Hyperprolactinemia (HPRL)

Prolactin is produced exclusively by the lactotroph cells in the pituitary gland. Consequently, elevated levels of prolactin, known as hyperprolactinemia, are typically the result of conditions that lead to increased prolactin secretion from these lactotroph cells. At our company, we've brought together a team of highly experienced professionals who are well-versed in addressing the complexities of drug and therapy development for hyperprolactinemia.

Introduction to Hyperprolactinemia

Hyperprolactinemia, characterized by elevated levels of prolactin in the blood, affects approximately 0.4% of the general adult population, with higher prevalence rates observed in women. The condition can result from various causes, including pituitary tumors (prolactinomas), medications, and hypothyroidism. Hyperprolactinemia may lead to symptoms such as galactorrhea, menstrual disturbances, and infertility in women, and hypogonadism and erectile dysfunction in men.

Pathophysiology of Hyperprolactinemia

Fig. 1 Model of mechanisms of hyperprolactinaemia-induced anovulatory infertility. (Bernard, V., et al., 2015)

The pathophysiology of hyperprolactinemia includes multiple factors. Elevated prolactin levels inhibit the secretion of gonadotropin-releasing hormone (GnRH), leading to reduced levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which result in anovulation and infertility. This inhibition is primarily mediated through the decreased secretion of kisspeptin-1, a crucial regulator of GnRH neurons.

Additionally, hyperprolactinemia can directly affect other GnRH-related neurons and non-neural factors, further impacting GnRH secretion. Genetic factors also play a significant role, such as loss-of-function mutations in the PRLR gene leading to inactivation of the prolactin receptor, thereby disrupting normal prolactin function.

Biomarker Development of Hyperprolactinemia

Research has found that certain proteins, such as cytokines and transcription factors, are abnormal in individuals with hyperprolactinemia. These proteins may be involved in the regulation of prolactin and could serve as new biomarkers.

Prolactin (PRL)

Prolactin itself is the primary marker of hyperprolactinemia, it is also an important indicator for assessing disease severity and therapy response.

Thyroid-Stimulating Hormone (TSH)

Abnormal levels of TSH may be associated with hyperprolactinemia, especially in cases where hypothyroidism is the cause of the elevated prolactin levels.

Insulin-Like Growth Factor 1 (IGF-1)

IGF-1 often shows abnormalities when prolactin levels are elevated, particularly in individuals with prolactinomas, where changes in IGF-1 levels may be related to the presence and activity of the tumor.

Therapeutics Development of Hyperprolactinemia

Small molecule drugs have been the cornerstone of hyperprolactinemia therapy. These drugs primarily target dopamine receptors to inhibit prolactin secretion from the pituitary gland.

Cabergoline: A long-acting dopamine D2 receptor agonist, cabergoline is highly effective in reducing prolactin levels. It has a favorable side effect profile and requires less frequent dosing compared to other agents.
Bromocriptine: An older dopamine agonist, bromocriptine is still widely used. It binds to dopamine D2 receptors, decreasing prolactin secretion. However, it often requires multiple daily doses and is associated with more side effects than cabergoline.
Quinagolide: Another dopamine agonist, particularly used in individuals who do not respond to or tolerate cabergoline or bromocriptine. Quinagolide binds to dopamine D2 receptors with high affinity.

Our Services

Our company adopts a collaborative approach, partnering closely with clients to create tailored and innovative therapy strategies for Hyperprolactinemia. Our focus on customized strategies ensures that we meet your individual needs with the highest level of support and guidance.

Platforms of Hyperprolactinemia Therapy Development

Animal Models of Hyperprolactinemia

We have considerable expertise in developing and employing animal models that accurately replicate the disease characteristics and therapeutic responses seen in Hyperprolactinemia. These models are instrumental in investigating the underlying mechanisms and assessing the safety and effectiveness of prospective therapies with precision.

Non-Genetically Engineering Models

They are biological systems used in research that do not involve the manipulation or alteration of an organism's genetic material.

Optional Models: Estrogen-induced Hyperprolactinemia Model; Dopamine Antagonist-induced Hyperprolactinemia Model

Genetically Engineering Models

Genetically engineering models involve the manipulation of genetic material to study specific disease mechanisms and therapeutic interventions.

Optional Models: Prolactin-overexpressing Transgenic Mice Model; Dopamine-related Knockout Mice Model

Moreover, we provide a variety of detailed animal model services focused on particular signaling pathways and molecular targets.

If you are interested in our services, please don't hesitate to contact us.

References

Bernard, V., et al., "New insights in prolactin: pathological implications." Nat Rev Endocrinol, (2015). 11(5): p. 265-275.
Capozzi, A., et al., "Hyperprolactinemia: pathophysiology and therapeutic approach." Gynecol Endocrinol, (2015). 31(7): p. 506-510.

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

Related Disease Solutions