Sunivera Immunotherapy

The Future of Immunotherapy - Today

Sunivera Immunotherapy


Sunivera ImmunotherapyTM combines one of the world’s most powerful immunotherapy agents, GcMAF, with synergistic therapies and nutraceuticals that work together to modulate the innate and adaptive immune systems. This proprietary Hope4Cancer therapeutic protocol combines 25 years of research expertise at leading Japanese and U.S.-based research centers with Hope4Cancer’s clinical experience in natural cancer therapies.

Why is Sunivera important for you? The immune system keeps our body free of pathogens and nips in the bud any abnormal cell growth that could lead to cancer. One of the major hallmarks of cancer is its ability to turn off or avoid the immune system, which allows its uninterrupted growth. Sunivera brings light into the immune-depleted darkness of cancer.

Treatment Highlights

  • Replaces a cancer-depleted, natural biomolecule, GcMAF, essential for the ability of the immune system to kill cancer cells.
  • Based on three generations of research optimization at some of the leading research and progressive pharmaceutical centers in Japan.
  • Avoids the pitfalls of conventional immunotherapies. Sunivera DOES NOT:
    • Risk over-activation of the immune system, causing serious autoimmune problems.
    • Require the alteration of genes in immune system T-cells with unknown downstream consequences.
    • No known side effects.
  • The complete Sunivera protocol is a holistic treatment approach that rebuilds the immune system from a variety of angles, even as it works synergistically with other Hope4Cancer therapies to maximize benefit.

How It Works

GcMAF (Gc Protein Derived Macrophage Activating Factor) is a naturally produced glycoprotein in cells obtained from the Vitamin D3-binding (serum Gc) protein. GcMAF is responsible for activating immune system macrophages into a form that can recognize and kill cancer cells. However, cancer cells produce an enzyme, a-N-acetylgalactosaminidase (Nagalase) that deglycosylates serum Gc protein, consequently preventing its conversion into GcMAF (Figure 1).1


[Sunivera Immunotherapy] Mechanism of Action of GcMAF in the Body
Figure 1. Mechanism of Action of GcMAF in the Body
Macrophages exist in a variety of forms, and in the absence of pathogens or cancer cells, can lie dormant awaiting an activating stimulus. Once activated, macrophages become capable of consuming and breaking down the invading cells (Figure 2). However, a dysfunctional activating mechanism can result in macrophages either lying dormant or getting subverted by the cancer in the tumor micro-environment.2-3

[Sunivera Immunotherapy] The role of macrophages in eliminating cancer cells, pathogens, and cellular debris
Figure 2. The role of macrophages in eliminating cancer cells, pathogens, and cellular debris.
However, more recent understanding of the complex mechanisms behind macrophage activation have shown that the nagalase model is too simplistic. While not fully understood, laboratory evidence has shown that GcMAF activates macrophages productively to attack pathogens and cancer cells, while having a positive impact on autoimmune conditions as well. Please keep an eye on this page and our blog for more information as we continue our study of the rapidly-growing world of cancer immunotherapy.

Next Generation Injectable and Oral GcMAF

In 2008, researchers reported that the administration of GcMAF resulted in regression of tumors and long-term benefits for cancer patients.4 Researchers at the University of Tokushima and Saisei-Mirai immunotherapy centers in Japan have now developed a patented process for the world’s most advanced injectable GcMAF (second generation GcMAF), 15 times more potent than the first generation product. After treatment of over 1000 patients at Saisei-Mirai, the researchers have found the product safe and effective against a variety of cancers.5-8

Colostrum MAF, an oral version of GcMAF is also available9 – both the injectable and oral forms cross the blood-brain barrier.

As part of our collaboration with Saisei-Mirai, the latest oral and injectable forms of GcMAF are now available at Hope4Cancer Treatment Centers as part of the Sunivera Protocol.

How Does Sunivera Differ from Existing Immunotherapies?

As an endogenous bioidentical molecule, GcMAF has a very big advantage over currently available immunotherapies.10 Besides less expense and ease of administration, it does not cause serious side effects through the over-stimulation of the immune system (PD1/PD-L1 immune checkpoint inhibitors) or introduction of genetically-altered immune system cells (adoptive T cell transfer). While the latter methodology has generated considerable excitement, it is significant to note that adoptive T cell transfer requires first that the patient go through “immunotransplant”, which essentially first involves killing off the patient’s immune system with chemotherapy or radiation.11-12

Synergistic Combination of Sunivera With Other Therapies

Clinical experience in Japan has shown that the benefits of GcMAF can be enhanced when used in combination with other non-toxic cancer approaches.5 Sunivera Immunotherapy represents the optimal integration of GcMAF with Hope4Cancer’s synergistic therapies and nutraceuticals that modulate both the innate (macrophages) and adaptive (NK cells and T cells) immune response. In combination with treatments such as Sono-Photo Dynamic Therapy and Tumor Treating Fields,4 Sunivera favorably alters the tumor microenvironment13 to a healthier state. This sets the patient on a steady path towards disease resolution and improved quality of life.

