This is a topical product that a UG lab is making, every time i see this it baffles me on why they put 25% DMSO in it if its for spot reduction.
Qfs Dinoprost-gel, Transdermal Fat Reduction, Pgf-2a
QFS Dinoprost-Gel, Transdermal Fat Reduction active ingredients
Dinoprost Tromethamine 150mg ( Prostraglandin F2 alpha) and
Dimethylsulfoxide (DMSO 25%)
Prostaglandin F2alpha is a potent inhibitor of adipocyte precursor
differentiation and a physiological negative modulator of adipocyte
function (ie triglyceride accumulation) through stimulation of
transforming growth factor-alpha mRNA expression. It initiates a
cascade of effects in the adipoctes which have physiological
importance to reducing the size and it appears number of mature
cells,long after PGf-2a is cleared from the system
Mature adipose cells only shrink in size in response to restricted
caloric intake or increased metabolic demand. Before now the only
method of reducing the number of fat cells was liposuction. It now
appears that Pgf-2a applied topically can have the same same
effects as diet and liposuction. Pgf-2a can reduce the size of
mature adipocytes and the number of mature adipocytes through
negative modulation and reversing the process of differentiation
There are no studies on topical application. DMSO does carry PGF-2a
through the dermal layers and the low concentration spread over a
large area is ideal for the intended purpose. One cannot spread
PGf-2a (or anyother substance) over the surface area that one can
with DMSO topical application. The idea being that you need to
interact as many molecules of PGF-2a with as many mature fat cells
as possible. The biggest asset to DMSO as a carrier is the ability
to spread the PGF-2a applicatiion over a large surface area,
thereby maximising the interactuion of the number PGF-2a molucules
with the maximum number of fat cells. This is where the DMOS method
really shines. QFS is not masking the smell of the DMSO. It is not
that bad and goes away in about 5 minutes.
It is important to remember that dinoprost tromethamine does not
burn the released fatty acids, aerobic exercise and or T3 will take
care of that. PGF-2a only changes the way fats are stored and the
formation and function of adipose tissue. As well I find that about
half of the time I feel a tickle in the back of my throat and
sometimes I have a full out coughing fit. This says to me that I
have applied a good dosage.
Here are some studies that support PGF-2a and negative modulation
of adipose tissue.
Endocrinology 1995 Aug;136(8):3222-9
Prostaglandin F2 alpha stimulates transforming growth factor-alpha
expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York
12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2
alpha (PGF2 alpha) are potent inhibitors of adipocyte
differentiation. We demonstrate here that TGF alpha messenger RNA
(mRNA) is expressed in freshly isolated fat pads and in primary
culture of adipocyte precursors cultivated in defined medium before
and after differentiation. We show that PGF2 alpha stimulated TGF
alpha mRNA expression in a dose-dependent manner. PGF2 alpha also
stimulated TGF alpha production in the culture medium of adipocyte
precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA
expression in both undifferentiated and differentiated cells. 9
alpha,11 beta-PGF2 alpha, which also inhibited adipose
differentiation, stimulated TGF alpha mRNA expression similarly to
PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA
expression. The time-course experiment indicates that the
stimulation of TGF alpha mRNA expression by PGF2 alpha is observed
within 6 h of exposure to PGF2 alpha and is inhibited by treatment
of the cells with actinomycin D. The effect of PGF2 alpha on TGF
alpha expression did not require activation of protein kinase C and
was fully reversible. As both TGF alpha and PGF2 alpha are
inhibitors of adipose differentiation, it is suggested that
stimulation of TGF alpha expression by PGF2 alpha could represent
an amplification mechanism to modulate adipocyte precursor
differentiation and adipocyte function within the adipose tissue.
Int J Obes Relat Metab Disord 1996 Mar;20 Suppl 3:S58-64 R
Endocrine and paracrine negative regulators of adipose
differentiation.
Serrero G, Lepak N.
W Alton Jones Cell Science Center, Inc, Lake Placid, NY 12946, USA.
Obesity which is characterized by an abnormal adipose tissue
development is a first degree public health hazard in
industrialized countries. One important aspect in the study of
adipose tissue development is to investigate the hormonal control
of proliferation and differentiation. Any qualitative or
quantitative change in these hormones or their receptors can result
in abnormalities in the process of proliferation and/or
differentiation possibly leading to obesity. Therefore, it is
important to identify these factors and investigate their mechanism
of action. We have concentrated our efforts in the study of factors
triggering differentiation (positive regulators) and also of
factors inhibiting differentiation (negative regulators). The
present paper provides evidence of the importance of EGF/TGF-alpha
and of PGF2 alpha as differentiation inhibitors for adipocyte
precursors in primary culture. Data presented here also demonstrate
that TGF-alpha is expressed in adipose tissue and that its
expression is specifically stimulated by PGF2 alpha, thus
suggesting the existence of an amplification mechanism between two
differentiation inhibitors within the adipose tissue. The
importance of these two types of differentiation inhibitors in the
regulation of adipose tissue development is discussed.
