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Hyperparathyroidism

Hyperparathyroidism is a condition characterized by overactivity of the parathyroid glands, leading to excessive production of parathyroid hormone (PTH). Our company excels in rare diseases like hyperparathyroidism by offering unparalleled one-stop services tailored to researchers and scientists dedicated to this field.

Overview of Hyperparathyroidism

Hyperparathyroidism is characterized by abnormal calcium and phosphorus metabolism caused by excessive secretion of PTH. The excessive secretion of PTH in hyperparathyroidism sets forth a cascade of events that disrupt the balance of calcium regulation in the body. When the parathyroid glands produce too much PTH, it can precipitate elevated calcium levels in the bloodstream, a condition known as hypercalcemia, ushering in a plethora of symptoms and potential complications for the afflicted individuals.

Synthesis and secretion of PTH.Fig.1 Decreased ionized calcium levels inhibit CaSR, stimulating PTH synthesis and secretion. (Lemoine, S., et al., 2022)

Pathogenesis of Hyperparathyroidism

The taxonomy of hyperparathyroidism delineates primary, secondary, and tertiary types, each with its unique etiological footprint.

  • Primary hyperparathyroidism (PHPT), is often triggered by the presence of a parathyroid adenoma on one of the parathyroid glands. Which can also arise from the hyperplasia of multiple parathyroid glands. This condition incidence rate ranges from 0.4 to 82 cases per 100,000 individuals.
  • Secondary hyperparathyroidism (SHPT), is frequently observed in individuals with chronic kidney disease or vitamin D deficiency. In response to low calcium levels in the body, the parathyroid glands become overactive, leading to the secretion of increased levels of PTH.
  • Tertiary hyperparathyroidism (THPT), is a consequence of long-term overstimulation of the parathyroid glands, leading to the development of nodules within the glands. It is characterized by the compensatory hyperfunction of the parathyroid glands in response to excessive PTH secretion.
Calcium homeostasis.Fig.2 The role of the kidneys in calcium homeostasis. (Lemoine, S., et al., 2022)

Therapeutics Development of Hyperparathyroidism

Types Drug Names Mechanism of Action Targets Research Phase
Phosphorus binders Calcium carbonate Inhibit the secretion of PTH / Approved
PA21 Relieve hyperphosphatemia and significantly decrease PTH levels Phosphates Phase III trials
Vitamin D and analogs Paricalcitol Combines with vitamin D receptors VDR Approved
DP001(2MD) Inhibit PTH synthesis and secretion VDR Phase II trials
Calcimimetics Cinacalcet Combines with the calcium-sensing receptors to inhibit PTH secretion CaSR Approved
Etelcalcetide Reduce levels of fibroblast growth factor 23 CaSR Approved
Monoclonal antibody Denosumab RANKL inhibitor RANKL Clinical research
Photodynamic therapy 5-aminolevulinic acid Destroy the parathyroid gland tissue / Preclinical research

Our Services

From cutting-edge laboratory facilities to expert consultancy services, we ensure that our clients have access to all the resources they need. Our animal model and therapeutic development platform, enable researchers and scientists to advance knowledge and therapeutics for rare diseases, ultimately driving progress in the field.

Therapeutics Development Platforms

Animal Models of Hyperparathyroidism

Animal models are crucial in studying diseases like hyperparathyroidism to understand underlying mechanisms and test potential therapeutics. Our company provides you with various animal models to help you gain a comprehensive understanding of hyperparathyroidism.

Diet-induced models.

Diet-induced Models

Diet-induced models of hyperparathyroidism involve manipulating the diet to induce changes in calcium and phosphorus metabolism, mimicking aspects of the disease.

Optional Models: High-phosphate diet induced model, etc.

Genetically engineered models.

Genetically Engineered Models

Genetic engineering animal models of hyperparathyroidism involve manipulating specific genes associated with calcium regulation to induce the disease.

Optional Models: Cdkn1btm1Mlf model; Pthtm1Dgo model; Men1tm1.1Ctre model, etc.

With a deep understanding of the complexities surrounding rare diseases, we provide a comprehensive suite of solutions including pharmacokinetic studies and drug safety evaluations. If you are interested in our service, do not hesitate to reach out to us for additional insights and detailed quotations about the specialized services we provide.

References

  • Lemoine, Sandrine et al. "Calcium homeostasis and hyperparathyroidism: Nephrologic and endocrinologic points of view." Annales d'endocrinologie 83.4 (2022): 237-243.
  • Minisola, Salvatore et al. "Epidemiology, Pathophysiology, and Genetics of Primary Hyperparathyroidism." Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 37.11 (2022): 2315-2329.
  • Zhang, Li-Xi et al. "Advances in the treatment of secondary and tertiary hyperparathyroidism." Frontiers in endocrinology 13 (2022): 1059828.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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