Lecirelin is a somatostatin analogue composed of 14 amino acids, including a circular structure formed by disulfide bonds connecting 6 amino acids (Cys Thr Lys Thr Phe Thr Cys), with 4 amino acids (Val Gly Leu Gln) extending from the ring. This unique cyclic and linear binding structure gives it a relatively stable conformation, which facilitates specific binding to somatostatin receptors. CAS 61012-19-9, Molecular formula C59H84N16O12. Usually soluble in water, physiological saline, or suitable buffer solutions. When dissolving, gently stir or shake to promote dissolution, but avoid vigorous stirring or ultrasonic treatment to avoid damaging its structure. Generally, it should be stored in a low temperature environment of 2-8 ℃, avoiding light and moisture. If it is a dissolved solution, it should be used as soon as possible. If it needs to be stored, it can be packaged and stored below -20 ℃ to avoid repeated freezing and thawing
Our product Form
Lecirelin COA
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| Certificate of Analysis | ||
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| Grade | Pharmaceutical grade | |
| CAS No. | 61012-19-9 | |
| Quantity | 60g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090053 | |
| MFG | Jan 9th 2025 | |
| EXP | Jan 8th 2028 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.45% |
| Loss on drying | ≤1.0% | 0.53% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.90% |
| Single impurity | <0.8% | 0.25% |
| Total microbial count | ≤750cfu/g | 80 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 400ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
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Lecirelin is an artificially synthesized octapeptide analogue of somatostatin, which exhibits unique therapeutic effects in the treatment of various diseases by simulating the mechanism of action of natural somatostatin.
Acromegaly
Acromegaly, as a chronic disease caused by excessive secretion of growth hormone (GH) by pituitary growth hormone (GH) adenomas, is closely related to the abnormal proliferation and hyperfunction of pituitary tumor cells in its pathogenesis. During the development of the disease, excessive growth hormone can act on multiple tissues and organs throughout the body, leading to a series of typical clinical manifestations. Patients often experience enlarged hands and feet, enlarged and clumsy fingers and toes, and difficulty wearing shoes and gloves; The facial features can also undergo significant changes, such as a raised forehead, deepened nasolabial folds, protruding jaw, and sparse teeth, which seriously affect the patient's appearance.
In addition, joint pain is also a common symptom. Due to the impact of growth hormone on the metabolism of joint cartilage and bone tissue, joint cartilage wear and bone hyperplasia can occur, leading to joint pain and limited mobility. Enlargement of internal organs should not be ignored. Important organs such as the heart, liver, and kidneys may enlarge due to the stimulation of growth hormone, which may affect their normal function and increase the risk of complications such as cardiovascular disease and respiratory system diseases.
This product occupies an important position as a first-line drug in the treatment of acromegaly, especially suitable for the following situations:
Postoperative residual or recurrence:
Pituitary tumor resection is one of the commonly used methods for treating acromegaly. However, some patients may not be able to completely remove pituitary growth hormone adenomas after surgery, resulting in serum growth hormone (GH) levels not reaching normal standards. At this point, it played a crucial role. It can specifically act on the anterior pituitary gland and tightly bind to the somatostatin receptor (SSTR2/SSTR5). This combination is like a precise key that opens the door to inhibiting the secretion of growth hormone, directly suppressing the synthesis and release process of growth hormone.
Meanwhile, it can also reduce the production of insulin-like growth factor-1 (IGF-1) in the liver. IGF-1 is an important mediator for the downstream effects of growth hormone, and a decrease in its level can effectively block the excessive stimulation of growth hormone on tissues throughout the body. Research has shown that after 12 months of standardized treatment with product, the proportion of patients with serum GH levels below 1 μ g/L can reach 56%, and the proportion of patients with IGF-1 levels returning to the normal range can reach 68%. This fully demonstrates the significant efficacy of product in controlling hormone levels in patients with residual or recurrent acromegaly after surgery.