Disclaimer: Hope4Cancer treats cancer patients with GcMAF only at its Mexico treatment centers; the product is not available for purchase outside the borders of Mexico. Our GcMAF brand is obtained from Saisei-Mirai clinics in Japan who have conducted extensive collaborative research on three generations of the product in association with Tokushima University.


  1. Yamamoto, N.; Kumashiro, R. Conversion of Vitamin D binding protein (group-specific component) to a macrophage activating factor by the stepwise action of ß-galactosidase of B Cells and sialidase of T Cells. J. Immunol. 1993, 151 (5), 2794-2802.
  2. Noy, R.; Pollard, J. W. Tumor-Associated Macrophages: From Mechanisms to Therapy. Immunity 2014, 41, 49-61.
  3. Sumiya, Y. U.; Inoue, T.; Ishikawa, M.; Inui, T.; Kuchiike, D.; Kubo, K.; Uto, Y.; Nishikata, T. Macrophages Exhibit a Large Repertoire of Activation States via Multiple Mechanisms of Macrophage-activating Factors. Anticancer Res. 2016, 36 (7), 3619-23.
  4. Yamamoto, N.; Suyama, H.; Yamamoto, N. Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF. Trans. Oncol. 2008, 1 (2), 65-72.
  5. Inui, T.; Amitani, H.; Kubo, K.; Kuchiike, D.; Uto, Y.; Nishikata, T.; Mette, M. Case Report: A Non-small Cell Lung Cancer Patient Treated with GcMAF, Sonodynamic Therapy and Tumor Treating Fields. Anticancer Res. 2016, 36 (7), 3767-70.
  6. Inui, T.; Katsuura, G.; Kubo, K.; Kuchiike, D.; Chenery, L.; Uto, Y.; Nishikata, T.; Mette, M. Case Report: GcMAF Treatment in a Patient with Multiple Sclerosis. Anticancer Res. 2016, 36 (7), 3771-4.
  7. Inui, T.; Kuchiike, D.; Kubo, K.; Mette, M.; Uto, Y.; Hori, H.; Sakamoto, N. Clinical experience of integrative cancer immunotherapy with GcMAF. Anticancer Res. 2013, 33 (7), 2917-9.
  8. Inui, T.; Makita, K.; Miura, H.; Matsuda, A.; Kuchiike, D.; Kubo, K.; Mette, M.; Uto, Y.; Nishikata, T.; Hori, H.; Sakamoto, N. Case report: A breast cancer patient treated with GcMAF, sonodynamic therapy and hormone therapy. Anticancer Res. 2014, 34 (8), 4589-93.
  9. Amitani, H.; Sloan, R. A.; Sameshima, N.; Yoneda, K.; Amitani, M.; Morinaga, A.; Uto, Y.; Inui, T.; Asakawa, A. Development of colostrum MAF and its clinical application. Neuropsychiatry (London) 2017, 7 (2), 640-647.
  10. Akiyama, S.; Inui, T. Cancer Immune Therapy in Clinic: 2016. Clinics in Oncology 2016, 1, 1-3.
  11. Bollard, C. M.; Gottschalk, S.; Leen, A. M.; Weiss, H.; Straathof, K. C.; Carrum, G.; Khalil, M.; Wu, M. F.; Huls, M. H.; Chang, C. C.; Gresik, M. V.; Gee, A. P.; Brenner, M. K.; Rooney, C. M.; Heslop, H. E. Complete responses of relapsed lymphoma following genetic modification of tumor-antigen presenting cells and T-lymphocyte transfer. Blood 2007, 110 (8), 2838-45.
  12. Dudley, M. E.; Wunderlich, J. R.; Yang, J. C.; Sherry, R. M.; Topalian, S. L.; Restifo, N. P.; Royal, R. E.; Kammula, U.; White, D. E.; Mavroukakis, S. A.; Rogers, L. J.; Gracia, G. J.; Jones, S. A.; Mangiameli, D. P.; Pelletier, M. M.; Gea-Banacloche, J.; Robinson, M. R.; Berman, D. M.; Filie, A. C.; Abati, A.; Rosenberg, S. A. Adoptive cell transfer therapy following non-myeloablative but lymphodepleting chemotherapy for the treatment of patients with refractory metastatic melanoma. J Clin. Oncol. 2005, 23 (10), 2346-57.
  13. Brown, J. M.; Recht, L.; Strober, S. The Promise of Targeting Macrophages in Cancer Therapy. Clin. Cancer Res. 2017, 23 (13), 3241-3250.

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