsuit against the drug maker, a B.C. judge has ruled.”

 

“The significant reduction in DFI within 3 months of finasteride cessation and continued improvement suggests a causal link between finasteride and sperm DNA damage. We hypothesize that low-dose finasteride may exert a negative influence on sperm DNA integrity, resulting in increased pregnancy losses. We suggest that in infertile men using finasteride, sperm DFI should be measured in addition to semen parameters, and a trial of discontinuation of finasteride may be warranted.”

 

The likely primary mechanism of most or all reported side-effects not due to nocebo-type effect is systemic action of 5-alpha reductase. When taken orally, 5AR drugs have systemic action and are in no way confined in their action to the peripheral (local) area of effect, namely the scalps of balding men. Topical applications of finasteride preparations may reduce systemic circulation, but will not prevent this issue, since, unlike cortexolone, the finasteride gel that absorbs into the dermal layer can still be circulated systemically in its active form.

 

The androgen-receptor-mediated mechanism is upstream of PGD2, meaning that it is hypothetically possible to reduce PGD2 levels to treat baldness without interfering with androgen levels. On the other hand, since PGD2 is likely associated in a general sense with inflammation, modulation of the androgen pathway may be an insufficient way to address baldness in some men if PGD2 elevation is caused by a pathway other than androgen receptor binding by DHT. Without more published PGD2 data, though, it is impossible to predict how future PGD2 inhibitor drugs may change the treatment landscape for AGA patients.

 

It is reasonable to state that the androgen receptor pathway of baldness is well-demonstrated, well-studied, and is an effective target for drug development in the interest of treating androgenic alopecia. Cortexolone, with a distinct yet similar mechanism (competitive inhibition/receptor inactivation, preventing DHT-binding) is a major step forward in addressing the major downside to 5AR inhibition as a baldness treatment because, if approved, it may be as effective as systemic, orally-dosed 5AR inhibitors, and would almost certainly be safer.

 

 

Interesting?

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