Igf-1 LR3 info

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This is a basic IGF cycle guide. It is meant to answer a lot of very simple questions. I will continue to update as I see fit

What is it? And what is the difference between huIGF-1 and LR3 IGF-1?
IGF-1 stands for insulin like growth factor. IGF-I is the primary protein involved in responses of cells to growth hormone (GH): that is, IGF-I is produced in response to GH and then induces cellular activities. One such example is muscle growth or hyperplasia
This compound also makes the human body more sensitive to insulin. It is the most potent growth factor found in the human body. IGF-1 causes muscle cell hyperplasia, which is an actual splitting and forming of new muscle cells, this is a good thing.

LR3 IGF-1 

Long Recumbent 3 IGF-1, which is an 83 amino acid analog of human IGF-1 sequence with the substitution of an arg for the glu at position 3 (hence R3), and a 13 amino acid extension peptide at the N-terminus (hence the long).

Clenbuterol info 2

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Clenbuterol is a beta2-adrenergic agonist.  Stimulation of the beta2-adrenergic receptors on bronchial smooth muscle produces bronchodilation.  However, clenbuterol, like other beta-adrenergic agonists, can produce adverse cardiovascular and neurological effects, such as heart palpitations, muscle tremors, and nervousness.  Activation of beta-adrenergic receptors also accounts for clenbuterol’s ability to increase lean muscle mass and reduce body fat, although the downstream mechanisms by which it does so have yet to be clearly defined. After ingestion, clenbuterol is readily absorbed (7080%) and remains in the body for awhile (25-39 hours).  As  a result of its long half life, the adverse effects of clenbuterol are often prolonged

Thymosin beta 4 TB500

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Previously, thymosin beta 4 (Tbeta(4)) was found to promote wound healing in full thickness skin wounds and heptanol debrided corneas. Here, the effect of Tbeta(4) was examined treatment on corneal wound healing and inflammation in vivo after alkali injury, a more severe wound of the eye. Corneas from 129 Sv mice were chemically burned with a 2 mm disc soaked in 1 N NaOH for 30 sec. Eyes were irrigated copiously with phosphate buffered saline (PBS) and then treated topically with either Tbeta(4) (5 microg/5 microl PBS) or 5 microl PBS twice daily. Animals were killed, the eyes were enucleated, fixed and embedded in plastic resin or prepared for mRNA analysis. Mouse corneas topically treated with 5 microg of Tbeta(4) twice daily after alkali injury demonstrated accelerated re-epithelialization at all time points and decreased polymorphonuclear leukocyte (PMN) infiltration at 7 days post injury (p.i.) when compared to PBS-treated controls. mRNA transcript levels were decreased several fold for interleukin (IL)-lbeta, and the chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, MIP-2 and monocyte chemoattractant protein (MCP)-1 from 1 to 7 days after injury in the Tbeta(4)- vs. PBS-treated corneas. Thus, Tbeta(4) may provide a new clinical treatment for severe traumatic corneal wound disorders by promoting rapid corneal wound healing and decreasing both PMN infiltration and inflammatory cytokine and chemokine mRNA levels.

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Helios

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Yes we now have HELIOS. Helios are a research chemical that is a mixture of clenbuterol and yohimbine. There is 40mcg clenbuterol and 5.4mg yohimbine per ml. 

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Clenbuterol info

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Every organism requires a means to rid itself of cells that are no longer required, are damaged, or that may be harmful to the organism. Cell death is a tightly controlled process and may occur by apoptotic or non-apoptotic means (necrosis). Apoptosis is the regulated destruction of a cell and may be triggered by either external or internal signals. Unlike necrosis, apoptosis does not result in an inflammatory response from the surrounding cells and the morphological features are quite distinct. Apoptosis, or programmed cell death, involves complex signaling that results in a molecular cascade triggering a series of proteases known as caspases. Caspases are central to the process of apoptosis and are activated specifically in apoptotic cells. Caspases cleave a limited set of proteins within the cell which are critical for cell survival, resulting in cell death.

