Synonym |
ACTH, Adrenocorticotropic Hormone |
Species |
Monkey, Human |
Protein Accession |
P01193, Pomc_Human |
Purity |
≥ 95% |
Endotoxin Level |
< 1.0 EU per 1 μg of the protein |
Biological Activity |
The ED50 for this effect is typically 2-10 ng/mL |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
2705 Da |
Formulation |
Lyophilized from a 0.2 μm filtered solution of 20% acetonitrile and 0.1% trifluoroacetic acid in
water |
Reconstitution |
Centrifuge the vial prior to opening. Reconstitute in sterile distilled water or aqueous buffer
containing 0.1% BSA to a concentration of 0.1-1.0 mg/mL. |
Storage & Stability |
Store lyophilized protein at -20°C. Aliquot the product after reconstitution to avoid repeated
freezing/thawing cycles. Reconstituted protein can be stored at 4°C for a limited period of
time. |
FAQ
What is β-MSH and how does it work in the body?
β-MSH, or Beta-Melanocyte-Stimulating Hormone, is
a peptide hormone that originates from the pro-opiomelanocortin (POMC) precursor, primarily produced in
the pituitary gland. Its primary function is related to the regulation of energy homeostasis and
appetite control. In the context of monkeys and humans, it plays a critical role in the stimulation of
melanocytes, cells that produce the pigment melanin. Melanin is key to protecting the skin against UV
radiation and also affects the coloration of skin, hair, and eyes. Beyond its role in pigmentation,
β-MSH has been implicated in various metabolic processes, including the regulation of energy balance and
lipid metabolism. It binds to melanocortin receptors, particularly MC3R and MC4R, which are
predominantly expressed in the central nervous system but also found in other tissues. Activation of
these receptors has been shown to reduce appetite and increase energy expenditure, making it a molecular
target of interest in the study of obesity and metabolic disorders. Additionally, β-MSH is involved in
the modulation of the immune response, anti-inflammatory processes, and possibly even behavioral
responses. Though not as extensively studied as its relatives, such as alpha-MSH, β-MSH still presents a
significant biological interest due to its comparable functions and potential therapeutic applications
in conditions where modulation of melanocortin receptors could be beneficial.
How does β-MSH
(5-22) differ from the full-length β-MSH in functionality and application?
β-MSH (5-22) refers to
a specific active fragment of the full-length β-MSH molecule, which consists of its amino acid sequence
from positions 5 to 22. This specific segment retains the core activity of the hormone as it includes
the key residues necessary for binding to melanocortin receptors. However, the truncated version has a
distinct functionality and application profile compared to the full-length molecule. The removal of
certain terminal residues can enhance the stability and receptor specificity of β-MSH (5-22),
potentially making it a more potent and targeted agent in research or therapeutic applications. The
smaller fragment may demonstrate increased stability under physiological conditions, which can be
advantageous for applications requiring prolonged activity or reduced degradation in biological systems.
Furthermore, the specificity of β-MSH (5-22) enables more precise interaction with specific melanocortin
receptors, which is particularly beneficial in research studies aiming to delineate the distinct roles
of various melanocortin receptors. This specificity can help in identifying new therapeutic targets and
the development of drugs with minimized off-target effects. Additionally, the use of peptide fragments
like β-MSH (5-22) allows for the exploration of novel delivery mechanisms. Due to their smaller size and
specific configurations, they offer enhanced permeability and reduced immunogenicity, critical factors
in drug design and therapeutic delivery systems. As a result, β-MSH (5-22) serves as a promising tool in
both experimental and applied contexts, fostering a deeper understanding of β-MSH's biological roles and
its potential implications in treating metabolic and dermatological disorders.
What research has
been conducted on β-MSH's role in obesity and metabolism?
Research concerning β-MSH's role in
obesity and metabolism has focused extensively on its interaction with melanocortin receptors,
particularly MC3R and MC4R. These receptors are integral to the regulation of appetite and energy
balance. Studies have demonstrated that β-MSH, through melanocortin pathways, plays a critical role in
appetite suppression and the modulation of energy expenditure. Animal models, particularly rodents and
primates, have been used to elucidate the mechanisms by which β-MSH influences feeding behaviors and
body weight regulation. For instance, experiments have indicated that β-MSH administration can lead to
reduced food intake and decreased body weight, suggesting its potential for therapeutic application in
obesity treatment. Additionally, genetic studies in humans have identified mutations in MC4R as a common
cause of monogenic obesity, thus highlighting the receptor’s critical influence in energy homeostasis
and further supporting β-MSH's significance in managing metabolic conditions. β-MSH has also shown
potential in influencing glucose metabolism, thereby offering possible benefits in mitigating conditions
like diabetes. Moreover, ongoing research delves into how β-MSH, often acting in concert with other
hormones like leptin and insulin, orchestrates complex neuroendocrine responses to maintain energy
equilibrium. Clinical research efforts strive to translate these findings into effective weight
management therapies and to design drugs that can harness β-MSH's properties to modulate metabolic
functions safely. As scientific understanding advances, β-MSH continues to stand out as a promising
candidate in addressing metabolic disorders across varied patient populations, reinforcing the need for
ongoing exploration into its therapeutic possibilities.