Qfs Dinoprost-gel, Transdermal Fat Reduction, Pgf-2a
QFS Dinoprost-Gel, Transdermal Fat Reduction active ingredients
Dinoprost Tromethamine 150mg ( Prostraglandin F2 alpha) and
Dimethylsulfoxide (DMSO 25%)
Prostaglandin F2alpha is a potent inhibitor of adipocyte precursor
differentiation and a physiological negative modulator of adipocyte
function (ie triglyceride accumulation) through stimulation of
transforming growth factor-alpha mRNA expression. It initiates a
cascade of effects in the adipoctes which have physiological
importance to reducing the size and it appears number of mature
cells,long after PGf-2a is cleared from the system
Mature adipose cells only shrink in size in response to restricted
caloric intake or increased metabolic demand. Before now the only
method of reducing the number of fat cells was liposuction. It now
appears that Pgf-2a applied topically can have the same same
effects as diet and liposuction. Pgf-2a can reduce the size of
mature adipocytes and the number of mature adipocytes through
negative modulation and reversing the process of differentiation
There are no studies on topical application. DMSO does carry PGF-2a
through the dermal layers and the low concentration spread over a
large area is ideal for the intended purpose. One cannot spread
PGf-2a (or anyother substance) over the surface area that one can
with DMSO topical application. The idea being that you need to
interact as many molecules of PGF-2a with as many mature fat cells
as possible. The biggest asset to DMSO as a carrier is the ability
to spread the PGF-2a applicatiion over a large surface area,
thereby maximising the interactuion of the number PGF-2a molucules
with the maximum number of fat cells. This is where the DMOS method
really shines. QFS is not masking the smell of the DMSO. It is not
that bad and goes away in about 5 minutes.
It is important to remember that dinoprost tromethamine does not
burn the released fatty acids, aerobic exercise and or T3 will take
care of that. PGF-2a only changes the way fats are stored and the
formation and function of adipose tissue. As well I find that about
half of the time I feel a tickle in the back of my throat and
sometimes I have a full out coughing fit. This says to me that I
have applied a good dosage.
Here are some studies that support PGF-2a and negative modulation
of adipose tissue.
Endocrinology 1995 Aug;136(8):3222-9
Prostaglandin F2 alpha stimulates transforming growth factor-alpha
expression in adipocyte precursors.
Lepak NM, Serrero G.
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York
12946, USA.
Transforming growth factor-alpha (TGF alpha) and prostaglandin F2
alpha (PGF2 alpha) are potent inhibitors of adipocyte
differentiation. We demonstrate here that TGF alpha messenger RNA
(mRNA) is expressed in freshly isolated fat pads and in primary
culture of adipocyte precursors cultivated in defined medium before
and after differentiation. We show that PGF2 alpha stimulated TGF
alpha mRNA expression in a dose-dependent manner. PGF2 alpha also
stimulated TGF alpha production in the culture medium of adipocyte
precursors in primary culture. PGF2 alpha stimulated TGF alpha mRNA
expression in both undifferentiated and differentiated cells. 9
alpha,11 beta-PGF2 alpha, which also inhibited adipose
differentiation, stimulated TGF alpha mRNA expression similarly to
PGF2 alpha, whereas other PGs had no effect on TGF alpha mRNA
expression. The time-course experiment indicates that the
stimulation of TGF alpha mRNA expression by PGF2 alpha is observed
within 6 h of exposure to PGF2 alpha and is inhibited by treatment
of the cells with actinomycin D. The effect of PGF2 alpha on TGF
alpha expression did not require activation of protein kinase C and
was fully reversible. As both TGF alpha and PGF2 alpha are
inhibitors of adipose differentiation, it is suggested that
stimulation of TGF alpha expression by PGF2 alpha could represent
an amplification mechanism to modulate adipocyte precursor
differentiation and adipocyte function within the adipose tissue.
Int J Obes Relat Metab Disord 1996 Mar;20 Suppl 3:S58-64 R
Endocrine and paracrine negative regulators of adipose
differentiation.
Serrero G, Lepak N.
W Alton Jones Cell Science Center, Inc, Lake Placid, NY 12946, USA.
Obesity which is characterized by an abnormal adipose tissue
development is a first degree public health hazard in
industrialized countries. One important aspect in the study of
adipose tissue development is to investigate the hormonal control
of proliferation and differentiation. Any qualitative or
quantitative change in these hormones or their receptors can result
in abnormalities in the process of proliferation and/or
differentiation possibly leading to obesity. Therefore, it is
important to identify these factors and investigate their mechanism
of action. We have concentrated our efforts in the study of factors
triggering differentiation (positive regulators) and also of
factors inhibiting differentiation (negative regulators). The
present paper provides evidence of the importance of EGF/TGF-alpha
and of PGF2 alpha as differentiation inhibitors for adipocyte
precursors in primary culture. Data presented here also demonstrate
that TGF-alpha is expressed in adipose tissue and that its
expression is specifically stimulated by PGF2 alpha, thus
suggesting the existence of an amplification mechanism between two
differentiation inhibitors within the adipose tissue. The
importance of these two types of differentiation inhibitors in the
regulation of adipose tissue development is discussed.