In rats, doses of clenbuterol on the order of 100 mcg (micrograms) per kg of body weight have been shown to induce necrosis of cardiac myocytes (muscle cells) (1). The same research group that examined necrosis recently showed that much smaller doses of clenbuterol, as low as 1 mcg/kg of body weight, could induce apoptosis in cardiac myocytes (2). Before looking at the mechanisms and implications of this, we must convert these figures to Human Equivalent Doses (HED) to see if there is any relevance to humans here. In some cases, when extrapolating animal doses to human doses a direct mg/kg to mg/kg conversion is adequate. Considering necrosis, using this conversion 100 mcg/kg would translate into 10,000 mcg for a 100 kg bodybuilder. It’s unlikely that anyone routinely consumes this much clenbuterol, so necrosis would not be an issue in humans. Apoptosis is a different story however. The 1 mcg/kg figure would amount to 100 mcg in a human. People routinely consume between 100 and 200 mcg of clenbuterol daily so apoptosis is a distinct possibility in humans.

For some drugs and routes of administration extrapolating from animals to humans works better if one takes body surface area into account:

http://www.fda.gov/cber/gdlns/dose.htm

In the case of rats in this study with an average weight of 289 grams, one multiplies the toxic dose in mg/kg by 0.15 to arrive at the HED in mg/kg. Using this algorithm for necrosis we arrive at an HED of 1500 mcg for the 100 kg bodybuilder. This is still far outside the range of clenbuterol doses used by people, so again necrosis is not relevant in the human heart. However, scaling this way for apoptosis gives us an HED of 16 mcg for or 100 kg subject. So regardless of how we calculate HED, clen doses commonly used by humans are well within the apoptotic range.

Clenbuterol is a relatively specific beta 2 receptor agonist, but it does show some degree of beta 1 binding at high doses. In addition to acting directly on beta receptors, clenbuterol facilitates release of norepinephrine (NE) from sympathetic nerve terminals by stimulating pre-synaptic beta 2 adrenoreceptors. (Ephedrine acts in a similar manner, both directly and indirectly by inducing NE release.) To test the mechanism of clenbuterol’s apoptotic action, the authors administered reserpine to deplete the NE releasing capacity of the sympathetic nerve terminals. This resulted in a 68% reduction in apoptosis. Similarly, prior administration of bisoprolol, a selective beta 1 antagonist resulted in a 98% reduction in apoptosis. Based on the above observations the authors concluded that NE is primarily responsible for cardiac apoptosis due to clenbuterol. Note that after administrtion of a single dose of clenbuterol the authors observed apoptosis at 4 hours. The long elimination time of clenbuterol allows for the buildup of high concentrations in the heart (3).

In the soleus muscle, 10 mcg/kg of clenbuterol was the minimum dose that induced apoptosis. In the soleus only beta 2 blockade was capable of reducing apoptosis. This latter observation implies that while NE is responsible for the cardiac toxicity of clenbuterol, the drug is acting directly on beta 2 receptors in the soleus to induce apoptosis.

An interesting possibility is that the clenbuterol induced cardiac apoptosis might be a protective response gone awry to the cardiac hypertrophy that accompanies chronic beta receptor stimulation, since both cardiac apoptosis and hypertrophy occur in humans with long term use of beta agonists :

"Accumulating evidence suggests that chronic stimulation of ß-adrenergic receptor (ß-AR) in patients causes progressive cardiac dysfunction, cell loss, and cardiac chamber remodeling. Consistent with this notion, it has been demonstrated that stimulation of the ß-AR causes hypertrophy and apoptosis in cardiac myocytes" (4).

Under physiologic conditions where the heart is exposed to normal levels of NE a balance is struck between hypertrophy and apoptosis. ICER (inducible cAMP early repressor) is upregulated by cAMP (cyclic adenosine monophosphate), which in turn is upregulated by exposure to beta agonists like NE. ICER initiates signaling that ultimately leads to apoptosis, as depicted in the diagram below, adapted from (5).

Schematic representation of ICER-mediated feedback signaling, with ICER-mediated effects italicized.