Preoperative preparation:
For some cases of acromegaly with large tumor volume or strong invasiveness, direct surgery often faces significant difficulties and risks. A large tumor volume may compress important nerve and vascular structures around it, increasing the risk of surgical injury; Strong invasiveness means that the boundary between the tumor and surrounding tissues is unclear, making it difficult to completely remove. In this case, preoperative pre-treatment with lecirelin has become a wise choice. Acetate lanreotide can regulate the growth environment of tumor cells and slow down their proliferation rate by inhibiting the secretion of growth hormone. Long term use can also induce apoptosis of tumor cells, leading to a gradual reduction in tumor volume. This not only creates more favorable conditions for surgery, reduces the difficulty of surgery, but also reduces damage to surrounding tissues during the surgical process, improving the success rate and safety of surgery.
Radiotherapy is another important treatment method for acromegaly, but its onset time is relatively slow lecirelin:, usually taking several months or even years to observe significant therapeutic effects. During this long transition period of radiotherapy, the patient's condition may continue to progress and various symptoms may worsen. It can quickly exert its effect and effectively control patients' symptoms during the period before radiotherapy takes effect. It can rapidly reduce the levels of growth hormone and IGF-1 in serum, alleviate symptoms such as hand and foot hypertrophy and joint pain, prevent further deterioration of the condition, buy time for radiotherapy, and improve overall treatment effectiveness.
The mechanism of action of lanrelitide acetate in the treatment of acromegaly is multifaceted:
Inhibition of GH secretion:
After binding to the anterior pituitary somatostatin receptor (SSTR2/SSTR5), acetic acid lanrelitide triggers a series of changes in intracellular signaling pathways. The changes in these signaling pathways can inhibit the transcription and translation processes of growth hormone genes, thereby directly reducing the synthesis of growth hormone. At the same time, it also affects the release process of growth hormone, preventing it from being released from pituitary cells into the bloodstream, thereby reducing the level of growth hormone in the serum.
Lowering IGF-1 levels:
Growth hormone primarily exerts its biological effects by stimulating the synthesis and secretion of insulin-like growth factor-1 (IGF-1) in the liver. Acetate lanreotide reduces the stimulating effect of growth hormone on the liver by inhibiting the secretion of growth hormone, thereby reducing the production of IGF-1 in the liver. In addition, it may directly act on liver cells, affecting the expression and synthesis process of IGF-1 gene, further reducing the level of IGF-1 in serum, and blocking the downstream effects of growth hormone.
Reducing tumor volume:
When used for long-term treatment of acromegaly, it can induce tumor cell apoptosis through various pathways. On the one hand, it can regulate the expression of apoptosis related genes in tumor cells, promote the activation of apoptosis signaling pathways, and enable tumor cells to actively enter the apoptosis program. On the other hand, it can also affect the nutritional supply and metabolic environment of tumor cells, leading to deterioration of their survival conditions and inducing cell apoptosis. Research shows that after long-term treatment, the median shrinkage rate of tumors can reach 30% -50%, which provides important guarantees for improving patients' condition and prognosis.
Gastrointestinal pancreatic neuroendocrine tumors (GEP NETs)
Gastrointestinal pancreatic neuroendocrine tumors (GEP NETs) are a group of heterogeneous tumors originating from the gastrointestinal tract and pancreas, with unique biological behaviors and clinical features. These types of tumors often secrete multiple hormones, which enter the bloodstream and have wide-ranging effects on multiple systems and organs throughout the body, leading to the occurrence of carcinoid syndrome. The typical symptoms of carcinoid syndrome include flushing, diarrhea, bronchospasm, etc. Redness is manifested as sudden redness and fever of the skin on the face, neck, and upper chest, which can last for several minutes to several hours; Diarrhea may be more severe, leading to dehydration, electrolyte imbalance, and malnutrition in patients; Bronchial spasm can cause symptoms such as difficulty breathing and wheezing, seriously affecting the quality of life of patients.
It is the standard treatment drug for advanced gastrointestinal, pancreatic, neuroendocrine tumors and plays an important therapeutic role in various situations:
Unresectable high/moderately differentiated tumors:
For some patients with advanced and unresectable high/moderately differentiated gastrointestinal, pancreatic, neuroendocrine tumors, the main goal of treatment is to prolong their progression free survival (PFS) and improve their quality of life. It exerts anti-tumor effects through multiple mechanisms. It can bind to the somatostatin receptors (SSTR2/SSTR5) on the surface of tumor cells, mediate cell cycle arrest, and keep tumor cells at specific cell cycle stages, preventing them from continuing to proliferate and divide. Meanwhile, it can also induce apoptosis of tumor cells and promote their death. In addition, lanreotide acetate also has anti angiogenic effects, as it can downregulate the expression of vascular endothelial growth factor (VEGF).
