IMULAN BioTherapeutics, LLC, headquartered in St. Joseph, Missouri, at the Kit Bond Life Science Incubator associated with Missouri Western State University. IMULAN is a veterinary immunobiology company developing a range of immune based therapies for veterinary medicine. IMULAN BioTherapeutics, LLC has several divisions related to immuno-biology and comparative medicine. IMULAN Clinical Trials, a clinical trial division of IMULAN BioTherapeutics, conducts a variety of comparative disease trials in oncology, asthma, sepsis, cardiology, and virology. In 2009, IMULAN started Veterinary Cancer Therapeutics, to develop new immunological approaches to cancer. [edit] Technologies [edit] Technologies in Development - Immune Selective Anti-Inflammatory Derivatives imsaids - small peptides which regulate granulocyte function, modulate neutrophil chemotaxis and activation, reduce the production of reactive oxygen species, and reduce the effects of endotoxin.[5]. Immune Selective Anti-Inflammatory Derivatives (ImSAIDs) are a class of peptides discovered to have diverse biological properties, including remarkable anti-inflammatory properties. ImSAIDs work by altering the activation and migration of inflammatory cells, which are immune cells responsible for amplifying the inflammatory response[6],[7]. The ImSAIDs represent a new category of anti-inflammatory and are unrelated to steroid hormones or non steroidal anti-inflammatories. The ImSAIDs were discovered by scientists evaluating biological properties of the submandibular gland and saliva. Early work in this area demonstrated that the submandibular gland released a host of factors which regulate systemic inflammatory responses and modulate systemic immune and inflammatory reactions. It is now well accepted that a the immune, nervous and endocrine systems communicate and interact to control and modulate inflammation and tissue repair. One of the neuroendocrine pathways, when activated, results in the release of immune regulating peptides from the submandibular gland upon neuronal stimulation from sympathetic nerves. This pathway or communication is referred to as the cervical sympathetic trunk-submandibular gland (CST-SMG) axis, an regulatory system that plays a role in the systemic control of inflammation[8]. Early work in identifying factors that played a role in the CST-SMG axis lead to the discovery of a seven amino acid peptide, called the submandibular gland peptide-T. SGP-T was demonstrated to have biological activity and thermoregulatory properties related to endotoxin exposure[9]. SGP-T, an isolate of the submandibular gland, demonstrated its immunoregulatory properties and potential role in modulating the cervical sympathetic trunk-submandibular gland (CST-SMG) axis, and subsequently was shown to play an important role in the control of inflammation. One SGP-T derivative is a three amino acid sequence shown to be a potent anti-inflammatory molecule with systemic effects. This three amino acid peptide is phenylalanine-glutamine-glycine (FEG) and its D-isomeric form (feG), have become the foundation for the ImSAID category[10]. Cellular Effects of feG: The cellular effects of the ImSAIDs are characterized in a number of publications. feG and related peptides are known to modulate leukocyte (white blood cells) activity by influencing cell surface receptors to inhibit excessive activation and tissue infiltration. One lead ImSAID, the tripeptide FEG (Phe-Glu-Gly) and its D-isomer feG are known to alter leukocyte adhesion involving actions on αMβ2 integrin ,and inhibit the binding of CD16b (FCyRIII) antibody to human neutrophils [11]. feG has also been shown to decrease circulating neutrophil and eosinophil accumulation, decrease intracellular oxidative activity and reduced the expression of CD49d after antigen exposure[12],[13],[14].
[edit] Technology Focus IMULAN's technologies currently focused on the following disease targets: Feline leukemia virus (FeLV) is a retrovirus that infects cats. As a retrovirus, the genetic information of FeLV is carried by RNA instead of DNA. FeLV is usually transmitted between infected cats when the transfer of saliva or nasal secretions is involved. If not defeated by the animal’s immune system, the virus can be lethal. There are many possible outcomes as to how successfully the cat’s immune system will react to the virus. About forty percent of cats extinguish the virus. Sixteen percent fight it off due to minimal exposure to it. The other twenty-four percent resist the virus at phase four, which will be described later. All of this usually occurs between sixteen to eighteen weeks after the FeLV infection begins. About twenty percent are able to put the virus into a latent stage, in which the virus will remain until the cat becomes stressed causing the FeLV to re-emerge. About five to ten percent of cats go through a sequestered stage in which viremia is limited, intermittent, or absent altogether. Approximately thirty percent of cats go through the disease from start to finish, normally resulting in death. Once the virus has entered the cat, there are six phases to a FeLV infection: Phase one is when the virus enters the cat, usually through the pharynx where it infects the epithelial cells and infects the tonsillar B-lymphocytes and macrophages. These white blood cells then filter down to the lymph nodes and begin to replicate. In phase two, the virus enters the blood stream and begins to distribute throughout the body. Phase three starts when the lymphoid system (which produces antibodies to attack infected and cancerous cells) becomes