Evidently under exposure to chronic supraphysiological levels of beta agonists ICER leads to deleterious levels of apoptosis while at the same time being unable to offset beta agonist induced hypertrophy. Hence the combination of apoptosis and hypertrophy mentioned in the quote above from (4).

Paraphrasing a passage from (2), the take home message for both cardiac patients and bodybuilders based on the research discussed here might be the following:

Clenbuterol has recently been used as an adjunct to the implantation of left ventricular assist devices (The Harefield Protocol) as a bridge to recovery and has been shown to aid the reverse remodelling of the myocardium. These patients also receive 'combination therapy' that includes beta 1-AR blockade. It is likely therefore, that in this case the heart will be protected from the myotoxic effects of clenbuterol, as explained above. However, their skeletal musculature will remain vulnerable to beta 2-AR-induced myocyte death. The potential additional loss of skeletal muscle bulk in already severely ill patients, together with the effects on their protein metabolism and exercise capacity, warrants further investigation before the use of clenbuterol becomes widely accepted as a standard therapeutic intervention. With regard to the illicit use of clenbuterol the philosophy of "the more you take, the greater the benefit" must engender a cause for concern.

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References

Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF. Myotoxic effects of clenbuterol in the rat heart and soleus muscle. J Appl Physiol. 2002 Nov;93(5):1824-32.

Burniston JG, Tan LB, Goldspink DF. {beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle. J Appl Physiol. 2004 Dec 10; [Epub ahead of print]

Soma LR, Uboh CE, Guan F, Luo Y, Teleis D, Runbo L, Birks EK, Tsang DS, Tissue distribution of clenbuterol in the horse. J Vet Pharmacol Therap 27: 91- 98, 2004

Tomita H, Nazmy M, Kajimoto K, Yehia G, Molina CA, Sadoshima J. Inducible cAMP early repressor (ICER) is a negative-feedback regulator of cardiac hypertrophy and an important mediator of cardiac myocyte apoptosis in response to beta-adrenergic receptor stimulation. Circ Res. 2003 Jul 11;93(1):12-22.

Sussman MA. ICER-capades: putting cardiac cyclic AMP signaling "on ice". Circ Res. 2003 Jul 11;93(1):6-8.

Melanotan 2 info

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MOLECULAR FORMULA : C50H69N15O9 MOLECULAR WEIGHT : 1024.2 CAS NO. : 121062-08-6

SEQUENCE: AC-NLE-ASP-HIS-D-PHE-ARG-TRP-LYS-NH2(CYCLIC 2-7)

DEVELOPED AT THE UNIVERSITY OF ARIZONA. FOR RESEARCH PURPOSES ONLY.

A PILOT PHASE I CLINICAL TRIAL CONDUCTED ON THREE MALES USING MT-2 BY THE COLLEGE OF MEDICINE, PHARMACOLOGY DEPARTMENT, UNIVERSITY OF ARIZONA IN TUCSON, ARIZONA PUBLISHED IN 1996 REPORTED THAT, "MT-2" HAS TANNING ACTIVITY IN HUMANS GIVEN ONLY 5 LOW DOSES EVERY OTHER DAY BY SUBCUTANEOUS INJECTION. ((MILD SIDE EFFECTS REPORTED INCLUDED SLIGHT NAUSEA AND INCREASED SPONTANEOUS PENILE ERECTIONS.

THE DEPARTMENT OF PHARMACOLOGY, UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE PUBLISHED A STUDY IN 1998 THAT INVOLVED TEN MEN WHO SUFFERED FROM PSYCHOGENIC ERECTILE DYSFUNCTION. THEIR TRIAL CONCLUDED THAT, "MELANOTAN-II IS A POTENT INITIATOR OF ERECTIONS IN MEN WITH PSYCHOGENIC ERECTILE DYSFUNCTION AND HAS MANAGEABLE SIDE EFFECTS AT A DOSE OF 0.025 MG./KG." [14]

