Seractide

1. Diagnosis and Treatment of Endocrine Diseases

In endocrinology, the core application of seractide lies in the diagnosis of adrenocortical insufficiency and the treatment of related rare diseases. Featuring high specificity and rapid onset of action, it has become an essential tool in clinical diagnosis and treatment.For the diagnosis of adrenocortical insufficiency, it is used in the rapid ACTH stimulation test, which serves as the gold standard for differentiating primary from secondary adrenocortical insufficiency. The standard procedure involves intravenous injection of 250 μg it, followed by measurement of serum cortisol levels at 30 and 60 minutes respectively.

A normal physiological response is defined as a peak cortisol level ≥ 550 nmol/L; a level below this threshold indicates abnormal adrenocortical function. Patients with primary insufficiency (lesions of the adrenal gland itself) show a markedly abnormal response, while those with secondary insufficiency (pituitary or hypothalamic lesions) may present a delayed or mild response.

Compared with natural ACTH, it has higher purity and better stability, and is not interfered by endogenous ACTH. It can more accurately reflect the reserve function of the adrenal cortex and reduce diagnostic errors.

In the treatment of rare diseases, it is a first-line therapeutic agent for infantile spasms (West syndrome), especially suitable for hormone-sensitive children patients. Infantile spasms is a severe epileptic encephalopathy in infants and young children, characterized by frequent spasms often accompanied by hypsarrhythmia on electroencephalography. Delayed treatment will lead to intellectual developmental disorders. It promotes glucocorticoid secretion by the adrenal cortex through activating MC2R, and meanwhile acts directly on central nervous system MC1R and MC4R to inhibit abnormal neuronal discharge, achieving spasm control via dual mechanisms.

In addition, it can be used as adjuvant therapy for acute relapse of multiple sclerosis. It reduces central nervous system demyelination and edema by stimulating glucocorticoid secretion, and directly activates central MC4R to protect neurons, inhibit apoptosis and excitotoxicity, shorten recovery time after relapse, and lower the risk of disability progression. It also maintains therapeutic efficacy in some hormone-resistant patients.

2. Treatment of Autoimmune Diseases

With potent immunomodulatory properties, it exhibits satisfactory therapeutic effects in a variety of autoimmune diseases, especially for some refractory cases.

In the treatment of rheumatoid arthritis (RA), it exerts anti-inflammatory effects through dual mechanisms: on the one hand, it activates the hypothalamic-pituitary-adrenal (HPA) axis to promote glucocorticoid secretion and inhibit synovial hyperplasia and inflammatory reactions in joints.

On the other hand, it directly acts on immune cells such as macrophages and T lymphocytes, downregulates the expression of pro-inflammatory factors (IL-1β, TNF-α, IL-6) and upregulates the level of anti-inflammatory factor IL-10, thereby alleviating joint swelling, pain and morning stiffness, and reducing disease activity (DAS28 score).For systemic lupus erythematosus (SLE), seractide is mainly applied to refractory cases, particularly patients complicated with central nervous system or renal involvement. SLE is a multisystem autoimmune disease closely associated with autoantibody production and immune complex deposition.

The product inhibits B lymphocyte proliferation and autoantibody secretion, reduces the deposition of immune complexes in the kidneys and central nervous system, alleviates renal inflammation and proteinuria, protects central neurons, and improves neuropsychiatric symptoms.

Compared with traditional high-dose glucocorticoid therapy, it uses a lower dosage with a significantly lower incidence of adverse reactions. It can effectively reduce disease recurrence rate and improve patients' quality of life. Moreover, it has limited clinical applications in ankylosing spondylitis, systemic sclerosis and other autoimmune diseases, mainly serving as adjuvant anti-inflammatory therapy and immune balance regulation.

As a highly selective MC2R agonist, it is a commonly used tool drug in endocrinology and neuroscience research. Its high purity (≥98%), strong specificity and excellent stability make it an ideal choice for in vitro cell experiments and in vivo animal model studies.

In research on HPA axis functional regulation, it is applied to explore the regulatory mechanism of the pituitary-adrenal axis. It is used to stimulate adrenocortical cells in vitro to observe the pattern of glucocorticoid secretion and clarify the regulatory effect of ACTH on adrenocortical cell differentiation and steroid synthesis. In in vivo experiments, injection of it into animals can simulate HPA axis activation under stress, facilitating research on the correlation between stress response and immunity, metabolism as well as neural function.

In neuroscience research, it is used to analyze the physiological functions of melanocortin receptors (especially MC1R and MC4R). For instance, in studies on neuroprotective mechanisms, it is adopted to verify the role of the MC4R-mediated PI3K/Akt signaling pathway in neuronal protection. In research on appetite regulation and energy metabolism, central MC4R activation by it is used to observe changes in food intake and energy consumption in animals, exploring the regulatory role of melanocortin receptors in metabolic homeostasis. Additionally, it is applicable to adrenocortical cell culture and neuronal protection experiments, providing technical support for research on the pathogenesis of related diseases.

1. Neurodegenerative Diseases and Neuroprotection

Basic studies have demonstrated that it possesses prominent neuroprotective effects, showing promising potential for the treatment of Alzheimer's disease, Parkinson's disease, cerebral ischemia/stroke, spinal cord injury and other neurological disorders.

In cerebral ischemia/stroke research, it acts through a glucocorticoid-independent pathway. At a concentration of 200–400 nM, it can significantly protect rat forebrain neurons from apoptosis and excitotoxicity induced by glutamate, NMDA and hydrogen peroxide, reduce infarct volume and improve neurological function scores.

Its mechanism involves MC4R-mediated activation of the PI3K/Akt pathway, inhibition of oxidative stress and inflammatory factor release, and upregulation of brain-derived neurotrophic factor (BDNF) expression.

In Alzheimer's disease research, seractide alleviates Aβ amyloid deposition and excessive tau protein hyperphosphorylation in the brain, improving cognitive function in model animals. In Parkinson's disease models, it protects dopaminergic neurons, inhibits excessive microglial activation, and delays motor function decline.

In spinal cord injury research, it suppresses excessive astrocyte proliferation and glial scar formation, while promoting axonal regeneration and myelin repair to enhance motor and sensory functional recovery in experimental animals. At present, relevant research remains in the basic experimental stage, yet its multi-target neuroprotective properties offer a new direction for the comprehensive intervention of neurodegenerative diseases.