VEGF is a key factor in promoting tumor angiogenesis, and its decreased expression reduces the formation of tumor blood vessels, thereby cutting off the nutritional supply and metabolic waste excretion pathways of tumors, inhibiting tumor growth and metastasis. The Phase III CLARINET study is an important clinical trial that showed a median progression free survival of 32.8 months in the group of patients treated with lecirelin , while the median progression free survival of the group treated with placebo was only 18.0 months. The difference between the two groups is highly statistically significant (HR=0.47, P<0.001), which fully demonstrates the significant advantage of lanrelitide acetate in prolonging progression free survival in patients with unresectable high/moderately differentiated gastrointestinal and pancreatic neuroendocrine tumors.
Cancer like syndrome control:
The symptoms of cancer like syndrome seriously affect the quality of life of patients, and effective control of these symptoms is crucial for improving the survival status of patients. The control effect on symptoms related to carcinoid syndrome is significant, with a control rate of over 80% for symptoms such as diarrhea and flushing. It reduces the levels of hormones such as serotonin and bradykinin that cause cancer like syndrome by inhibiting tumor cell secretion, thereby alleviating symptoms such as flushing and diarrhea. After treatment with product, patients can significantly feel a reduction in symptoms, a significant improvement in their quality of life, and are able to better engage in daily activities and social interactions.
Functional tumors:
Gastrointestinal pancreatic neuroendocrine tumors also include some functional tumors, such as insulinoma, gastrinoma, etc. Insulin tumors can secrete insulin excessively, causing patients to experience symptoms of hypoglycemia such as palpitations, hand tremors, sweating, hunger, and even coma in severe cases. Gastrinoma secretes a large amount of gastrin, which stimulates an increase in gastric acid secretion and causes peptic ulcers, leading to symptoms such as abdominal pain, bloating, nausea, and vomiting. It can inhibit the excessive secretion of hormones by these functional tumor cells, thereby alleviating complications such as hypoglycemia and peptic ulcers. For patients with insulinoma, lanreotide acetate can reduce insulin secretion, maintain normal blood glucose levels, and reduce the frequency and severity of hypoglycemic episodes; For patients with gastrinoma, it can reduce the level of gastrin, decrease gastric acid secretion, promote the healing of peptic ulcers, and alleviate symptoms such as abdominal pain.
The anti-tumor mechanisms for treating gastrointestinal, pancreatic, neuroendocrine tumors mainly include the following aspects:
Inhibition of cell proliferation:
After binding to the somatostatin receptor (SSTR2/SSTR5) on the surface of tumor cells, it activates a series of signaling pathways within the cell, which regulate the expression and activity of cell cycle related proteins, keeping tumor cells in the G1 or S phase and preventing them from entering the next cell cycle stage, thereby inhibiting tumor cell proliferation and division. At the same time, it can also induce apoptosis in tumor cells, promoting programmed cell death by activating apoptosis related signaling pathways such as the mitochondrial pathway and death receptor pathway.
Anti angiogenesis:
The growth and metastasis of tumors depend on the formation of new blood vessels, and vascular endothelial growth factor (VEGF) is a key factor in promoting tumor angiogenesis. It can downregulate the expression of VEGF in tumor cells and vascular endothelial cells, reducing the synthesis and secretion of VEGF. At the same time, it can also inhibit the binding of VEGF to its receptors, block the transmission of VEGF signaling pathway, thereby inhibiting the proliferation, migration, and lumen formation of vascular endothelial cells, reducing the generation of tumor blood vessels, cutting off the nutritional supply and metabolic waste excretion pathways of tumors, and inhibiting tumor growth and metastasis.
Regulating the immune microenvironment:
The occurrence and development of tumors are closely related to the functional status of the body's immune system. It can regulate the tumor immune microenvironment and enhance the activity of natural killer (NK) cells. NK cells are important effector cells in the body's immune system, capable of recognizing and killing tumor cells. Lecirelin promotes the proliferation, activation, and cytokine secretion of NK cells, enhancing their ability to recognize and kill tumor cells, promoting tumor immune surveillance function, enhancing the body's anti-tumor immune response, and thereby inhibiting tumor growth and metastasis.
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