A CLINICAL STUDY PUBLISHED IN 2000 OF 20 MEN WITH PSYCHOGENIC AND ORGANIC ERECTILE DYSFUNCTION CONDUCTED AT THE SECTION OF UROLOGY OF THE UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE CONCLUDED, "THAT MELANOTAN II IS A POTENT INITIATOR OF PENILE ERECTION IN MEN WITH ERECTILE DYSFUNCTION." [15]

AFTER SYNTHESIZING AND SCREENING HUNDREDS OF MOLECULES, THE RESEARCHERS HEADED BY DR. VICTOR HRUBY, FOUND A PEPTIDE THAT AFTER TRIALS AND TESTING SEEMED TO NOT ONLY BE SAFE BUT ALSO APPROXIMATELY 1,000 TIMES MORE POTENT THAN NATURAL Α-MSH. THEY DUBBED THIS NEW PEPTIDE MELANOTAN-II (MT-2). SINCE THEIR DISCOVERY, NUMEROUS STUDIES DATING BACK TO THE MID-1980S HAVE SHOWN NO OBVIOUS TOXIC EFFECTS OF MELANOTAN-2. BECAUSE SKIN CANCER (MELANOMA) TODAY IS A MAJOR HEALTH CONCERN, MELANOTAN II (MT-2) IS EXPECTED TO BE USED AS A DRUG TO COMBAT IT. MT-2 WILL DO THIS BY STIMULATING THE BODY'S NATURAL TANNING MECHANISM TO CREATE A TAN WITHOUT FIRST NEEDING EXPOSURE TO HARMFUL LEVELS OF UV RADIATION. THIS IN TURN WILL REDUCE THE POTENTIAL FOR SKIN DAMAGE THAT CAN EVENTUALLY LEAD TO SKIN CANCER.

MELANOTAN-II (MT-2) IS A CYCLIC HEPTAPEPTIDE ANALOG OF THE ALPHA-MELANOCYTE STIMULATING HORMONE (A-MSH), WITH THE FOLLOWING MOLECULAR STRUCTURE:

IT HAS BEEN DESCRIBED TO HAVE SUPERPOTENT MELANOTROPIC ACTIVITY IN VITRO. ITS EFFECT ON TANNING, LIKE THE EFFECT OF ITS SIMILAR PEPTIDE MELANOTAN I, WAS ALSO INVESTIGATED (DORR ET AL. 1996).

THE EFFECTS OF MELANOTAN II ON THE DIET AND FOOD INTAKE OF THE LABORATORY MICE HAVE ALSO BEEN INVESTIGATED. IT HAS BEEN DEMONSTRATED THAT THE CENTRAL MELANOCORTIN (MC) HAS BEEN ACTIVATED BY MELANOTAN II WHEN FED AND INDUCED IN THE MICE. THE SIX-DAY TREATMENT OF MT-2 HAS SHOWN THAT MELANOTAN II ACTUALLY REDUCED THE BODY WEIGHT AND THE ADIPOSE TISSUE IN THE VISCERA OF THE MICE AND SUPPRESSED THE CALORIC INTAKE OF THE ORGANISM. THIS HAS IMPLICATIONS IN CLINICAL APPLICATIONS OF THE POSSIBLE TREATMENT TO REDUCE CARBOHYDRATE OR CALORIE INTAKE ESPECIALLY FOR THE OVERWEIGHT AND THE OBESE. FURTHERMORE, THE SAME STUDY HAS ALSO DEMONSTRATED THAT THERE WAS A SUSTAINED INCREASE IN THE AVAILABLE OXYGEN CONSUMPTION IN OBESE ANIMALS. MELANOTAN II (MT-2) ALSO HELPED REDUCED THE LEVEL OF SERUM INSULIN AND THE CHOLESTEROL LEVELS WHEN COMPARED WITH THE CONTROL TREATMENTS. FURTHERMORE, IT HAS BEEN SUGGESTED THAT MELANOTAN ACTUALLY LOWERS THE LEVEL OF ACETYLCHOLINE A CABOXYLASE EXPRESSION AND EVEN PREVENTED THE REDUCTION OF CARNITINE AND PALMITOLTRANSFERASE I MRNA IN MUSCLE-TYPE TISSUES BY PAIR-FEEDING IN THE MUSCLES OF THE OBESE RATS. MOREOVER, THE MELANOTAN II ACTUALLY INCREASED THE FAT CATABOLISM IN THE MUSCLES AND EVEN IMPROVED THE CHOLESTEROL METABOLISM (LI ET AL. 2004).