In what ways might β-MSH contribute to
treatments for skin disorders or conditions?
β-MSH, given its intrinsic role in melanogenesis,
holds substantial promise in the treatment of various skin disorders. The mechanism through which β-MSH
exerts its effects is primarily via stimulation of melanocytes to produce melanin, the pigment
responsible for the coloration of skin, hair, and eyes. This capability is foundational in treating
conditions characterized by hypopigmentation, such as vitiligo. β-MSH could potentially restore pigment
to affected areas, thereby offering a therapeutic pathway significantly different from current
treatments, which may include steroids or phototherapy. In addition to its role in pigmentation, there
is evidence to suggest that β-MSH possesses anti-inflammatory properties, making it a potential
candidate for treating inflammatory skin conditions like psoriasis or eczema. By influencing immune
responses and reducing inflammation, β-MSH could help alleviate symptoms such as itching, redness, and
swelling. Furthermore, β-MSH's interaction with MC1R, a receptor found in skin cells, proposes
additional mechanisms by which it may confer protective effects against ultraviolet (UV) radiation. By
enhancing melanin production, β-MSH augments the skin’s natural defense against UV damage, thus
potentially mitigating the risk of skin cancer development. Current research is investigating peptide
analogs of β-MSH to maximize these beneficial effects while minimizing systemic activity, aiming to
develop topical formulations that could be directly applied to the skin. These advancements are crucial
in targeting specific skin conditions effectively with reduced side-effects. Thus, β-MSH presents a
multifaceted potential in dermatological therapies, promoting not only cosmetic benefits but also
enhancing the skin's intrinsic health and resilience against external aggressors.
How does the
use of β-MSH in research help in understanding neurological conditions?
The utilization of β-MSH
in research has opened new avenues for understanding neurological conditions, particularly those related
to energy balance, appetite control, and behavior. β-MSH interacts with melanocortin receptors in the
central nervous system, making it pivotal in regulating neurological pathways that govern feeding
behavior and energy metabolism. By examining these interactions, researchers gain insights into
conditions such as obesity, anorexia, and metabolic syndromes that are further tied to neurological
processes. For instance, dysregulation in melanocortin signaling has been linked with alterations in
mood and behavior, indicating a role for β-MSH in neuropsychiatric disorders. Ongoing studies focus on
the potential of β-MSH to modulate synaptic transmission and plasticity, processes crucial for learning
and memory, and thus hold implications in neurodegenerative diseases like Alzheimer's. Additionally,
β-MSH's impact on inflammation and neuroprotection presents it as a candidate for investigation in the
context of neurological disorders characterized by an inflammatory component, such as multiple
sclerosis. In laboratory settings, knocking out or modifying melanocortin receptors provides valuable
models for understanding the pathophysiology of these conditions and opens pathways for developing
targeted therapies. Moreover, by exploring the role of β-MSH and its receptors beyond traditional
metabolic pathways, researchers can identify novel therapeutic targets that could ameliorate or
potentially reverse brain-related diseases. These studies underline the complex interaction between
hormones like β-MSH and neurochemical pathways, showcasing β-MSH's value not just in metabolic health
but as an exploratory tool in deciphering the intricacies of neurological disorders. Thus, β-MSH serves
as a crucial link in integrative research approaches, merging endocrinology and neuroscience for
holistic understanding and treatment development.
What safety considerations should be considered
with β-MSH research or therapy?
When considering β-MSH for research or therapeutic use,
comprehensive safety evaluations are paramount. β-MSH, like any bioactive peptide, can have systemic
effects, thus necessitating careful examination of its therapeutic window and potential for adverse
effects. One primary concern is the possibility of off-target activity, given the presence of multiple
melanocortin receptors in various tissues. Ensuring that β-MSH or its analogs interact specifically with
intended receptor subtypes is crucial to minimizing unintended physiological responses. Developing
receptor-specific analogs and delivery mechanisms can mitigate such risks. Additionally, the
immunogenicity of peptide-based therapies needs to be assessed, as immune reactions could lead to
diminished efficacy or hypersensitivity. In this context, modifying peptide structures to enhance
stability and reduce immunogenic potential is an active area of research. Another core concern involves
the long-term effects of β-MSH therapies, especially if used for chronic conditions. Chronic stimulation
of melanocortin pathways might lead to desensitization or down-regulation of receptors, possibly
negating therapeutic benefits or necessitating dose adjustments over time. Researchers must also
consider β-MSH’s impact on pigmentation, as its potent melanogenic effects could pose cosmetic or
skin-related concerns in therapies not involving skin-based conditions. Such aspects necessitate
detailed dermatological evaluations during clinical trials. Furthermore, in the framework of safety
pharmacology, comprehensive toxicological tests, including chronic toxicity, genetic toxicology, and
potential impacts on reproductive health, should be undertaken. Lastly, ethical considerations must
guide the use of β-MSH in experimental settings, prioritizing informed consent and the welfare of study
participants, whether human or animal. Addressing these safety considerations ensures that β-MSH can
transition from promising research findings to safe, effective clinical applications, maximizing its
therapeutic potential while minimizing risks.