infected, with further distribution throughout the body. Phase four is the main point in the infection, where the virus can take over the body's immune system and cause viremia. During this phase the hemolymphatic system and intestines become infected. If the cat's immune system does not fight off the virus, then it goes onto phase five where the bone marrow becomes infected. At this point, the virus will stay with the cat for the rest of its life. In this phase, the virus replicates and is released four to seven days later in infected neutrophils (white blood cells), and sometimes lymphocytes, monocytes (white blood cell formed in the bone marrow), and eosinophils (another white blood cell). At phase six the cat's body is overwhelmed by infection and mucosal and glandular epithelial cells (tissue that forms a thin protective layer on exposed bodily surfaces and forms the lining of internal cavities, ducts, and organs) become infected. The virus replicates in epithelial tissues including salivary glands, oropharynx, stomach, esophagus, intestines, trachea, nasopharynx, renal tubules, bladder, pancreas, alveolar ducts, and sebaceous ducts from the muzzle. Cats diagnosed as persistently infected by ELISA testing may die within a few months or may remain asymptomatic for up to 4 years. The fatal diseases are leukemias, lymphomas, and non-regenerative Anemias. Although there is no known cure for the virus infection, in 2006 the United States Department of Agriculture approved Lymphocyte T-Cell Immunomodulator as a treatment aid for FeLV and/or FIV infections Feline immunodeficiency virus (FIV) is a lentivirus that affects domesticated housecats worldwide and is the causative agent of feline AIDS. Approximately 11% [1] of cats worldwide, and about 2.5% of cats in the USA, [2] are infected with FIV. FIV differs taxonomically from two other feline retroviruses, feline leukemia virus (FeLV) and feline foamy virus (FFV) and is more closely related to human immunodeficiency virus HIV. Within FIV, five subtypes have been identified based on nucleotide sequence differences coding for the viral envelope (env) or polymerase (pol). FIV is the only non-primate lentivirus to cause an AIDS-like syndrome, but FIV is not always a death sentence for cats, as they can live relatively healthily as carriers and transmitters of the disease for many years. [edit] Management - Chief Executive Officer - Craig Woods DVM, MS, MBA
- Chief Scientific Officer - Daniel Gingerich DVM, MS
- Chief Operating Officer - Randall Woods DO (ophthalmologist)
- General Manager - Gerhard Poppel MS
- Clinical Director - Brett Cordes DVM
- Business Director - Tom Overbay DVM
- Operations - Heather Hurst
[edit] Address and Contact - Kit Bond Science and Technology Incubator
- 4221 Mitchell Avenue
- St. Joseph, MO 64507
- 816.749.4016 Phone
- www.IMULAN.com
[edit] Company Partners - AIM Therapeutics, Inc. - license agreements - (ImSAIDs anti-inflammatory platform)
- University of Arizona - license agreements
- T-Cyte Therapeutics, Inc. - license agreements (Lymphocyte T-Cell Immune Modulator)
- ImmunoPhotonics, Inc. - license agreements (cancer laser)
- ProLabs Animal Health, a division of Agri Laboratories - distributor agreement
[edit] Sources and notes - ^ United States Department of Agriculture. Veterinary Biological Products; Licensees and Permittees, December 2006.[1]
- ^ Beardsley, et al. "Induction of T-Cell Maturation by a Cloned Line of Thymic Epithelium (TEPI) Immunology 80: pp. 6005-6009, (Oct. 1983).
- ^ Beardsley, Terry R. Patent # 7,196,060; Method to enhance hematopoiesis. Method to enhance hematopoiesis - Google Patents at www.google.com
- ^ "TCR Vax Technical Summary". http://www.imulan.com/Resources/TCR_Peptide_Summary.pdf.
- ^ "ImSAIDs Technical Summary". http://www.imulan.com/Resources/ImSAIDS_Tech_Summary.pdf.
- ^ Bao F, John SM, Chen Y, Mathison RD, Weaver LC. The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord. Neuroscience. 2006 Jul 7;140(3):1011-22. Epub 2006 Apr 3.
- ^ Mathison RD, Befus AD, Davison JS, Woodman RC. Modulation of neutrophil function by the tripeptide feG. BMC Immunol. 2003 Mar 4;4:3. Epub 2003 Mar 4
- ^ Mathison R, Davison JS, Befus AD. Neuroendocrine regulation of inflammation and tissue repair by submandibular gland factors. Immunol Today. 1994 Nov;15(11):527-32. Review.
- ^ Mathison RD, Malkinson T, Cooper KE, Davison JS. Submandibular glands: novel structures participating in thermoregulatory responses. Can J Physiol Pharmacol. 1997 May;75(5):407-13.
- ^ Dery RE, Mathison R, Davison J, Befus AD. Inhibition of allergic inflammation by C-terminal peptides of the prohormone submandibular rat 1 (SMR-1). Int Arch Allergy Immunol. 2001 an-Mar;124(1-3):201-4.
- ^ Mathison RD, Christie E, Davison JS. The tripeptide feG inhibits leukocyte adhesion. J Inflamm (Lond). 2008 May 20;5:6.
- ^ Dery RE, Ulanova M, Puttagunta L, Stenton GR, James D, Merani S, Mathison R, Davison J, Befus AD. Frontline: Inhibition of allergen-induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro-endocrine pathway. Eur J Immunol. 2004 Dec;34(12):3315-25
- ^ Mathison RD, Davison JS. The Tripeptide feG Regulates the Production of Intracellular Reactive Oxygen Species by Neutrophils. J Inflamm (Lond). 2006 Jun 15;3(1):9
- ^ Mathison R, Lo P, Tan D, Scott B, Davison JS. The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation. Neurogastroenterol Motil. 2001 Dec;13(6):599-603.
IMULAN website - Medical News Today
- DVM Newsmagazine
- Veterinary Products News
- BioSpace - website
- Flinn Foundation website
- Arizona BioIndustry website
[edit] External links |