ANOTHER STUDY THAT HAS IMPLICATIONS FOR CLINICAL APPLICATIONS IS THE TREATMENT OF MELANOTAN II (MT-2) AND ITS EFFECT ON SEXUAL STIMULATION AND MOTIVATION ALONG WITH ENHANCED ERECTIONS IN ANIMALS AND HUMANS. IN A STUDY CONDUCTED BY WESSELLS ET AL. (2000), THEY HAVE SHOWN THAT MELANOTAN II (MT-2) ACTUALLY INCREASED SEXUAL DESIRE AND EVEN CONCLUDED THAT MELANOTAN II (MT-2) IS A POTENT INITIATOR OF PENILE ERECTION IN MEN ESPECIALLY WITH THAT OF ERECTILE DYSFUNCTION.

OTHER CHEMICAL ACTIVITIES OF MELANOTAN II (MT-2) WHEN TESTED IN VIVO ARE INHIBITION OF FEEDING, SUPPRESSION OF NPY OREXIGENIC ACTION AND REDUCTION IN BASAL INSULINAEMIA (RAPOSINHO ET AL. 2003). 

MELANOTAN AND MELANOTAN II ARE BOTH ANALOGS OF THE PEPTIDE HORMONE ALPHA-MELANOCYTE STIMULATING HORMONE (Α-MSH) THAT TEND TO INDUCE SKIN TANNING. UNLIKE MELANOTAN THOUGH, MELANOTAN II (MT-2) HAS BEEN SHOWN TO HAVE THE ADDITIONAL EFFECT OF INCREASING LIBIDO. MELANOTAN II (MT-2) HAS BEEN SHOWN TO HAVE APHRODISIAC PROPERTIES.

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Cabergoline in solution tested against Tablet form.

Pharmacodynamics and relative bioavailability of cabergoline tablets vs solution in healthy volunteers.

Persiani S, Sassolas G, Piscitelli G, Bizollon CA, Poggesi I, Pianezzola E, Edwards DM, Strolin Benedetti M.

Source

Pharmacia-Farmitalia Carlo Erba R&D, Nerviano (MI), Italy.

Abstract

The effect of formulation on the urinary pharmacokinetics, pharmacodynamics, and relative bioavailability of cabergoline was investigated. Twelve healthy female volunteers, aged 23-35 years, were treated, according to an open, randomized, crossover design, with cabergoline (1-mg single oral dose) both as tablets and as a solution. The two administrations were separated by a 4-week wash-out period. Cabergoline and prolactin were measured in urine and plasma, respectively, by specific radioimmunoassays. Blood samples were collected before and up to 30 days after dosing. Urine was collected before and up to 8 days after dosing. Cabergoline elimination half-lives calculated from urinary data were 68 and 63 h after administration of the tablets and the solution, respectively. Urinary excretion of unchanged cabergoline accounted, on average, for 1.92% (range, 0.14-3.26) and 1.80% (range, 0.67-3.09) of the dose after administration of the tablets and the aqueous solution, respectively. Relative bioavailability of tablets vs solution was 99% (geometric mean with the 90% confidence intervals of 68-144%). Prolactin levels in 10 out of 12 subjects fell below the detection limit of the assay (1.5 micrograms/L) after both treatments. The mean maximum prolactin decrease (ca. 70%) was achieved by 2 or 3 h after dosing; the effect persisted up to 9 days, being completely exhausted 23-28 days after dosing. The analysis of variance performed on the pharmacodynamic effects of the two cabergoline formulations indicated that the percent decreases of plasma prolactin levels were not significantly different for tablets and solution. These results indicate that the pharmacodynamics and relative bioavailability of cabergoline are not influenced by formulation, as tablets or solution.

PMID: 7884663 [PubMed - indexed for MEDLINE]

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